Photoreceptor response Hearing Olfactory signal transduction

Resting potential caused by Dark current: Flows in through cation channels, flows Sound: perception of pressure waves, waves are alternating compression and thining of air, --Odorant receptor proteins are GPCRs
out through potassium channels in outer segment compression propagates through air --Olfactory specific G-protein Golf
Light response produced by: Closure of cation channels, Reduction in circulating Period: time b/w compression peaks -- Golf targets adenylyl cyclase
dark current, Potassium channels still open, Hyperpolarization Frequency (pitch) =1/period --Activates cAMP
Light response Amplitude (loudness) =amount of compression and thinning --Cyclic Nucleotide gated Na+/Ca2+ chan
1.photon absorbed by rhodopsin, a gprotein coupled receptor. 2. Phase=time b/w peaks of diff sine waves --Depolarization amplified
Photon changes the 11 cis retinal into all-trans retinal. 3. All trans Human ear by Ca2+ gated Cl- channel
is an active enzyme call metarhodopsin. 4. Metrahodopsin Outer ear: Collect sound waves (called Pinna)
-- Cl- channel inactivated by CaM
catalyzes activation of transducin 5. Transducin activates Middle ear: Amplify pressure waves, Transmit waves to inner ear
--Na+/Ca2+ channel inactivated by
phosphodiesterase (PDE) that hydrolyzes cGMP. 6. Ligand of light Inner ear: transduction
Outer ear phosphodiesterases
sensitive channel is cGMP which is permeable to NA, K and Ca, 3 --Generates AP
cGMP bind to channel to keep it open. 7. When cGMP is hydrolyzed Auditory meatus : Hole into the skull
--Ends at ear drum = tympanic membrane Olfactory Receptor Protein :
there is a reduction in free cGMP which causes dissociation of --GPCR homologous to β -adrenergic receptor and mACHR
Middle ear
cGMP from channel. 8. Unbinding of cGMP causes channel closure --Largest known gene family – 3 to 5 percent of mammalian genes
--Function is impedance (resistance to movement) matching
and reduction in Na and K influx Human ~400 transcribed
--Air provides low resistance medium for movement of molecules while Fluid provides high
resistance for movement of molecules Mouse ~1200 transcribed
---When transferring sound waves from air to water, 99.9% of energy is lost Dog ~1100 transcribed
Role of middle ear: Two mechanical processes to boost energy transmitted Each olfactory neuron expresses only one or a few odorant receptor proteins
--Focusing of force from large tympanic membrane to small oval window Different odors activate distinct subsets of receptor neurons
--Lever action of interconnected bones (ossicles) Stimulus Selectivity
--Individual ORNs show a range of specificity
-- Some are highly selective for specific stimuli
-- Others activated by many odorant molecules
Challenges
No chemical or physiological data showing a correspondence between high
affinity binding of odorant molecule, and perception of a specific odor.
