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GENERAL Fasciculus = bundle of axons in the CNS Funiculus = cord areas (stains black) Lemniscus = ribbon shaped fiber tract (stains black) Ipsilateral = same side Contralateral = opposite side Bilateral = both sides Decussate = crossover
Afferent = sensory Efferent = motor
Prosencephalon (forebrain) Telencephalon Diencephalon
Mesencphalon (midbrain)
Rhombencephalon (hindbrain) Medulla Pons Cerebellum
Aphasia = speech deficits Paraplegics do have reflexes due to intrinsic wiring in spinal cord “reflex arch”
Spinal Cord DORSAL (mainly sensory) Dorsal columns = discriminating touch and proprioception (don’t cross in spinal cord) Spinothalamic = pain and temperature (decussates at anterior white commissure)
VENTRAL (mainly motor) Corticospinal tract = efferent, voluntary skilled motor
- anterior median fissure (anterior spinal artery) - posterior median fissure - posterior intermediate fissure - posterior lateral fissure
Coverings - dura mater - arachnoid mater - pia mater
Denticulate ligaments = made of pia: connects spinal cord to arachnoid and dura mater Conus medularis = end of spinal cord L1- L2 Filum Terminale = made of pia: connects spinal cord to dura mater at end of canal
SACRAL LEVEL: Small with cauda equina ¯ white matter; gray matter
LUMBAR LEVEL: Ventral horn = hearts, anterior horn cells = alpha motor neurons
THORACIC LEVEL white matter; ¯gray matter Why? Haven’t given off as much motor and have taken up more sensory Intermedial lateral gray (origin of sympathetic fibers) Nucleus dorsalis of Clark Dorsal columns (discriminating touch and proprioception): Fasciculus gracilis (medial): info from below mid thoracic level Fasciculus cuneatus (lateral): info from the mid thoracic level and up
CERVICAL LEVEL ventral gray matter (for brachial plexus)
Brain Stem
CRANIAL NERVES Midbrain CN 3 oculomotor -midline CN 4 trochlear – from the dorsal side of brainstem Pons CN 5 trigeminal –exits from the substance of pons Pontomedullary junction CN 6 abducens CN 7 facial CN 8 vestibulocochlear Medulla CN 9 glossopharyngeal CN 10 vagus CN 11 accessory –coming up from spinal cord CN 12 hypoglossal –between medullary pyramid and olive
MEDULLA CLOSED Corticospinal tract decussates at medullary spinal jct; travel in pyramids Damage rostral to decussation = contralateral motor damage Damage caudal to decussation = ipsilateral motor damage Nucleus gracilis and cuneatus – seen grossly as gracilis and cuneatus tubercles Medial lemniscus Fibers from the dorsal columns: (already crossed in reticular formation) Obex – most caudal point of 4th ventricle OPEN Tegmentum of 4th ventricle at level of medulla: Medial bump is hypoglossal trigone (hypoglossal nucleus) Lateral bump is vagal trigone (dorsal motor nucleus of vagus) Inferior cerebellar peduncle appears PONS Inferior cerebellar peduncke – sensory info spinal cord ® cerebellum Middle cerebellar peduncle – pons ® cerebellum Superior cerebellar peduncle – carries output of cerebellum Basilar artery on ventral side of pons
MIDBRAIN Cerebral peduncle Cerebral aqueduct Roof: inferior and superior colliculi Superior cerebellar peduncle fibers cross (decussation of brachium conjuctivum) Substantia Nigra = produces dopamine, degenerates in Parkinson’s disease
Tectum = roof Tegmentum = floor
Cerebellum
Cerebellar nuclei (seen in x-sec of caudal pons) - 4 pairs composed of giant efferent neurons - only neurons of cbl that have axons that leave the cerebellum - medial ® lateral fastigial globose emboliform dentate
cerebellar lobes (lobes ® lobules ® folia) - anterior lobe –degeneration in chronic alcoholism and in hereditary ataxias primary fissure – best seen from sagittal view - posterior lobe - flocculonodular lobe anterior of cerebellum midline: nodulus (part of vermis) wings: flocculous
vermis – longitudinal strip in midline hemispheres –right and left each having lateral and intermediate portions tonsils – can herniate through foramen magnum
inferior cerebellar peduncle (restiform body) sensory info spinal cord ® cerebellum juxtarestiform body – communicating axons between vestibular structures and cbl
middle cerebellar peduncle pons ® cerebellum
superior cerebellar peduncle carries OUTPUT of cerebellum ® brainstem these axons arise from cerebellar nuclei
CEREBELLAR HISTOLOGY
Cerebellar cortex (3 layers) gray matter: homogeneous structure 1. molecular layer (outermost) - ¯ cells, mostly axons and dendrites Basket cells – interneuron, inhibitory Stellate cells – interneuron, inhibitory
2. purkinje layer (middle) – monolayer of large cell bodies only cell bodies to have axons that leave the cbl cortex to end in cbl nuclei
3. Granule layer (innermost) – density of neurons (most dense in entire brain) Granule cells Granule cells head toward molecular layer. There they bifurcate to become parallel fibers These parallel fibers have direct input into purkinje cell dendrites Golgi cells Interneurons
White matter (2 fiber types) 1. Climbing fibers Arise: ONLY in olivary complex Run: ONLY in inferior cerebellar peduncle Terminate: Purkinje cell dendrites in molecular layer Memorize the letter “i” for climbing, olive, inferior cbl peduncle *Direct synapse onto Purkinje (which then sends its axon out cbl cortex)
2. Mossy fibers Axons of all other inputs Arise: spinal cord, medulla (except olive), pons Run: inferior and middle cerebellar peduncles Terminate: granule cell layer on glomerulus Mossy® glomerulus ® granule cell ® molecular layer ® purkinje ® cbl nuclei *Indirect input to Purkinje cells via granule cells
cerebellar function
Planning movements Coordination Execution of movement Postural maintenance Motor learning and adjustments
DIENCEPHALON
PARTS
1. Thalamus 2. Hypothalamus 3. Epithalamus 4. Subthalamus
LIMITS Anterior limit (separates 3rd ventricle from subarachnoid space) Lamina terminalis – runs between optic chiasm and anterior commissure
Posterior limit (separates diencephalon from mesencephalon) Dividing line between the mammillary bodies and posterior commissure
Internal division Hypothalamic sulcus (depression in wall of 3rd ventricle; separates thalamus from hypothalamus)
THALAMUS
