neurobio final review
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jessieannsmith on April 29, 2012
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modules 1-4 only
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145 terms
Terms | Definitions |
|---|---|
 auditory pathway from hair cell to primary auditory cortex | 1. hair cells of the basilar membrane 2. brain stem neurons fire aps 3. MGN thalamic neurons fire aps 4. auditory cortex neurons fire aps |
| cochlea | - a pressure wave reaches the oval window and pushes it inward and increases pressure above the basilar membrane - basilar membrane moves downward as pressure is released by bulging out of the round window at base of cochlea - 3 components 1. scala vestibuli 2. sale tympani - scala media |
| scala vestibuli | - connected to the oval window - where sound waves enter the cochlea - have perilymph fluid |
| scale tympani | - compartment connected to round window - has perilymph fluid |
| sacal media | - bounded by basilar & ressner's membranes - has endolymph fluid |
| ossicle | - amplify the sound wave n air to produce a force on the oval window 20 times greater than on the tympanic membrane so that the fluid in the cochlea us moved |
| basilar membrane | - narrow at the base near oval window - wide at apex - hair cells have cilia will depolorize to different extents in response to frewuency of sound wave - 100 times stiffer than the apex -moves up an down in response to waves of pressure impinging on the oval window and transmitted through to round window - hair cells connect to sensory neurons that live in spiral ganglion inside cochlea |
| oval window | - connection of middle ear stapes bone with opening of cochlea - flexible membrane |
| primary auditory cortex | - tonotopic & recieves precisely mapped information from MGN - process combination of frequencies - process modulations of amplituure or frequency |
| spiral ganglion | - sensory neurons each have a synapse with a hair ceel is "turned in" or most sensitive to a particular freqency - almost all contact inner hair cells |
| sensory pathways | - dorsal column-medial leminiscus pathway - spinothalamic pathway |
| dorsal column-medial leminiscus pathway | - touch/pressure. vibration & body position (proprioception) info travels to the brain seperate from pain/temp - afferent/central axon of large sensory fibers ascend ipsilaterally in dorsal comumns with tacile info and imb position info - DC also have 2nd ascending axons from dorsal horn neurons - in the post central gyrus of the parietal lobe - the neurons that projects to the cortex is called the thalamo-cortical neuron |
| spinothalamic tract | - DRGN enters dorsal horn at each spinal cord level - pain, temp, some touch - ascend/descend in lissaur's tract - synapse in substanita gelatinosa - decussate in ventrcal spinal cord - ascend ventrally in spin cord as spinothalamic tract - synapse in thalamus - thalamic axons travel to Si somasensory cortex and synapse in layer 4 |
| primary somatosensory cortex | - in partietal lobe, posterior to central sulcus - carriers on higher order processing of sensory info - receives synaptic input from vp nucleus of thalamus - respond to somatosensory info - thalamic input it to cortical layer IV which sends axons to other layers in the same area - reciprocal (bidirectional) connections between cortical areas & association pathways |
| lesions on primary somatosensory cortex S1 | - impair somatic sensation |
| electrically stimulate S1 | - "feel" sensation on the appropriate body part |
| S1 cortex restriction of information | - some cortex areas specialize in decoding texture, shape, and size |
| columnar organization of S1 | - alternating columns with nerons that have neurons with rapid or slow adapting properties recieving information from a given body area - same concept as in auditory & visual cortex |
| first-order neurons | - has the sensory receptor - innervates skin by right & left dorsal roots of a single spinal segment |
| second order neurons | - aka interneurons - gets information from the primary & can project info or modify locally activity of primary neurons - recieve synaptic input form DRG neurons - reside in dorsal horn and trigger reflex responses - also aascend to brainstem & thalamus - also reside in brain stem & are involved in perception |
| location of synapsa involved in reflexes | - midbrian |
| perilymph | - in scala bestibuli and tymppani - same composition as csf - bathes the hair cells |
| endolymph | - in scala media - hi K concentration - bathes stereocilia of hair cells - inward K+ flux leads to depolarization |