Taste
--Less sensitive than olfaction
-- Most sensitive to bitter, harmful substances
-- Five perceptually distinct categories: salt, sour, sweet, bitter, umami
--Taste cells on tongue, palate, epiglottis, and esophogus – three different
cranial nerves
Tastant response vs position
--Tip responds to sweet, umami, and salty – nutritious substances
--Sides and back respond to bitter and salty – aesthetic qualities, dangerous
substances
Anatomy of tasting
--Papilla – protruberances surrounded by local invaginations
-- Fungiform (25% of taste buds)
-- Circumvallate (50% of taste buds)
--Foliate (25% of taste buds)
--~4000 taste buds

Amplification: 1 metarhodopsin can activate 800 gt, 1 PDE can

degrade 6 cGMP, 4800 cGMP degraded from 1 metarhodopsin
causing closure of 200 channels so 1 photon produces 1 mV of
hyperpolarization
Inactivation of light response:
Phosphorylation by rhodopsin Kinase
Binding of arrestin: promoted by phosphorylation
Arrestin bound metrahodopsin is inactive
Inactivation of Transducin:GTPase accelerating proteins increase
inactivation
Guanyl cyclase re-synthesizes cGMP
Light Adapation: to maintina sensitivity over wide range
1.Closure of channels reduces calcium influx 2.Low calcium boosts
Guanyl Cyclase activity – restores cGMP levels 3. Low calcium
increases activity of rhodopsin kinase – faster inactivation of
metarhodopsin 4. Calcium increases affinity of channels for cGMP
– more conversion to GMP required to close
Rods and Cones
Sensitivity to light
Scotopic (starlight) vision: Rod vision, High sensitivity, Low
resolution
Photopic (Good lighting or sunlight), Cone vision, rods saturated,
Low sensitivity
High resolution
Mesopic: rods and cones
Cones adapt faster, cones do not saturate in bright lights
Convergence
Cones: 1 cone contacts 1 cone bipolar, 1 cone bipolar contacts one
cone ganglion, No pooling of light signals, small receptive field
produce high resolution
Rods: 15-30 rods contact each rod bipolar, rod bipolar contact
many amacrine cells, Pooling of signals from many rods, large
receptive field produce low resolution, because source of photon
unknown
Cones: 4.5 million, mostly in fovea
Rods: 90 million, non foveal
Cones
3 classes of cones each with diff photopigment
Cochlea:
Taste Buds
- Taste cells – neuroepithelial cells
- Apical and basal domains
-Taste pore – concentrates tastants
- Microvilli – receptor molecules
Taste Transduction
--Different mechanisms for different taste categories
--Apical sensors signal basal voltage gated channels
--Graded receptor potentials lead to graded transmitter release
-- Serotonin and ATP (?)
--Taste receptor cells specialized for specific taste - Taste Receptor Neurons –
Inner Hair cells transduce sound graded neurotransmitter release
--Embedded in basilar membrane
--Stereocilia protrude from apical end of hair cell
Outer hair cells help to tune frequency response of membrane
Sterocilia: Up and down movement of basilar membrane (and hair cells)
produces back and forth movement of stereocillia
30 – 100 stereocilia: stiffened with actin cytoskeleton, Graded in height
Each stereocilia tapers at insertion into apical aspect of hair cell: Forms
hinge at insertion point, Due to stiffness, they pivot (not bend) at the
insertion point when tip is deflected
Tip Links: Connect tips of adjacent stereocilia, Mechanism for generating
receptor potential
Mechanoelectrical transduction mediated by hair cells
--Tip links are attached to cation channels
--Displacement of hair cells stretches tip link which opens cation channels
by direct force, when moved toward tallest cilia
--Movement in opposite direction compresses tip ink and closes cation
channels by direct force
--Resting potential: -45 to -50 mV
--Channel opening allows depolarization: Depolarization leads to opening of
voltage dependent calcium channels, calcium influx, release of
neurotransmitter
--Channel closure leads to hyperpolarization : Below resting potential, Not
as large as depolarization because more channels are closed at rest
--Channel opening allows fast potassium influx: Scala media is filled with
endolymph , High K+ of endolymph maintained by pumps

Molecular Mechanisms
--Salt – Na+ channel
Protanopia: missing Long cones -- Acids – Non selective cation channel permeant to H+
Deuteranopia: missing M cones --No Gating (?)