· relay between cerebrum and brainstem · we are responsible for 5 nuclei 1. Lateral geniculate body - located: posterior-inferior side near junction of the midbrain and diencephalon - associated with optic tract - sensory relay nucleus for visual system 2. Medial geniculate body - located: medial to lateral geniculate body - relay nucleus for auditory system 3. Centromedian nucleus - located: posterior middle part of thalamus always just medial to VPM - lies within the internal medullary lamina 4. Anterior nucleus - walled off by internal medullary lamina - destination of mamillothalamic tract - degenerates in Alzheimer’s disease and senile dementia 5. External reticular nucleus - Thin layer that lies between the external medullary lamina and internal capsule · Internal capsule lateral to thalamus (if you can see thalamus must be posterior limb of internal capsule) connects cerebrum to brainstem corticospinal fibers found here · Interthalamic adhesion or massa intermedia
HYPOTHALAMUS
· 3 parts 1. Optic (anterior) part (over optic chiasm) 2. Infundibular (middle) part 3. Mamillary (inferior) part · Divided into medial and lateral portions by the fornix · Hypothalamus axons (from mammillary bodies) ® mamillothalamic tract ® anterior nucleus of thalamus · Pituitary gland 1. Posterior lobe (neurohypophysis) is formed from outgrowth of hypothalamus - Neural connections to nuclei that produce oxytocin and vasopressin 2. Anterior lobe (adenohypophysis) grows out of Rathke’s pouch (roof of mouth)
EPITHALAMUS
· Located: dorsal inferior part of thalamus · Most caudal aspect of diencephalon · Contains: 1. Posterior commissure 2. Habenular nuclei 3. Pineal gland · Pineal gland - lies caudal to posterior commissure and habenular nuclei - produces melantonin - secretion of melantonin is controlled by light
SUBTHALAMUS
· located: ventral to thalamus · includes: 1. subthalamic nucleus 2. zona incerta 3. prerubral fields of forel (fiber bundles rostral to red nuclei)
SUBCORTICAL TELENCEPHALIC NUCLEI
BASAL GANGLIA = CORPUS STRIATUM Neostriatum (new part) 1. Caudate nucleus 2. Putamen Paleostriatum (old part) 3. Globus Pallidus
Lenticular nucleus = putamen and globus pallidus
Involved in planning stages of motor function
Caudate Nucleus · Associated with lateral ventricle · Internal capsule separates caudate from lenticular nucleus Anterior limb = lenticulo-caudate limb (ID: if you see septum pellucidum medially) Posterior limb = lenticulo-thalamic limb (ID: if you see thalamus medially)
Meynert’s Nucleus Degenerates in Alzheimer’s Located: ventral to anterior commissure Substantia Nigra Degenerates in Parkinson’s disease
LIMBIC SYSTEM Involved in initiation of behavior necessary for survival and propagation of the species Follows a C – shape Degenerates in Alzheimer’s disease
CORTICAL PART (rostral – caudal along C) 1. Subcallosal gyrus 2. Cingulate gyrus 3. Parahippocampal gyrus 4. Uncus
DEEP TO CORTICAL PART (rostral – caudal along C) 1. mallillary bodies 2. Fornix columns body crura 3. hippocampus 4. amygdaloid bodies
Both amygdala and hippocampal formation connect to hypothalamus
STRIA TERMINALIS Connects amygdala ® hypothalamus and septal nuclei STRIA MEDULLARIS Connects habenular nuclei ® septal nuclei
CEREBRAL HEMISPHERES
SULCUS Medial longitudinal fissure – divides right from left Central sulcus – divides frontal lobe from parietal lobe Lateral fissure – insular lobe is deep to it, temporal lobe lies ventral to it Parieto-occipital sulcus – most prominent in mid-sagittal section Calcarine sulcus Collateral sulcus – between parahippocampal and occipitotemporal gyrus more caudal Rhinal sulcus - between parahippocampal and occipitotemporal gyrus more rostral Olfactory sulcus – between gyrus rectus and orbital gyri
LOBES Frontal lobe Parietal lobe Temporal lobe Occiptal lobe Insular lobe
GYRUS Frontal Lobe: Precentral gyrus = motor Postcentral gyrus = sensory Superior, Middle, and Inferior Frontal Gyrus Gyrus rectus Orbital gyri
Temporal Lobe: Superior Temporal gyrus = primary auditory cortex lies on section in lateral fissure Middle and Inferior Temporal gyrus
Temporal, Occipital, and Parietal Lobes Supramarginal gyrus = horseshoe around lateral fissure Angular gyrus = adjacent to supramarginal in a traingular shape
Insular Lobe: Transverse Temporal gyrus (Heschl’s gyri) = part of primary auditory cortex
Occipital Lobe: Primary Visual Cortex = located bilaterally on either side of calcarine fissure Cuneus (wedge shaped portion dorsal to calcarine fissure) Lingula (tongue shaped portion ventral to calcarine fissure)
Ventral ® Dorsal - Corpus callosum - Sulcus of corpus callosum - Cingulate gyrus ® isthmus ® parahippocampal gyrus - Cingulate sulcus
Uncus = Medial directed bump on parahippocampal gyrus / amygdala lies deep to it Occipito – temporal gyrus = lies lateral to parahippocampal gyrus BRODMAN NUMBERS
Primary somatosensory 3, 1 and 2 postcentral gyrus Primary motor cortex 4 precentral gyrus Supplementary motor cortex 6 Broca’s (motor speech) 44 and 45 inferior frontal gyrus Wernicke’s (sensory speech) 22 superior temporal gyrus Primary auditory cortex 41 and 42 superior temporal gyrus and transverse temporal gyrus Primary visual cortex 17 occipital pole / sides of calcarine fissure (cuneus + lingula) Visual coordinating areas 18 and 19
4 TYPES OF WHITE MATTER
1. Commmisural fibers · Corpus Callosum Rostrum Genu (knee) Body/Trunk Splenium · Anterior commisure Most dorsal aspect of lamina terminalis Splays out laterally Communicates: temporal lobes ® olfactory lobes · Other comisures that are not telencephalic Posterior commissure Part of diencephalon (epithalamus) Communicates: left superior and inferior colliculi ® right sup. and inf. colliculi Habenular commisure Part of diencephalon (epithalamus) Communication: diecephalon ® limbic
2. Corona radiata Fanned out white matter directly underneath the cortex Collect into internal capsule
3. Projection fibers Origin in a neuron cell body in cortex Goes out of cortex to underlying structures
4. Association fibers Ipsilateral communication Uncinate fasciculus Communicates: frontal lobe ® temporal lobe Cingulum Communicates: limbic ® cortex Arcuate fasciculus Communicates: Broca’s area ® Wernicke’s area
VENTRICULAR SYSTEM
LATERAL VENTRICLES Anterior horn Body Posterior (occipital) horn Inferior (temporal) horn Trigone (atrium) – where all three horns meet
THIRD VENTRICLE Located: between medial thalamic walls Lamina terminalis – anterior limit of ventricular system Supra-optic recess Infundibular recess Pineal recess
CEREBRAL AQUEDUCT Located: only in midbrain Communicates: 3rd and 4th ventricles