| basal ganglia | - nuclei surrounding thalamus with a common function - putamen, globus pallidus, caudate nucleus (aka striatum) - substantia nigra - subthalamic nuclei - a group of deep brain nuclei involved in plannng of voluntary movement including starting & stoping a movement and tone of antigravity muscle - lesions cause parkinson's disease |
| basal ganglie-striatum | - 3 fore brain nuclei involved in motor control - putamen - globus pallidus - caudate nucleus |
| dsyfunction of which nucleus is associated with parkinson's disease? | - substrantia nigra |
| TRPA1 | - cilia on hair cells are tethered to each other at the tips by connecting filaments that act like springs that transmit tension to cation channels in membrane of cilia |
| 8intermediolateral cell column | - lateral horns in the grey matter of the spinal cord - only at lower thoracic and upper lumbar levels - contain autonomic sypmathetic neuronal somas |
| trigeminal touch pathway | - two trigeminal nerves CNS - eachh diveded into 3 PNs that innervate face, mouth, and anterior 2/3 tongue & dura matter - synapse ipsilaterally on trigeminal nucleus in pons - deccusate and ascend contralaterally to synapse on VP nucleus in thalamus - thalamic axons project to S1 cortex |
| trigeminal pain pathway | - carriers information about sensations from the face |
| sensory neurons | - innervate skin and muscle - soma is in the dorsal root ganglion of the spinal cord at each level - afferent |
| motor neurons | - innervates muscle - soma is in the ventral horn grey matter of the spinal cord at each level - efferent |
| afferent neurons | - carry information into the cns - incoming |
| efferent neurons | - carry information out of the cns - out going |
| interneurons | - another name for an association neuron |
| agnosia | - inability to recognize objects, including your own body part - injury caused neglect syndrome - astereoagnosia |
| neglect syndrome | - injury caused - do not recognize body part as your own - do not dress it or wash it |
| astereoagnosia | - inability to reognize something by touch - but recognize by sight |
| sound intensity | - encoded by rate of firing and # of active neurons - the greater the amplitude wave, the greater distance along basilar membrane that moves - activate more hair cells and more SGNs |
| sound frequency | - phase locking: consistent firing of cell at same sound wave phase - neurons fire in phase with some point of the sound wave - either at the peak, valley, or inbetween, but it is constant for that neuron - indicated by the ap firing rate |
| sound locallization methods | - interaural time delay - interaural intensity difference |
| interaural time delay | - sound location method - difference in time it takes for sound to reach each ear if sound is not coming from directly in front or behind you - use for detecting direction of a sudden sound |
| interaural intensity difference | - your head blocks sound, so intensity is less in the ear away from the sound - your brain detects and computes this difference in intensity to localize sound direction |
| postsynaptic potentials | - the change in membrane voltage caused by Ach - membrane must be depolarized to threshold to initiate an ap - each quantum causes 1mV deoplarization of membrane - EPSP or IPSP |
| ESPS | - depolarization of the post-synaptic membrane caused by the neurotransmitter brings the membrane potential close to the threshold for firing an ap - influx of Na or Ca |
| excitatory transmission | - synaptic transmission that causes depolarization of the postsynaptic neuron - increases the probability that the post synaptic neuron will fire an ap - increases amount of neurotransmitter released from prost synaptic neuron by presynaptic facilitation - ie. neurmuscular junction |
| inhibitory transmission | - synaptic transmission that causes transcient hyperpolarization of the post synaptic neuron - decreases the probability that the ppost synaptic neuron will fire an action potential |
| IPSP | - caused by increase in potassium permeability similar to the undershoot of the ap - decreases the likelihood that the axon hillick reaches threshold depolarization for firing an ap - influx Cl or efflux K - if Ecl=V then no change in V - ex. GABA & glycine |
| temporal summation | - time constant - time it takes for a constant applied voltage to build up to 63 % of final value |
| spital summation | - length constant - distance that the constant applied voltage will decay to 37 % of final value - determined by resistance; igh membrane resistance & low internal reistance -> high constant8 |
| time constant | - the amount of time that a psp will last at a given membrane location = tau - time it takes for constant applied voltage to build up to 63% of its final value |