Genetics of color deficiency: unequal recombination --Heterodimeric GPCR
Luminance perception ----One subunit same in sweet and umami transduction
Ganglion cells are sensitive to light surrounding the ----G-protein activates PLC/IP3 signal pathway
central spot ----Gates Ca2+ channel TRPM5
On center-off surround: decerase activity in response to light in --Bitter – GPCR
surrounding area --- Specialized G-protein – Gustducin
Off center – on surround: increase activity in response to light in ---30 different T2R genes
surrounding area ---Multiple T2R subtypes expressed in same cell
90 % of info is black and white ---Same pathway as Sweet & Umami
On center ganglion cell: Increase activity in response to light spot,
decerase activity in response to dark spot Nueural coding of taste
Off-center ganglion cell: increase activity in response to dark spot, --Labeled line code – specific receptor cells correspond to specific tastes (unproven)
decrease activity in response to light spot. --Knockout specific receptors abolishes sensitivity in behaving animal
Two classes of ganglion cells becauseTwo classes allow increases --Action potentials specific to tastant disappear
--Mapping of responses to tastants in cortex shows focal activity correlates to tastant
and decrease to be signaled reliably: Equal numbers of on center
--Coding not well established
and off center ganglion cell and Overlapping receptive fields
Gangion cells are contrast detectors, not light detectors, due to Chemotransduction
center surround Olafaction
Bipolar Cells Oldest sensory system -
Graded potentials: No action potentials --Unique among sensory systems – does not include a thalamic relay from
Off center: Sign conserving, AMPA and kainate receptors, primary sensors
Depolarize when glutamate released from photoreceptors, --Olfactory response neurons (ORNs) project to the olfactory bulb and then
Hyperpolarize to light, same as photoreceptors to the pyriform -----cortex in the temporal lobe
On center: mGluR6 receptors, Glutamate leads to closure of cGMP -- Less well understood than other sensory systems
gated sodium channels, Decrease in inward current produces --Widely ranging sensitivity from 0.01 nM to 2 mM for different odorants
hyperpolarization --Significant commonalities and some differences in receptor neurons
Light stimulation → decreased glutamate release → sodium compared to other sensory receptors
channel opening → depolarization Olfaction receptor neurons:
Sign inverting --generate action potentials
--Bipolar Neurons
-- Unmyelinated axon – basal
Molecular Signaling with Nuerons
Mechanisms: 1.Synaptic: targeted chemical release 2.Paracrine: local release of chemical in vicinity
of neurons. 3 Endocrine: release of chemical into blood-Acts on distant cells
Signal transduction: 1. Signaling cell 2. Molecular signal such as Glutamate 3. Receptor
molecule such as AMPA 4. Target molecule such as AMPA channel 5. Response Nuclear signaling Somatic Sensory system
Target and receptor molecule can be the same 2nd messengers elicit prolonged changes in neuronal function by promoting synthesis of new RNA Receptive field: part of stimulus that a single neuron responds to.
Amplification: 1. Each molecule/receptor complex may produce many G proteins 2. Each G and protein. Intracellular signal transduction cascades regulate gene expression byconverting Somatasenory afferents: cell body located in dorsal ganglia and cranial nerves,
protein bound enzyme may produce many second messenger molecules transcriptional activator proteins from inactive to activate states long afferent fiber, receptor ending in skin and muscle, remainder of fiber is
time scales: 1.Ionotropic responses are brief. 2.Metabotropic responses are slow & long lasting CREB-cAMP response element binding protein axon. Axon terminal in spinal cord
3 classes of signaling molecules Binds to cAMP response element (CRE) on DNA which is a transcription factor --unipolar: single fiber, functions as axon and dendrites
-Cell impermeant : 1. Vesicular release 2. Bind to receptor 3. Neurotransmitters, neurotrophic --Normally unphosphorylated and inactive --bipolar neuron: two fibes emanante from fibers, axon and dendrite
factors --Phosphorylation potentiates transcription, phosphrylated by these kinases: PKA, MAPK, CaMKIV --multipolar neuron: multiple dendrites, single axon emanating from soma
-Cell permeant: 1.Cross plasma membrane 2.Lipid soluble and water insoluble 3.Special transport --Genes regulated include c-fos, BDNF, Tyrosine Hydroxylase, neuropeptides --pseudopolar: dendrite is structurally and functionally an axon, except at its
proteins. 4. Steroids, thyroid hormones Nuclear receptors: are also transcriptional activators terminal receptor.