FOURTH VENTRICLE Located: inbetween open medulla / pons and cerebellum Tectum (roof) = superior medullary velum CSF exits ventricular system into the subarachnoid space - Foramen of Magendie: on the midline - Foramen of Luschke: lateral
CSF
CHOROID PLEXUS Formed by: Choroid epithelium (modified ependyma) Blood vessels Connective tissue
Blood suppy: Anterior choroidal artery (branch of internal carotid artery) Posterior choroidal artery (branch of posterior cerebral artery)
Found: Ventral floor of lateral ventricles Posterior horn ® trigone area ¯ Foramen of Monro (interventricular foramen) – connects: lateral ventricles and 3rd ventricle ¯ Dorsal roof of 3rd ventricle ¯ NO CHOROID PLEXUS IN CEREBRAL AQEDUCT ¯ pops up in 4th ventricle
Ependyma
Cuboidal cells that line ventricles in a continuous single layer Gap junctions (leaky) Cilia to aid movement of CSF Modified form of these cells make choroid plexus
Capillary Endothelial Cells
Blood brain barrier Tight junctions Few pinocytotic vesicles mitochondria for active transport Astrocytic feet (podocytes) Surround endothelial cells Protectors of blood brain barrier Maintain ion balance
FORMATION OF CSF
CHOROID PLEXUS is major producer Hydrostatic pressure between brain capillaries and choroid epithelium pushes water and ions out and into ventricles \an in serum osmolality ¯ CSF formation (does not favor filtration) Active transport Vitamin C Nucleotides Folates Pyridoxal phosphate Ion Exchange Sodium Chloride Potassium
EXTRACHOROIDAL FORMATION Transependymal movement (leakage of water through gap junctions in ependymal cells)
ABSORPTION OF CSF Rate of absorption = rate of formation pressure, absorption
Arachnoid villi and granulations Major absorptive components of CSF Herniations of arachnoid Penetrate gaps in dura Protrude into lumen of superior sagittal sinus Vacuoles in arachnoid cells pick up CSF ® empty into venous system
FUNCTIONS OF CSF Physical support Buoyancy reduces weight Cushioning against shock Excretory No lymphatics for brain CSF carries away metabolic wastes Intracerebral transport Control of chemical environment
COMPOSITION OF CSF Colorless Lot less protein than blood
DISEASES Meningitis Bacterial - protein, WBC, ¯ glucose Viral – protein and glucose normal, WBC Fungal - protein, WBC, ¯ glucose Fungal Infections Multiple sclerosis Demyelination or sclerotic plaques WBC, protein IgG present Viral Infections CSF not valuable diagnostic tool Brain Tumor Increased pressure in cranium (hydrocephaly) Decreased pressure in cord \Spinal Taps Are Not Recommended (danger of herniation) Reyes Syndrome (Hepatitic Encephalopathy) Children Viral disease of liver Aspirin ammonia ® brain causes deimensia and night terrors
VACULATURE
REGULATION OF BLOOD FLOW 3 mechanisms 1. Autoregulation Vessels constrict and dilate depending on blood pressure 2. Response to metabolites Vessels dilate when ¯ oxygen, CO2, ¯ pH 3. Autonomic nervous system
CEREBRAL VASCULAR DISEASE 1. Occlusive disease –extracranial 2. Thrombus – blood clots 3. Embolism – caused by blood clots or plaques breaking free 4. Hemorrhage 5. Aneurysm – dilation of vessel wall due to thinning or weakness
ARTERIES
Spinal Cord Vertebral artery Anterior spinal artery (anterior 2/3 of spinal cord) Posterior spinal artery (dorsal 1/3 of spinal cord) Radicular arteries Come from intercostal arteries or descending aorta Supply cord, vertebra, and meninges Artery of Adamkiewicz from descending aorta major supply of bottom 2/3 of cord
Brain Internal Carotids Carotid canal ® cavernous sinuses (zig-zags to form carotid siphon) ® branches Branches Opthalmic artery Anterior choroidal artery Posterior communicating artery Bifurcates Anterior cerebral artery – supplies medial side Medial striate arteries caudate part of internal capsule Middle cerebral artery – supplies lateral side Lenticulostriate arteries rest of internal capsule globus pallidus putamen
Verterbral arteries –transverse through cervical vertebra’s transverse foramen PICA – posterior inferior cerebellar artery Basilar artery –formed from union of vertebral arteries AICA - anterior inferior cerebellar arteries Labyrinthine artery (auditory) Pontine arteries Superior cerebellar artery Posterior cerebral artery Thalomogeniculate arteries
Anastomotic connections Circle of Willis Internal carotid or middle cerebral artery Anterior cerebral arteries Anterior communicating artery Posterior communicating artery Posterior cerebral Terminal ends of cerebral arteries
VEINS
straight sinus ®transverse sinus ® sigmoid sinus ® jugular vein
Lateral superficial veins ® sinuses or jugular vein
Deep veins ® straight sinus
Internal cerebral veins ® great vein of Galen ® straight sinus
Thalamostriate vein –associated with stria terminalis
DEVELOPMENT OF NEURAL SYSTEM
3rd week nervous system first appears
notochord (medoderm) induces ectoderm ® neural plate now these cells have neural fate
neural groove forms neural crests rise on either side
neural crests meet at midline ® neural tube ectoderm closes over it Anacephaly: failure of anterior neuropore to close Spina Bifida: failure of posterior neuropore to close
Neural tube ® will form entire CNS (brain and spinal cord) Neural Crest cells ® many migrate and form most of PNS (site of migration determines fate) - Dorsal root ganglia - Cranial ganglia - Autonomic ganglia - Enteric neurons in gut - Glia in PNS - Adrenal medullary (chromaffin cells) Neural Canal (lumen of neural tube) ® ventricular system
4th week – 3 vesicle stage
prosencephalon mesencephalon rhombencephalon
cephalic flexure at midbrain develops
5th week – 5 vesicle stage
Prosencephalon Telencephalon –cerebral cortex, basal ganglia, limbic system, and olfactory Diencepalon – thalamus, hypothal., epithal., subthal., neural retina, and optic tract
Mesencephalon - midbrain
Rhombencephalon Metencephalon – pons / cerebelllum myelencephalon – medulla
Sulcus Limitans
Divides neural tube into dorsal and ventral portions Alar plate Dorsal = Sensory
Basal plate Ventral = Motor
Persists into 4th ventricle Continues as hypothalamic sulcus in diencephalon
EMBRYO / HISTOLOGY
Neural Tube (stratified epithelium) cells move:
Pial surface (DNA synthesis) ¯ ventricular surface (mitosis)
Daughter cells then divide and differientiate Neuroblasts Glioblasts Ependymal (line venticles) Radial (important in migration railroad track)