| neurons with membranes that have a long time constant | - show more temporal summation for conduction of psp |
| membrane resistance & temporal summation | - is reflected by number of open channels and channel density |
| length constant | - distance that a psp can spread along the membrane - distance along a neurite at which constant applied voltage will decay to 37% of its original value - the greater the membrane resistance (ie. no channels) the longer the psp travels |
| excitatory nts | - cause an EPSP on the post synaptic neuron - glumate is the most common cns nt - aspartic acid is also a nt |
| exocytosis | - a calcium dependent process - membrane bound individual vesicles fuse with the plasma membrane - spill the intracellular contents of the vesicle into the extracellular space, referred to as the synaptic cleft |
| synaptic proteins involved in exocytosis | - synaptobrevin - syntaxin - SNAP-25 - synaptotagmin |
| synaptobrevin | - needed for vesicle exocytosis - binds to voltage sensitive calcium channel so that it is physically close to the two opposing membranes that will fuse after synaptotagmin binds calcium |
| synaptotagmin | - needed for vesicle exocytosis - a protein with 2 binding sites for calcium that trigger the vesicle fusion once calcium has entered throught the voltage sensitive calcium channel - binds the core complex - binds calcium - calcium sensor |
| neurotransmitter release | - exocytosis 1. presynaptic ap 2. deoplarization of synamtic terminal - released by the first neuron at the presynaptic terminal, release site: active zone - triggered by the arrival of an ap in the axon terminal - released nt is bounded by the second neuron at the postsynaptic membrane - leads to transient depolarizaton of the membrane |
| metabotropic receptors | - open ion channels from cell interior - bind nt directly and cause an ion channel to open indirectly through second messengers |
| g-protein coupled receptors | 1. binding of the neurotransmitter to the receptor protein 2. activation of g protein 3. activation of effector syndrome - can inhibit or activate downstream molecules to increase or decrease levels of second messengers |
| GPCRs basic structure | - single polypeptide with seven membrane spanning alpha-helices |
| GPCR effector systems | - second messenger cascade - push-pull method - phosphorylation & dephosphorylation |
| second messenger cascade | - g protein couples nt with downstream enzyme activation - bind guanosine di & triphosphate |
| push pull method | - different g proteins or stimulate annd inhibit adenylyl cyclase - causes formation of cAMP and activation of PKA - PKA phosphorylates serine & threonine residues on target proteins |
| phosphorylation and dephosphorylation | - phosphate group added to or removed from a protein - changes conformation and biological activity - the function of signal cascades; signal amplification by GPCRs |
| iontrophic receptor | - with thier associated proteins form one complex |
| deep cerebellar nuclei | - main output nerons from cerebellum into spinal cord to innervate motor neurons in ventral horn - emoboliform - denate - globose - fastigial |
| synotxin | - keeps Ca2+ channel closed so that Ca2+ is where it needs to be |
| metabrotrophic | - slower but long lasting widespread effect |
| g-protein process | 1. NT binds to meabrotrophic receptor 2. metabrotrophic receptor splits g-protein into 2 halves (alpha and betagamma) 3. to halves go different ways to affect different proteins, enymes, molecules, ect. |
| neurotransmission | 1. AP comes to axon terminus & causes depolarization 2. depolarization opens up Ca2+ channels 3. Ca2+ binds to SNARE proteins (esp. synaptotgmin) 4. vessicle membrane & axon membrane fuse together 5. exocytosis of NT-bind receptors 6. vessicle membrane is recycled -> via clathin mediated endocytosis and -> dynamin for hydrolysis of GTP (energy for recycling) |
| action potential | - depolarization - threshold - rising phase - overshoot - falling phase - undershoot - refractory period |
| depolarization | - a less negative membrane pontential triggers the firing of an ap |
| threshold depolarization | - needed to trigger the ap - opens K channels |
| rising phase | - inward Na current - m gate open |
| overshoot | - positive inside as predicted by Ena - h gate closes & blocks m gate |
| falling phase | - outward K current |
| undershoot | - return to membrane potential to a more negative potential than at rest - n gate takes a long time to close |
| refractory period | - follows an ap - cannot be fired even if there is a transient depolarization - due to Na channel inactivation, h gate slow to reopen - membrane is negative for h gate to reopen - ends when the K channel closes - subquent ap cannot be generated until membrane is repolarized |