-Cell associated: 1. On extracellular surface of plasma membrane 2.Only act on cells in physical Glucocorticoid hormone receptors: Located in the cytoplasm, Bind to soluble glucocorticoids Mechanoreceptors: stretch sensitive cation channels, stronger the stimulus,
contact 3. Example: neural cell adhesion molecules --Binding of glucocorticoids causes receptor to translocate to the nucleus stronger the response
4 types of receptors --Bound receptor is a transcription factor, binds to recognition site on DNA Free nerve endings: Higher AP threshold: Pain, temp, itch
Ligand gated channel receptor: signal binds, channel opens, ions flow across ---Activates transcription and gene expression Specialized receptors: lower AP threshold Ia=muscle sensory Abeta=touch
Enzyme linked receptors: intracellular domain is an enzyme, activated by molecule binding Thyroid hormone (thyroxin) receptors: Bound to DNA in the absence of thyroxin, Suppresses Merkel: slow adapating, superficial receptors, small recepetive fields, form and
extracellular domain Ex. Receptor tyrosine kinases, neutrophin, growth factor transcription Inner Ear texture perception
G protein coupled receptor: signal binds, g protein binds, g protein activated, examples: Beta- c-fos: Transcriptional activator,Fluid
Proteinpressure wavesinconverted
is normally into nerve
low quantities in cells, Stimulation causes Meissner: rapid adapting, superficial receptors, small recepetive field, motion
adrenergic, metabotropic ACh, mGlutamate, Dopamine, GABAB impulses
transcription and translation within 30-60byminutes
cochleawhich
(Latinisfor
thesnail)
Immediate early gene, Induces detection, grip control
Intracellular receptors: 1. activated by cell permeant molecules, 2. Inhibitory protein complex synthesis of delayed response genesSpiral structure , bisected by chochlear Pacinian: rapid adapting, deep receptors, large receptive field, tool use,
dissociates when signaling molecule binds 3. DNA binding domain revealed 4. Activated molecule partition
Nerve growth factor binds to tyrosine Receptor Kinase A, which then dimerizes, phosphorylates and transmitted vibrations
moves into nucleus 5. New mRNA is transcribed triggers RAS
Synpatic activation,
plasticity: change inCochlea:
activates
synapse Cochlear
kinase strength
that partition
translocate
caused toby
nucleusconsists of to
andthought
training, activate transcription
be underlying Ruffini: deep receptors, slowly adapating, large receptive field, hand shape,
G protein activator proteins
mechanism Tectorialand
in learning and memory membrane and Basilar
development Membrane
of neural circuits motion detection, tangential force
GTP binding proteins: Bind to GTP or GDP, GDP bound form is inactive, GTP bound form is active Short term: not involved in memory Creates fluid filled
storage, areas:
duration lessScala
than Vestibuli,
ten minutes, mechanisms are all Propioreceptors
Two types: Heterotrimeric: Three different subunits, Monomeric presynaptic Scala Tympani, Scala Media -Provide information about position of limbs in space
Hetetrtrimeric: 3 subunits Increase in strength: Pressure of Stapes on oval window produces -Receptors are within skeletal muscles and tendons
-Alpha: Binds to guanosine nucleotides: GDP or GTP, Many different subtypes vibration
--facilitation: increase of PSP (seen of basilar due
in amplitutde) membrane
to brief high frequency stimulation, effect -Three main types
-Beta and Gamma: Binds to alpha subunit, Stabilizes G protein in membrane, Blocks alpha from decays rapidly, cause: residual Ca Amplitude
binding of to vibration depends
synpatotagmin on properties
causes additional vesicle release ==Muscle spindles: embedded parallel to extrafusal fibers,sensory afferents
interacting with effector, Can be effectors --augmentation: Steadily increasingof membrane and frequency
amount of vibration