SPINAL CORD Ependymal layer (from glial cells) Mantle layer ( H-shaped gray matter) Marginal layer (myelinated axons / white matter)
New neurons: pre-natally only New glial cells: pre- and post-natally Myelination: pre- and post-natally
MIGRATION · Radial cell scaffold Interacts with growth cone of leading process of neuron Contact – mediated guidance · Guidepost cells Surface molecules guide neurons · Molecular events Chemoaffinity Cell adhesion to ECM (fibronectin, laminin, and collagen) · Growth cones Guide axons to target Have lamellapodia and filopodia · Neurites Baby axons and dendrites
GROWTH AND DIFFERENTIATION
Regional Identity Rostral – caudal axis determined by gastrulation Dorsal – ventral determined by sulcus limitans Floor plate ® expresses shh
Cell Identity Intrinsic factors –genetic within cells Extrinsic factors – diffusable factors, neurotrophic factors, environment, cell –cell interactions
Neurons differentiate first then glial cells
Neuroblasts = spherical baby neuron One neurite process becomes axon
SYNAPTOGENESIS Nerve gets to muscle and causes Ach receptors to aggregate around axon Basal lamina is established
MYELINATION In CNS: oligodendrites Develops relatively late Sensory areas are done first Continues after birth (clumsy baby)
MATURATION More processes ® greater area of synapses ® greater functional interaction Elaboration of dendritic tree is sign of maturity
CELL DEATH Function: reduce population to appropriate # of nerve cells with appropriate connections
Intrinsic cell death (apoptosis – programmed) Extrinsic cell death (fail to form appropriate conneciton)
NEURON HISTO
Cell body = soma = perikaryon Dendritic thorns ® increase surface area
NEURON TYPES Multipolar – most abundant Pseudounipolar – found in dorsal root ganglion Bipolar – special sensory organs
Projection Neuron = long axon = Golgi type II Interneuron = short axon = Golgi type II
ORGANELLES · Centrally located light staining nucleus (due to euchromatic DNA) · Deep staining nucleolus (RNA activity) · Nissl substance (dark staining RER / very metabolically active) –not found in axon · Cytoskeletal elements - Neurotubules (microtubules) Maintain shape of neuron Involved in axon transport Orthograde – in direction of action potential uses kinesin Retrograde – back towards cell body uses dynein - Neurofiliaments (intermediate filaments) Lined longitudinally in axons Form bundles called neurofibrils - Actin (microfilaments) Found in growth cones Function in developmental extension
MYELINATION PNS: Schwann cells / one cell provides one segment of myelin CNS: oligodendrite / one cell provides many axons myelin
Node of Ranvier: gap between myelinated segments thickness of myelin, faster action potention
neurolemma = cell membrane of Schwann cell Satellite Cells: PNS non-myelinating cells function to isolate cell bodies from synapses
SYNAPSES- action potential cascade leads to Ca++ into cell and vesicle release into synapse types Axodendritic Axosomatic Axoaxonic (presynaptic inhibition)
Components Presynpatic terminal Mitochondria Sypnaptic vesicles Presynaptic release sites Sypnaptic cleft Postsynaptic component receptors
Neuropil = space between neuron cell bodies
Tau ® MAP (microtubule associated protein) ® neurofibrillary tangles in Alzheimers
GLIAL HISTO
Glial cells Retain capacity to divide (cancer) Do not form synapses Processes are all similar (no axon vs. dendrites) Do not conduct action potentials
CLASSES OF CNS GLIA 1. Macroglia Astrocyte Oligodendrite Ependymal cells 2. Microglia – macrophages / not derivative of nervous system
FUNCTIONS General: Structural support Myelination Repair and regeneration Development of nervous system Uptake and release of neurotransmitters Isolate neurons Nutritive role Maintain blood brain barrier (do not create, tight junctions do that)
Oligodendrocyte CNS Myelination Mainly found in white matter
Astrocyte CNS Structural support Repair processes (reactive astrocytes become phagocytic) Endfeet provide protection to pia mater “glia limitans” Metabolic exchange between neurons and glia Mainly found in gray matter
Ependymal cells CNS Cuboidal cells that line venticles and have cilia + microvilli Choroid plexus is modification Tanycytes – single central cilium and microvilli
Microglia CNS Resident macrophages Very small and have squiggly processes
Schwann cell PNS Myelination Divide and help in repair of nerves
Satellite cell PNS Non-myelinating cells Isolate ganglion cell bodies
** Absolutely diagnostic for Astrocytes are end feet that project to capillaries or to pia. ** Never see neuron cell bodies in white matter
CYTOARCHITECTURE OF PERIPHERAL NERVE Epimeurium = Surrounds whole nerve Perineurium = Surrounds each nerve fascicle (bundle) Endoneurium = Surrounds individual nerve axons
DORSAL ROOT GANGLION Surrounded by connective tissue Pseudo-unipolar neurons Satellite cells present ID: alternating bands of circular cells bodies and wavy layers of peripheral nerve bundles
SPINAL CORD H-shaped gray matter in center Laminar arrangement of gray matter Layers 1- 6 dorsal horn sensory layer 2 = substantia gelatinosa Layers 7 –9 Ventral horn Motor Layer 10 Central canal
CEREBRAL CORTEX 1. neocortex 1. molecular layer –mostly dendrites / activity on EEG 2. outer granular 3. outer pyramidal 4. inner granular 5. inner pyramidal 6. polymorphic
2. archicortex - hippocampus 3. paleocortex - olfactory
vertical columns of cells act as functional units
INJURY AND REGENERATION
Crush injuries have best prognosis
Complete severence of PNS nerve
Degeneration Events distal to lesion Wallarian degeneration (anterograde degeneration) complete Axon Motor end plates Myelin sheath Schwann cell bodies remian Some divide and form cells Others phagocytize damaged material Events proximal to lesion Axon and myelin sheath degenerate for a node or two Neuron cell body swells Nucleus is pushed off center Chromatolysis: Nissl substance dissolves (ribosomes detach form RER and disperse)
Regeneration Schwann cells form neurolemma or Von Bungner tubes Tips of regenerating axon on proximal side of lesion sends out many growth cones If one of these tips reaches the tube it may reach the target organ again Neroma = when non-connecting tips persist (painful) There is an appropriate time period If appropriate contact is made, there will be re-myelination but not to same degree All the while cell body is restored Closer to spinal cord less chance of regeneration If axon fails to regenerate, cell body will die