| 2 ways to increas ap propagation | 1. increase internal diameter of axons which decreases the internal resistance to ion flow 2. increase the resistance of the plasma membrane to charge flow by insulating it with myelin |
| myelin | - facilitates current flow of ap - has high capacitance so the membrane stores charges and ions do not move acress the membrane |
| conductance | - the recipical of resistance and measures the ease with which current flows in an object |
| capacitance | - the ability of plasma membrane to store or seperate cherges of opposite signs |
| changes in ion permeability | - allows inward Na flux and triggers an increased outward K flux through voltage gated ion channels - causes transient changes in membrane potential - triggered by transient depolarization of the membrane |
| Sodium Channel | - triggered be depolarization (has a voltage gate) - reverse polarity - refractory period (inactivation gate) - m gate - h gate |
| m gate sodium channel | - activation gate - opens quickly when membrane is depolarized |
| h gate sodium channel | - inactivation gate - closes slowly after membrane is depolarized - causes the absolute refactory period for AP generation |
| resting period | - m gate closed |
| peak of action potenial | - h gate closes |
| potassium channel | - has one gate, n - threshold depolarization opens K channels - n gate opens more slowly than m gate on Na channels - Na and K currents do not offset each other right away |
| nerst equestion | - calculates the exact value of the equilibrium potential for each ion in mV |
| goldman equation | - used to calculate membrane potential - assumes that electrical field of the membrane potential is equal across the span of the membrane |
| equilbrium potentials | - large changes in Vm - net difference in electrical charges - rate of movement of ions across the memebrane - concenetration difference; equilbrium potential can be calculated |
| if relative permeability of sodium increases by 5x, what would be the expected result? | - increased outward K flux through voltage gate ion channels - increase depolarization |
| othodromic | - ap travels in one direction |
| antidromic | - ap travels backward propagation |
| somatic motor system | - motor neurons synapse directly on muscle or glands - release Ach - PNS |
| sympathetic system | - ANS - innervates all organs, glands, and smooth muscles - always active, under the influence of hypothalamus to maitian homeostasis - readies body for action, increase heart rate, bp, moves blood to muscles away from viscera - fear; neurons in hypothalamus and brain stem activate adrenal glands that secrete adrenalin aka epinephrine |
| sympathetic ns anatomy | - short preganglionis fibers in the lateral horns of thoracic and lumbar spinal cord levels only - long postganglionic fibers - preganglionic; Ach - postganglionic; NE, EP - innervates smooth muscle, cardiac muscle, gland cells |
| parasympathetic system | - ANS - innervate all organs except liver, skin & arteries - always active to maintain homeostasis - causes relaxation & ihibits activity of innverated end organs - except increases digestion - bp, hr decrease, blood flow directed from muscle to viscera |
| parasympathetic ns anatomy | - long preganglionic fibers synapse in ganglia close to or in the innervated organ - short postganglionic fibers - innervates smooth muscle, cardiac muscle, gland cells - preganglionic; Ach - postganglionic; Ach |
| neurotransmitters classes | - amine, "-ine" or "-in" - amino acids, starts with "g" & aspartate - peptides, everything else |
| criteria for NT | 1. substance must be in presynaptic neuron 2. released by Ca+ dependent depolarization 3. here must be receptors on post-synaptic membrane |
| amine | - end in "-ine" or "-in" - made in axon terminus (synaptic vesicles) - DA, ACh, histanine |
| ACh | - precursor: acetyl CoA, chloine - made by cholineacetyltransferase ChAT - degraded by acetylchlolinsterase AChE - nicotinic receptor (NAChR) - muscle contraction - mesacrarisic receptor - slow down heart rate |
| catecholamines | - DA, NE, Epi - tryosine -> l-dopine - > DA -> NE -> Epi - degraded by monosamineoxidase MAD - DA: pleasure seeking behavior; addiction; cocain, amphatamine - parkinson's disease: lack of DA in substrate nigria, treated w/l-dops; DA cannot cross bbb |
| serotinin | - 5-HT - tryptophan -> 5-HTP -> 5-HT - degraded by MAD - regulates sleep, mood, emtions - prozac: blocks reuptake - ecatsy: damages signal |
| GABA | - main IPSP in brain - precursor: glutmate, pryuvate, glucose - made by GAD (requires vitamin B6) - most common inhibitory NT in CNS - gates Cl- channels - barbiturates (sleeping pills): increase duration - benzodiazephines ( tranqualize): increase frequency |