of neurotransmitter release during a coiled around fiber, sense change in length of muscle fibers
train of action potentials,Apex onset is wide
and and flexible:about
duration Vibrates better for
100ms to seconds, caused
by accumulation of Ca in low axonfrequencies
terminal
--potentiation: Increase inBase PSC is that
narrow isand stiff: lasting
longer Vibrates better
than for
augmentation, Onset
and Duration - seconds tohigh frequencies
minutes, Requires more prolonged stimulation than
augmentation, Mechanism Location
is calciumof maximum
mediatedvibration depends
release of on
vesicles from reserve
Process: 1. Bound receptor increases affinity to G tone
pool, Phosphorylation of synapsin (by CaMKinase)
protein. 2. Coupling with receptor reduces Decrease in strength:
affinity of Ga to GDP 3.After GDP dissociation, Depression: Decrease in neurotransmitter release during sustained synaptic
GTP usually binds because its concentration is activity, Amount of depression depends on the amount of neurotransmitter
higher released previously (it is inversely proportional)
Consequences of GTP binding: 1. Alpha
--Mechanisms thought to be depletion of vesicles
dissociates from beta-gamma. 2 Alpha
---Rate of release decreases till release rate balances replenishment rate
dissociates from receptor
1. Binding of neurotransmitter to metabotropic ---More depression when reserve pool is smaller
receptor ---More depression when release probability is higher
2.Activation of GTP binding protein Tendency of facilitate or depress differs between synapses, Both facilitation and
-Either alpha or beta-gamma subunit depression can occur depending on characteristics of spike trains, Generally
3.Diffusion of G subunit within membrane observed that high p synapses exhibit paired pulse depression, and low p
4.Activation of effector protein synapses exhibit paired pulse facilitation
-Ion channel (direct activation) muscle stretch causes intrafusal fibers to stretch, mechanically gated ion
-Enzyme (indirect activation) channels open, depolarization generates action potential
Monomeric GTP binding protein
--production of second messengers Types of learning: -Group Ia afferents: Rapidly adapting, Sense velocity and direction
--Specific to G protein subtype Non-Declarative or Implicit memory: Group II afferents: Sustained response, Sense static position
-- Non-Associative Learning: Gamma motor neurons: Change tension (length) of intrafusal fibers to enhance
----Habituation: Decrease in behavioral response that occurs during repeated sensitivity of afferents
Vision
presentation of stimulus. Decrease in PSP from sensory to motor neuron Golgi Tendon Organ
Inner layer:Retina: contains neurons,
Role: Relay signals from cell surface ----Sensitization: Enhancement of reflex response by introduction of strong or Detects change
Outer layer: in muscle
schlera tension,
= white, In outside
fibrous series with extrafusal fibers,Ib
surfacecornea: afferent
transparent to allow
receptors to cytoskelaton, vesicle noxious stimulus branches
light are distributed among collagen of tendon
transmission
trafficking -- Associative Learning: Classical Conditioning Middle layer: choroid: capillary beds, nourishment. Ciliary body: muscle of
Five subfamilies Declarative or Explicit Memory: lens. Iris: controls pupil opening and amount of light entering
-Ras is involved in cell differentiation and division --Memory for facts and events Anteroir chamber: aqueous solution, changed 12 times a day
Termination of signaling for both heteromeric Posterior chamber: vitrious humor-maintains shape of eye
Short term Sensitization in aplysia
and monomeric: Refraction: bending of light, done by cornea for the most part, lens provides
During tail shock, interneuron from tail synpases on sensory neuron of siphon,
-GTPase Activating Protein (GAP) less refraction
-Hydrolysis of GTP to GDP this interneuron releases serotonin.