Regeneration in CNS Does not occur as well Lack of trophic factors from target organs Oligodendrites secrete inhibitory factors Astrocyte scarring
Stroke Abrupt onset of neurologic deficit Matches cerebral function perfused by vessels Any size vessel can be involved Permanent damage to neuron Symptoms are usually maximal acutely Spasticity occurs chronically
TIA (transient ischemic attack) Abrupt onset of neurologic deficit Matches cerebral function perfused by vessels Neurologic deficit completely resolves over 15 minutes Occurs in big vessels No neurons permanently damaged
A Pure motor stroke is most likely in the internal capsule
Monro – Kellie Doctrine If you put something in your head something else has to come out or the pressure
CPP = MABP – ICP Cerebral Perfusion Pressure = mean arterial blood pressure – intracranial pressure When ICP exceeds blood pressure there is no cerebral blood flow--death
Hydrocephalus is usually caused by obstruction of CSF pathway cerebral aqueduct is most common site of blockage
ION CHANNELS
TYPES OF CHANNELS
1. Non-gated - Responsible for passive properties of membrane (membrane resistance) - Responsible for resting potential
2. Gated Voltage gated channels - responsible for action potentials Ligand gated channels - responsible for PSP’s, EPP’s, and receptor potentials - intracellular ligand or external ligand stretch or pressure gated - responsible for receptor potentials
Ions bind briefly to charged groups within the walls of the channel’s pore. \ flux through channel is not a linear process and channels can be saturated.
CHANNEL SELECTIVITY (not all channels are selective)
· valence of ion (cation channels do not conduct anions and vice versa) · size of hydrated ion (smaller ions have larger hydration shell \ Na+ is “larger” than K+) · shape of hydrated ion · distribution of polar amino acid residues lining pore · affinity of ion for binding to amino acid residues
Selectivity filter – the narrowest region of the channel Ex. Na+ enters channel with 2 water molecules Dissociates from one water Binds to oxygen in an amino acid residue in pore Re-associates with another water on intracellular side
Inward currents (-) Outward currents ( +)
Conductance = 1/R (ohms: V = IR) Resistance = V/I Conductance = I/V
For some channels, flow (I) vs. voltage (V) is linear (ohmic) where slope = conductance
Inward rectification – conductance is greater for inward current (slope is steeper on negative side) Outward rectification – conductance is greater for outward current (slope is steeper on positive side)
Focal process – local conformational change
Activation: closed ® open
Inactivation: open ® inactive closed ® inactive
Removal of inactivation: inactive ® closed (never to open from inactive state)
INACTIVE OR REFRACTORY STATE Non-conduction of ions even when channel is “open”
Mechanisms: 1. Voltage induced– depolarization causes amino or carboxy end of channel protein to block pore. repolarization causes channel to close
2. Ca++ binds to site on inside surface of channel 3. Ca++ induced dephosphorylation
MOLECULAR STRUCTURE OF ION CHANNELS
Sodium and Calcium channels - A single polypeptide with 4 domains of 6 membrane spanning a - helices - The 4th membrane spanning region is a voltage sensor - P – domain forms the pore between 5th and 6th
Potassium channels - one domain of 6 membrane spanning a -helices and a P region between the 4th and 6th - four of these subunits come together to make a channel (\ K+ channel has more diversity)
PATCH CLAMP TECHNIQUE
Single channel recordings Seal pipette on membrane patch Measure conductance of single channel Measure probability that channel will open and close
Whole cell recordings Rupturing membrane patch Measure kinetics and voltage dependence of whole cell trans-membrane ionic currents
Membrane potential – caused by a separation of charge across a membrane
DEVELOPMENT OF K+ EUILIBRIUM POTENTIAL (Ek+ = - 95mV)
Membrane permeable only to K+ K+i > > K+o
Efflux of K+ (non-gated channels) \ positive charge outside & negative inside Diffusion continues until positive charge on outside repels K+ and prevents further net diffusion No net force on ion (Fe = - Fc) electrostatic force is equal and opposite to chemical force Influx K+ = efflux K+ This equilibrium does not occur in the cell. There is a net efflux of K+)
CALCULATION OF EQUILIBRIUM POTENTIALS
Euilibrium potential is proportional to the concentration gradient E µ Co / Ci when Co > Ci E µ Ci / Co when Ci > Co
E is positive if a positive charge on the inside of the cell would oppose diffusion (Na+) E is negative if a negative charge on the inside of the cell would oppose diffusion (K+ & Cl-)
RESTING POTENTIAL (-70 mV) Steady state condition in which there is no net current across cell membrane (sum of all I = 0)
Generated by: Constant diffusion of K+ and Na+ Cl- in skeletal muscle
Depends on: [gradients] of permeable ions (primarily EK & ENa) relative conductances of membrane (gK & gNa)
Calculation: RP = [gK / (gK + gNa)] EK + [gNa / (gK + gNa)] ENa]
“weighted average” – fraction of K conductance times it E plus fraction of Na times its E RP is closer to EK because gK > gNa
ELECTROCHEMICAL DRIVING FORCES DF = (RP – E) DFNa > DFK
CURRENTS I = g (V – E) or I = g (RP –E)
Na+ & K+ aren’t at equilibrium at RP. (K+: Fc > Fe net efflux) & (Na+: Fc & Fe are both directed inward net influx)
Na-K pump Electogenic: makes RP 2 – 4 mV more negative Prevents run down of gradients: maintains RP / amount pumped = amount diffused Stimulated by: increase of intracellular [Na+] Inhibited by: reduction of ATP (hypoxia or ischemia) or cardiac glycosides (ouabain, digitalis) –will depolarize
Hyperkalemia - [Ko], ¯ [Ki]/ [Ko], ¯EK, ¯ K+ efflux, ® depolarize RP I = g (V-E) is decreased \ IK ¯ Hypokalemia - ¯ [Ko], ¯ gK, ® depolarize RP I = g (V-E) is decreased \ IK ¯
Review Driving Force = RP – E Na+ driving force >> K+ driving force K+ conductance > Na+ conductance I = g (Vm – E)
At RESTING POTENTIAL: IK = INa - Hyperpolarization/repolarization (net outward current) IK > INa - Depolarization (net inward current) INa > IK Vm = membrane potential (separation of charge) - moves closer to EK in hyper/repolarization - moves closer to ENa in depolarization
depolarization - opens Na+ channels - opens K+ channels - inactivates Na+ channels (slow or sustained depolarization) repolarization - closes K+ channels - removes inactivation of Na+ channels