| GABA receptor subtypes | - GABAa & GABAc - iontrophic (fast acting & short) - GABAb - metrotrophic (slow, long lasting, widespread) |
| glycine | - IPSPs - precursors serine (prefered) glucose (for all IPSP) - less common inhibitory NT - stychine: antagonist (blocks CL- channels) to gly receptor on Cl- channel -> effects: uncontrolled depolorization in the brain (no inhibition) |
| glutomate | - EPSPs - precursors glutamine (from astrocytes) glucose - made by glutaminase (from mitochandria) - most important excitatory NT for brain function - long term pententatration - binds to AMPA (opens) & NMDA (closed, Mg+ blocks) - Na2+ current from AMPA depolarizes membrane to remove Mg2+ block for NMDA to open --> Na + Ca2+ enter |
| amino acids | - start with "g" - also aspartate - made in axon terminus (synaptic vesicles |
| peptides | - everything else - soma -> axon terminus -rough ER -> golgi apperatus -> axon terminus |
| acetylcholine in muscle contraction | - nicotinic receptor (NAChR) - binds at NMJ causes muscle to contract - triggers ap in the endplate of the muscle - excitation-contraction coupling |
| neuronal integration | - summing of all IPSP and EPSP to determine if threshold has been met for AP generation - based on temporal & spatial summation |
| schwann cells | - in PNS - myelinate only a single axon in the PNS - participates in the development & regeneration of the PNS |
| oligodendrocytes | - in CNS - provide myelin sheaths around axons in the brain & spinal cord |
| ependymal cells | - line ventricles with in the brain |
| astrocytes | - in CNS - makes bbb - "clean up system" of the brain - most numerous glie in the brain - regulates the chemical content of extracellular space - two types -> protoplasmic; found in grey matter -> fibrous; found in white matter |
| microglia | - carry out immune function - function as phagocytes to remove debris left by dead or degenerate neuron and glia |
| agonists | - a drug or compund that mimics the action of the naturally occuring NT |
| antagonist | - a drug or compund that inhibits the action of the naturally occuring NT |
| excitatory NTs | - catecholaminergic - dopamine - serotonin - glutamate - aspartic acid |
| inhibitory NTs | - GABA - glycine |
| precentral gyrus | - motor control - neurons control voluntary movement |
| postcentral gyrus | - sensory control - neurons are involved in somatic sensation (touch) |
| frontal lobe | - process conscious control of movement, behaviors & personality |
| parietal lobe | - processes sensory information from muscle and skin |
| occipital lobe | - involved in vision |
| temporal lobe | - involved in processing hearing and language |
| wernicke's area | - in secondary cortex - when damaged patients cannot understand speech because the sounds or out of order |
| Broca's aphasia | - understands - cannot speak clearly - motor defect (left frontal lobe) |
| cerebellum | - involved in controlling movement, by sequentially activating muscles - lesions cause ataxia - derieved from hindbrain, but not part of the brain stem - connected to pons & medulla - coordinate muscle activity - posutre - equilibrium - spatial reasoning - right & left hemispheres |
| cerebellar lobes | - rostral/anterior - caudal/posterior - vermis - flocculonodular |
| flocculondular | - primary connection with vestibular nuclei - recieves visual & sensory input - damage to it causes disturbance of balance and gait |
| node of ranvier | - gaps along the myelinated axon where myelin is missing |
| axon hillick | - beginning of axon - influenced sesnsitivity by shunting inhihibtion; inhibiting current flow from soma to axon hillock |
| relative refractory period | - ends when K channel closes - a stimulus can excite an ap, but it must be stronger than the minimum stimulus required to elict an ap at rest |
| absolute refractory perod | - due to Na channel inactivation because h gate is slow to reopen - the membrane has to be negative for h gate to reopen; so another ap cannot occur - the time between one ap and then not enough voltage-gated sodium channels are de-inactived and able to generate a new ap in response to stimulus |
| hodkin & huxley | - voltage clamp - identified the ion species that flowwed during ap - clamped Vm at 0mv to remove electric driving force that varied external ion concentration and onbserve ion efflux during a voltage step |
| otto lowei | - chemical nature of nerve transmission - proved that some soluble chemical released by the vagus nerve was controlling the heart rate |
| nernst | - calculate equilibrium potential |
| goldman | - calculate membrane potential |
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