Adjustable refraction=accomadation, distant objects less flat-less refraction,
-GAPs for both types of G proteins 1.serotonin is released by modulatory interneuron and binds to Gprotien couple
nearby obojects is lens fat-more refraction
Effector pathways of G protein coupled receptors receptor. 2 Gprotein coupled receptor produced GTP that binds to adenyl
Retina
1.neurotransmitter, 2. Receptor, 3. G protein binds to enzyme, 4. Effector protein: enzymes produces cyclase which produces cAMP 3. cAMP then binds to PKA. 4 catalytic subunits of Fovea: highest density of photoreceptors, sharpest vision, cell layers pushed
intracellular, diffusible 2nd messenger (adenyl cyclase, phospholipase C) 5. 2nd messenger: diffuses PKA phosphorylate K channels. 5 decreased opening of K channels prolongs AP away
in cytosol to target protein (Ca, cyclic nucleotide, phospholipid metabolites) 6. Later effectors: ion which increases Ca influx. 6. Increased Ca causes more vesicles of transmitter Macula lutea: larger area of high acuity vision
channels, kinases, phosphotases 7. Target action to release onto motor neuron. Optic disk: axons of neurons meet here to form optic nerve, blind spot
Second messengers – regulate neuronal function Long-term sensitization in aplysia: -Photoreceptors
By modulating the phosphorylation of intracellular proteins 1 PKA phosphorylates CREB which binds to CRE, increasing transcription of --Cell bodies in outer nuclear layer
genes, ubiqutin hydroxlyase stimulates degradation of regulatory subunit of --Transduce light into depolarization
5-10% are short, ratio of medium to long PKA allowing persistence of free catalytic unit of PKA, which allows CREB to No axon, but synaptic terminals in outer plexiform layer
wavelength is b/w 1:1, and 1:4 keep operating. -Bipolar cells
Color Perception: Long term plasticity (more than an hour) --Cell bodies in inner nuclear layer
One cone not enough for color, need Long Term Potentiation: increased strength, high frequency stimulation --Synapse in inner plexiform layer
comparison of response of multiple cone produces increased EPSP and EPSP amplitude for over an hour. -Ganglion cells
classes to indicate color Property of LTP: --Generate action potentials
Trichromacy: ability to match any color --Axons form optic nerve, carry information to CNS
by adjusting intensity of 3 Interneurons
monochromatic lights -Horizontal Cells
Dichromacy: just 2 wavelengths, missing --Cell bodies in inner nuclear layer
cone pigment, color blind --Processes are in outer plexiform layer
--Mediate lateral interactions between photoreceptors and bipolar cells
-Amacrine cells
--Cell bodies in inner nuclear layer
--Processes in inner plexiform layer
--Channel closing allows fast K+ efflux --Mediate lateral interactions between ganglion cells
From cell body into perilymph
--Fast changes in membrane potential
Gradient persists with continued activity
Three mechanisms produce frequency
tuning
Molecular mechanisms underlying LTP
--Properties of basilar membrane
NMDA receptor is responsible. Low hair
--Outer frequency
cells stimulation causes release of
glutamate which binds to AMPA and NMDA,
--Intrinsic channels but because NMDA pore is blocked
by Mg, EPSP at low frequencyResponse
is due entirely
propertiestoofAMPA opening.
auditory nerve During high
fibers of EPSP occurs and the cell post synaptic
frequency stimulation, summation
membrane is depoloraized and --Action
Mg ispotentials
expelled,occurnowduring
Ca the
can enter through NMDA
receptor and trigger LTP. NMDA depolarizing
thus acts phase
asofa the receptor potential
coincidence detector. Specifity
due to NMDA opening only where ---AP are “locked” toisparticular
glutamate phase of Associativty
being released.
caused by other inputs beingoscillation
stimulated and causing depol enough to remove
Mg block.
LTP mechanisms: Ca influx through NMDA receptor causes activation of protein
kinases, these can phosophrylate themselves and can initate gene expression
(LTP). Speciifically increase Ca causes CaMKII and PKC to activate which
phosphorylates AMPA receptors which leads to higher conductance, insertion of
new receptors and increased sensitivity to glutamate.