STRUCTURAL BASIS OF CHANNEL GATING - Open: depolarization rotates four S4 a-helices clockwise - Inactivation: depolarization moves a positively charged ball into pore (slow) - Close: repolarization rotates four S4 a-helices counter-clockwise - Removal of inactivation: repolarization removes ball
Na+ channels vs. K+ channels Slow depolarization inactivates Na+ channels but not delayed rectifier K+ channels Depolarization increases conductance for both Na+ influx is regenerative but K+ efflux is not
PHASES OF ACTION POTENTIAL
Resting potential IK = INa
Subthreshold IK > INa
Threshold IK = INa
Upstroke IK < INa
Peak IK = INa
Repolarization IK > INa (Na+ channels inactivated, K+ channels open)
Hyperpolarization after a.p. IK > INa
Resting potential IK = INa (K+ channels close due to repolarization)
INa > IK for an action potential to be generated
ALL-OR-NONE All - Amplitude, shape and duration are always the same regardless of stimulus strength Once threshold is reached is action potential is self generating None- If stimulus fails to depolarize to membrane threshold there will be no action potential
ELECTRICAL SYNAPTIC TRANSMISSION
Excitatory actions only No plasticity Bidirectional Faster - No synaptic delay - Channels have ¯ resistance and conduction
Agent of transmission: Ionic current Cytoplasmic continuity bewteen pre and post synaptic terminals Gap junctions 2 connexons each made of 6 connexins passage of ionic current, 2nd messangers, and small molecules
CHEMICAL SYNAPTIC TRANSMISSION Inhibitory (hyperpolarizing) or Excitatory (depolarizing) Plasticity: long lasting changes Myelination Dendritic arborization Axon redirection activity ® thicker, firing rate Unidirectional Slower - synaptic delay (time for transmitters to be released)
Agent of transmission: chemical transmitters Synaptic cleft
Presynaptic terminal Mitochondria and ER to make sure intracellular Ca++ is low Local [Ca++]i is key to transmitter release Active zones(fuzzy dark thickenings) – docking and release
THE STORY 1. presynaptic action potential depolarizes terminal 2. depolarization opens voltage gated Ca++ channels (Ca++ influx) 3. Ca++ allows release of transmitter enriched vesicles from cytoskeleton and exocytosis into cleft 4. Transmitters react with postsynaptic receptors 5. Movement of ions and development of postsynaptic potentials 6. Upon reaching threshold, action potential occurs in postsynaptic neuron
RECEPTORS Membrane spanning Direct / ionophoric / fast / channel and receptor are one in the same / ex: cholinergic and nicotinic Indirect / metabotropic / slow / channel and receptor are two separate entities / use of 2nd messangers
Property of receptor determines action of transmitter
NEUROMUSCULAR JUNCTION (NMJ) Characteristics 1 Muscle fiber (at end plate region) : 1 motor axon Directly gated chemical transmission Transmitter: Ach Receptor: Nicotinic Ach receptors
Presynaptic: Synaptic boutons Active zones Postsynaptic: Junctional folds AchE
EPP Unusually large Always produces an action potential in muscle fiber (by activating regenerative Na+ channels) Has decremental decay with distance (leaks charge)
Ach degradation - major means of Ach inactivation - AchE located in junctional folds - High affinity choline uptake process
VOLTAGE GATED VS. CHEMICALLY (LIGAND) GATED Channel size: smaller larger Ion selectivity: more selective less selective Regenerative: yes no Pharmacology tetrodotoxin (Na+ channel) bungarotoxin and curare (nicotinic AchR)
Note: Chemically (ligand) gated channels and voltage gated channels are in parallel \ EPP’s depolarize activate regenerative Na+ channels.
MOLECULAR STRUCTURE OF AchR
- Direct / ionophoric - Recognition site: - 2 a subunits (bind Ach) - 5 subunits form pore - Negatively charged amino acid in pore - After transmitter binds, conformational change causes opening of channel - Na+ flows in while K+ flows out simultaneously
SYNAPTIC TRANSMISSION MEDIATED BY SECOND MESSANGERS - Slower in onset (modulating) - Longer in duration - Many transmitters / few 2nd messenger pathways - Receptor and effector are separate molecules and can be coupled by a G protein
RECEPTORS Seven membrane spanning domains
G – PROTEINS a,b, and g subunits a subunit conveys specificity and has GDP transmitter (NE /Ach/histamine) binding to receptor (b-adrenergic, muscarinic, histamine) allows G-protein (with ADP) to bind to receptor this causes the GDP to be replaced by a GTP this causes the a subunit (bearing GTP) to dissociate from the b and g subunits the a subunits then binds to the primary effector (adenylyl cyclase/phospholipase C/phospholipase A) this affects catalytic activity of primary effector hydrolysis of GTP to GDP causes a subunit to dissociate from primary effector a subunit then reassembles with b and g subunits
cAMP pathway External signal (1st messanger): NE
Receptor: b - adrenergic receptor Transducer: Gs Primary effector: Adenylyl cyclase
Second messanger: cAMP Secondary effector: cAMP dependent protein kinase
IP3 – DAG system External signal (1st messanger): Ach
Receptor: Muscarinic Ach receptor Transducer: Go Primary effector: Phospholipase C
Second messanger: IP3 and DAG Secondary effector: IP3 ® Ca++ release and DAG ® protein kinase C
Arachindonic acid External signal (1st messanger): Histamine
Receptor: histamine receptor Transducer: Go Primary effector: Phospholipase A2
Second messanger: Arachidonic acid Secondary effector: lipoxygenase and cyclooxygenase (eicosanoids) 2nd messengers MODULATE can act directly (fast) to OPEN or CLOSE ion channels can act indirectly (slow) through protein phoshorylation to OPEN or CLOSE ion channels
2nd messengers and DESENSITIZATION loss of receptor responsivelness due to pronlonged exposure to transmitter due to phosphorylation of cytoplasmic domains of the receptors alters G-protein binding or channel subunit
2nd messengers and GENE EXPRESSION Phosphorylation of transcriptional regulatory proteins causes changes in protein synthesis
OTHER 2ND MESSENGER PATHWAYS (do not use G-proteins)
Tyrosine kinases - used by growth factors - span the membrane only once - phoshorylate tyrosine residues
cGMP - cGMP synthesis is stimulated by nitric oxide - cGMP dependent protein kinase
Differences in SYNAPTIC TRANSMISSION in CNS vs. NMJ
CNS NMJ excitatory & inhibitory excitatory only
PSP’s < 1mV EPP’s » 70mV