Silent synpases: synpases with NMDA receptors, very few AMPA receptors. No
PSC at resting potential during glutamate release (Mg block). Adding AMPA Retinal pigmented epithelium
Second Messenger Targets: Protein Kinases and Phosphates receptors wakes synpases up . Prevelant in developing brains -photoreceptors are behind other cells to allow contact with RPE
Phosphorylation state of protein modulates activity Early Phase LTP: first hour, requires activation of protein kinases RPE has long process extending into photoreceptor layer
-Depends on balance between kinases and phosphatases Late Phase: more than anhours, Ca-calmodulin activates adenly cyclise which Two critical roles: 1. Regnerate photopigment-“Exposed” rhodopsin
Horizontal
-Phosphorylation targets include enzymes, ion channels, cells
structural and regulatory proteins produces cAMP which activates PKA which activates CREB and transcription 2. Cycling of outer segment disks: Disks form at inner part, Move toward outer
-Mediates plasticity involved in learning receive glutamatergic input from and synapse growth Also requires protein synthesis part, Shed into REP
Kinases: puts 2 phosphate groups onto amino acid, cones, Connected
usually act on with
Serinegapand Threonine Photoreceptors
Genetic experiments on flies shows cAMP critical for learning and memory
residues junctions, Activity represents -Morphology
New denditirc spines after LTP
illumination
3 essential domains: catalytic domain (ATP and substrate bindingover a broadautoinhibitory
domains), area, domain --Outer segment: Specialized for Phototransduction, "Disks" of membrane in
Releasedomain(
GABA causes
onto photoreceptor Long Term Depression
(blocks catalytic domain), activator/2nd messenger binding conf change) rods, Infolding of plasma membrane in cones
terminals, Decrease release of LTP leads to maximum efficacy of synpases and thus no new encoding of info,
Protein Kinase A: cAMP activates this kinase by reducing affinity of regulatory unit for catalytic unit --Inner segment: Mitochondria enriched area, Cell body with nucleus and nissl
neurotransmitter from LTD must selectively weaken synpases. This occurs during low frequency
Ca/Calmodulin dependent protein kinase type II (CaMKII): calmodulin binds and displaces the substance
inhibitory domain and results in active enzyme subunit stimulation, seen in hippocampus, LTD reverses LTP.
--Terminal: Connected by axonlike process (fibre of Henle), Storage and
Protein Kinase C: binding sites for DAG and Ca and PS Mechanism: Low calcium elevation activates protein phosphatases
release of neurotransmitter
Protein Tyrosine Kinase: preferentially, Dephosphorylation of AMPA receptors leads to lower
Phototransduction
-Two types: conductance, Internalization of AMPA receptors Receptors respond differently from all other sensory receptors
photoreceptors
--Receptor tyrosine kinases: TM with extra cell domain that binds to protein ligands (growth factors, LTD in cerrebullum: -No action potentials generated, graded potentials
neutropic factors, or cytokines) and intracell domain that phosphorylates substrate protein. Associative LTD: LTD requires concurrent stimulation of parallel fibers and -In response to light:
--Non-receptor Tyrosine Kinases: Cytosolic and membrane associated, Indirectly activated by climbing fibers, Long term decrease in parallel fiber EPSP Ion channels close, instead of open
extracellular signals Mechanism: Climbing fiber depolarizes dendrite, Calcium influx through VDCC, Hyperpolarization, instead of depolarization
-Role: involved in cell growth and differentiation Parallel fiber releases glutamate, which binds to metabotropic glutamate Reduced neurotransmitter release, instead of increased
Mitogen Activated Protein Kinases: activated by phosphorylation of other kinases receptor, Production of DAG and IP3, ,Release of calcium from the ER, Activation Photoreceptor response:
--phosphroylates transcription factors and regulates gene expression of protein kinase C, Phosphorylation of substrates, Internalization of AMPA In dark: light channels open, depoloarization causes Ca channel opening, Ca
Phosphates: Oppose action of kinases by removing phosphate groups from proteins receptors. influx causes neurotransmitter release
-Three major types: Accomplished without NMDA receptor and phosphotases In Light: light sensitive channels close, hyperpolarization, Ca channels close
--PP1:Most prevelant, Regulated by inhibitory proteins Spike Timing Dependent Plasticity and neurotransmitter release stops, mag and dur depend on intensity
--PP2A: multi-subunit Recent experiments show that relative timing of action potentials plays a