Neurons receive input from 1 motor neuron : 1 muscle fiber 100’s of presynaptic neurons
Postsynaptic potential properties - transmitter generated - graded potentials – variable amplitude - local potentials – decremental decay - no threshold - no refractory period - long duration allows summation
EXCITATORY PROCESSES IN THE CNS
EPSP’s - depolarizing - produce influx of Na+ ions moving Vm towards ENa
GLUTAMATE RECEPTORS Classification Ionophoric - NMDA (N-methyl-D-asparate) Agonists: Glutamate and NMDA Channel selectivity: Na+, K+, Ca++ Ca++ has long lasting changes Modifier: glycine required (an inhibitory amino acid) Gated: Voltage (Mg++ regulated) and chemically - Non – NMDA Agonists: Glutamate (endogenous), kainate, AMPA, and quisqualate Channel selectivity: Na+and K+ Metabotropic
Function Depolarization Produce EPSP’s
Pathology Glutamate toxicity Excessive influx of Ca++ Excessive activation of proteases and free radicals Status epileptics Huntington’s chorea Stroke INHIBITORY PROCESSES IN CNS
2 Methods
1. Hyperpolarization (IPSP’s) Prevents membrane from reaching threshold Channels for ions having a E more negative than RP open (K+efflux, Cl- influx)
Agonists: GABA – inhibitory tramsmitter in the brain and spinal cord synthesized from glutamate (an excitatory amino acid) Glycine – inhibitory transmitter in spinal cord
Method: Cl- influx
2. Stabilization or Clamping Vm If RP = ECl- cannot have IPSP’s (GABA does nothing) Stabilize/clamp Vm at ECl- ¯ size of EPSP’s (when GABA released with glutamate smaller PSP created) ECl-
NEURONAL INTEGRATION in the CNS
- PSP’s summate at the initial segment (axon hillock) - If temporal and spatial summation reaches threshold an action potential will be generated - Long length and time constants increase summation increase probability of reaching threshold - amplitude of summated potentials determines the rate of discharge
Final integrator: axon hillock Site of neuronal integration Lowest threshold Highest density of voltage gated Na+ channels Converts summated PSP’s into an action potential
TRANSMITTERS - neuronal synthesis - present in presynaptic terminal - exerts an action upon release into synaptic cleft - exogenous and endogenous effects mimic each other - inactivation mechanisms exist
RECEPTORS - Receptor type is defined by the neurotransmitter that interacts with the receptor. - A receptor type can be subdivided into subtypes on the basis of selective agonists and antagonists. - Receptor determines action of transmitter.
ACETYLCHOLINE Ach synthesis (in presynaptic terminal) choline + AcetylCoA ® acetylcholine (choline acetyltransferase)
Inactivation: Acetylcholinesterase and then uptake of choline
Ach location - Motor neurons: All Preganglionic neurons Parasympathetic Postganglionic neurons - Nucleus Basilis of Meynert - Septal nucleus - Striatum - Lateral hypothalamus
NEUROPEPTIDES - Composed of two or more amino acids - There exists more than 50 - Peptide effects are slower in onset (develop gradually) - Effects have a longer duration
Synthesis Proteolytic cleavage by peptidases from large precursor proteins (preprohormones and prohormones) Precursors often are polyproteins that contain different peptides Synthesized by ribosomes located in cell body and transported down axon to terminal in vesicles
Inactivation No evidence for re-uptake DEGRADED BY EXTRACELLULAR PROTEASES Peptidergic receptors have a higher affinity for peptides than classical transmitter receptors
Morphine vs. endorphins - similar receptor binding site - produce analgesia - produce drug tolerance and dependancy - antagonized by naloxone (opiate antagonist)
Substance P - transmitter in pain afferents from the
periphery to spinal cord
CATECHOLAMINES - synthesized form tyrosine - inactivated principally via re-uptake - MAO and COMT secondarily - Synthesis: Phe ® tyrosine ® dopa ® dopamine ® NE ® Epi Phenylalanine Tyrosine hydroxylase hydroxylase *Rate limiting step (deficient in PKU)
Dopamine (DA) Location: substantia nigra ventral tegmental area arcuate hypothalamus
Function: movement psychosis neuroendocrine function
Major metabolites: homovanillic acid
Norepinephrine (NE) Location: locus ceruleus subceruleus projects throughout CNS except striatum solitary nucleus dorsal motor nucleus of vagus
Function: alerting center
Major metabolites: MHPG (centrally) Vanillylmandelic acid (peripherally)
OTHER BIOGENIC AMINES Serotonin (5-HT) - synthesized form tryptophan - inactivated by re-uptake and the MAO enzyme - synthesis: trptophan ® 5-hydroxytrptophan ® 5-hydroxytryptamine (serotonin) trptophan hydroxylase 5-hydroxytryptophan decarboxylase
Located: brainstem raphe nuclei to reticular formation
Function: mood –depression obsessive-compulsive disorders alcoholism food intake
Histamine
TRANSMITTER RELEASE
Channel Blocker V- Na+ TTX V- K+ TEA Ca++ Mg++
CALCIUM IS ESSENTIAL FOR TRANSMITTER RELEASE L type calcium channels ® slow rate inactivation N type calcium channels ®more rapid rate of inactivation
TRANSMITTER IS RELEASED IN QUANTAL UNITS Unit synaptic potential at muscle end plate (mEPP) results from a fixed sized quantum of transmitter sum of unit potentials = synaptic potential 1 vesicle contains 1 quantum
classical vesicles - Small - clustered in rows at dense bodies - some are positioned at active zones (release sites) - transmitter discharged by exocytosis at active zones
biogenic amine and neuropeptide vesicles - larger - do not release their contents from active zones
Calcium responsibilities - Calcium influx µ # of quanta released ( [Ca++]e doesn’t affect size of quantum) - Mobilization of vesicles from the cytoskeleton into active zone release sites Ca++/calmodulin dependent protein kinase phoshorylates synapsin causing vesicles to be freed Vesicles move to active zone under guidance of other proteins - Docking - Fusion of vesicle with plasma membrane at the active zone release sites - Fusion pore forms and dilates as exocytosis occurs - synaptic delay ® it takes for calcium to diffuse to its site of action to trigger vesicle release
Intrinsic cellular mechanisms regulate the [Ca++] Posttetanic potentiation: postsynaptic potential persists after tetanic (high-frequency) stimulation due to build up of free Ca++ presynaptic facilitation and inhibition involve changes in [Ca++] stimulated by axo-axonic synapses
Concentration of Ca++ channels (Ca++ influx) is greatest at the active zone.
SYNAPTIC VESICLES
Transmitters are stored in vesicles Protect transmitter from degradation
Transmitter is actively taken up into vesicles (carrier mediated transport)
Small molecule transmitters are synthesized in the nerve terminal Peptide transmitters are synthesized in the cell body, packaged and transported to the terminal
Cholinergic Aminergic Small clear vesicles Small and large vesicles Facilitated by active zones Not facilitated at active zones Contain: little/no core protein Contain: transmitter, core proteins, and peptides Concentrated by ion trapping Concentrated by ion trapping Complex formation Complex formation Inside acidic
Vesicular proteins Anchoring - synapsins (dephosphorylated = attached)
Bind Ca++ - annexins
Fusion - synaptotagmin - synaptophysin
Synaptic vesicles are recycled either locally in terminal through lysosomal degradation and return to cell body
If retrieval of vesicles is blocked, the terminal membrane is enlarges
Not all transmitter release is by exocytosis - carrier mechanisms (pumps) - diffusion - reversal of transporters that normally mediate transmitter re-uptake
Removal of Transmitter from synaptic cleft: terminates synaptic transmission - diffusion - enzymatic degradation - re-uptake (not for peptides)
OVERVIEW OF SENSORY ANATOMY
PRIMARY AFFERENT FIBERS - first neuron in sensory pathway - comprise the dorsal root - cell bodies in the dorsal root ganglia - peripheral process (distal to DRG) specialized sensory receptors at endings - central process (proximal to DRG) enter spinal cord to project to higher levels or make synaptic contact with relay neurons
DORSAL ROOTS - enter spinal cord at all levels from cervical to sacral - impart anatomical segmentation to spinal cord representing dermatomes
Dermatome = skin innervated by single dorsal root
SPINAL CORD Anterior/Ventral/basal = motor Posterior/Dorsal/alar = sensory
Anterior lateral sulcus ® emergence of ventral roots Posterior lateral sulcus ® entrance of dorsal roots
Dorsal Columns and spinocervical: fine discriminative touch and proprioception Fasciculus gracilis = sacral thru cervical Fasciculus cuneatus = upper thoracic and entire cervical Spinocervical = just lateral to dorsal horn
Anterolateral Columns: crude touch, pain, pressure, temperature, tickle and itch Spinothalamic tract Spinoreticular tract Spinotectal tract
Gray Matter All synaptic contact between 1o afferents and relay neurons All synaptic contact between descending neurons and relay or motor neurons Ten Lamina Dorsal horn Sensory/alar plate deriverative I – marginal layer (2o relay neurons) II – substantia gelatinosa (interneurons) III-VI – nucleus proprius (2o relay neurons & interneurons) Ventral horn Motor/basal plate deriverative VIII – interneurons IX – motor neurons VII & X – Clark’s column and intermediolateral cell column
Primary afferent terminations Large fibers: medially Majority do not make synaptic contact Synaptic contacts in nucleus proprius (lamina IV - VI) Smaller fibers enter more laterally Distributed via Lissauer’s tract Synaptic contact in lamina I, II, V
Somatotropic organization Dorsal columns = ipsilateral deficit Sacral medial Cervical lateral Spinothalamic, spinoreticular, and spinotectal = contralateral deficit Sacral lateral Cervical medial
Relay Points Dorsal horn of spinal cord Dorsal column nuclei (gracilis and cuneatus) Lateral cervical nucleus (spinocervical tract) Thalamus Reticular formation Primary and secondary cortex
Function of Relay Nuclei Give rise to higer order afferent fibers Integration (modify and tune output)
Somatosensory thalamic nuclei VPL and VPM Specific (somatotopic map maintained) Lateral division, medial lemniscus and spinothalamic tract from body Medial division, trigeminal input from face Interlaminar nuclei (CL, CM, PF) Nonspecific (multiple diffuse profections) Direct input from reticular formation Behavioral activation and motivation via hypothalamus and limbic system
Primary sensory cortex (3,1 & 2) Input from VPL and VPM via posterior limb of internal capsule Transfers input to 2o sensory cortex and association cortex
PERIPHERAL MECHANISMS FOR SOMESTHESIS
Ab large heavily myelinated fast lowest threshold well localized: fine discriminative touch and proprioception ischemia (leg falls asleep)
Ad smaller lightly myelinated intermediate conduction velocity
C smallest unmyelinated slow highest threshold poorly localized: crude touch, pain, pressure and temperature anesthetics
Labeled Line Code fibers have specialization: convey only information arising from separate modalities of natural stimuli
SENSORY RECEPTORS Types specialized afferent nerve endings separate specialized cells that directly affect the afferent nerve terminal
Exteroceptors – sense external environment Interoceptors – sense internal environment Proprioceptors – sense position and movement of limbs
Function Transduce natural stimulus energy to neural activity (ion flow produces receptor or generator potential)
Cutaneous Exteroceptors Mechanoreceptors Fast adapting Slow adapting Thermoreceptors Warm Cold Nocioceptors Mechanical Thermal Polymodal
RECEPTOR MODALITY Receptor type is specialized such that activation always gives rise to a particular sensation
Adequate stimulus Type of stimulus energy for which the receptor has the lowest threshold (most sensitive to)
Receptor Potentials Elicited by adequate stimuli (transduction) Graded Local Trigger action potentials in afferent nerve (neural encoding of intensity and duration)
Receptor adaptation ¯ receptor potential and firing frequency of ap’s on afferent nerve with presence of adequate stimulus causes morphological: receptor changes shape biophysical: ion channel phosporylation types fast adapting on/off response (dynamic) Ab & Ad signals changes, movements and location slow adapting on response followed by sustained response (dynamic and static) Ad and C fibers Signals location and continued presence |
