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120 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Ionotropic Receptors |
a receptor that functions directly by opening ion channels that enable specific ions to stream in an out of the cell. ex: NMDA, KA, AMPA receptors |
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Metabotropic Receptors |
an indirect receptor which initiates an intracellular biochemical cascade after it is triggered by an agonistic ligand. function through second messengers, transduction pathways ex: g-protein linked |
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Ischemia |
a decrease in the blood supply to a bodily organ, tissue, or part caused by constriction or obstruction of the blood vessels. = low oxygen and glucose = low cellular energy supply = depolarization |
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Ion Channel-Linked Receptors |
Ligand-gated channels NT binds to the receptor, ions flow in or out changes membrane potential ex: glutamate receptors |
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Enzyme-Linked Receptors |
Bind a hormone (many growth factors work this way) and get a dimer (two subunits coming together and phosphorylating receptor. Enzyme generates product ex: tyrosine-kinase receptors |
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G-protein-coupled receptors |
ligand or NT binds to the receptor, which is linked to a g-protein. This Turns on cascade of effects |
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intracellular receptors |
signalling molecule passes right through the membrane, binds to receptor in cytoplasm or nucleus |
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Mechanoreceptors |
touch receptors (encapsulated) |
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Nociceptors |
pain receptors (free nerve endings) |
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thermoreceptors |
temperature receptors |
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reticular formation |
(RF) - neuron tracts across the lower brain stem. Many interconnections btw neurons wide spread projections from ascending portions primary nt is norepinephrine |
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functions of the Limbic System |
sets emotional tone of the mind filters external event based on internal state notes events as internally important modulates motivation stores highly charged emotional memories controls appetite/sleep cycle directly processes sense of smell info modulates libido |
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somatogenic pain |
direct injury ex: heart attack, lacerations |
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Psychogenic pain |
no physical cause can be equally as distressing as somatogenic |
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Acute Pain |
Protective mechanism alert to harmful situation sudden onset mediated by nociceptors relieved when nociceptors are no longer activated |
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Chronic Pain |
persistant (> 6 months) unknown cause or "intractable" behavioral implications |
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pain afferent pathways |
nociceptors in peripheral tissues, information carried to the spine and to the brain |
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Rapid Desensitization |
Loss of activity and responsiveness over time.
Different conformational change from activation to inactivation mediated at extracellular domain High NT concentration = rapid loss of function Low NT concentration = down regulation of channel expression |
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What type of NT receptor is important for serotonin? |
G-Protein Linked Receptors |
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G-protein-linked receptor process |
NT binds to receptor Activates G-protein Stimulates effector alters second messengers (inside cell) alters cellular response |
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α subunit of trimeric G-protein complex |
has GTPase Is active when bound to GTP Is inactive when bound to GDP |
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βγ subunit of trimeric G-protein complex |
anchors G-protein to plasma membrane on cytoplasmic face (covalently linked) activates other proteins |
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Heterotrimeric G-protein |
αβγ activation by phosphorylating a protein on effector protein. The alpha subunit dissociates and activates the effector protein. Over time, α subunit has endogenous GTPase activity. This breaks down GTP to GDP which inactivates the α subunit. Turns itself off. Transient and quick |
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Monotrimeric G-protein. |
NT binds on to a receptor and is passed onto a protein like RAS whichis active again. It changes conformation, drops a GDP binds a GTP and is active and GAP is now active and it's a GTPase activating protein and activatesthe ras protein for instance. Can activate and turn itself off with time. |
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Ras |
Protein that relays info from tyrosine kinase to nucleus of cell Regulates big things like cell differentiation, proliferation, and growth Inactive when bound to GDP, Active with GTP GTPase activating protein, turns itself off |
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Viral Ras |
Ras protein is abnormal Lost or Low GTPase activity, so Was remains active for long periods of time. Long proliferation, growth and division. Results in unregulated cell growth = cancer |
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NMDA subunits |
NR1 NR2A-D NR3A |
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Glutamate |
Excitatory NT. |
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What happens to NMDA glutamate receptor when membrane is hyperpolarized? |
Becomes less negative, loses affinity for binding Mg++, Mg++ block is removed |
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What are the coagonists for NMDA receptor |
glutamate (2) glycine (1) NEED ALL 3 |
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Why do we have differential expression/ different subunits for NMDA receptor in different parts of brain? |
allows for different function. moves same ion but functions differently. |
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How does pH regulate NMDA receptor? |
If channel opens, the opening is reduced with proton binding. (as pH goes down, opening is reduced) |
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What can cause depolarization of cell membrane? (spec. NMDA) |
Reduction in energy stores. results in lower efficiency of energy dependent ionic pumps (Na/K ATPase), which keep cell negative. This gradually depolarizes the cell. Stressed cells. Changes in metabolism like B amyloid that causes neurons to run out of energy Ischemia blocks blood flow, inc. oxygen and glucose. no energy. Trauma. |
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What does depolarization do to the presynaptic cell? |
Causes NT to be released. |
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Excitotoxicity in NMDA channel. Steps: |
1. Depolarization of membrane 2. Release of glutamate 3. Release of Mg++ block 4. Glutamate binds to NMDA channel 5. Without Mg block, channel opens 6. Rapid influx of neurotoxic Ca++ 7. Neuronal injury/death |
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What evidence is there for excitotixicity of NMDA channel? |
NMDA receptor blockers are neuroprotective. When given NMDA receptor blockers and induced stress, blocks or reduces damage. |
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Ischemic Pathway of neuronal injury |
1. Ischemia leads to free radical release and decrease in energy supply 2. Cell depolarizes 3. This opens Ca++ channel and releases glutamate 4. NMDA and AMPA receptors activate 5. This increases Ca++ and further depolarizes cell. 6. Neuronal injury |
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What is the benefit of receptor diversity? |
Increases plasticity, increases the way cells can respond to particular stimuli |
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G-protein linked receptor structure |
single polypeptide chain crosses membrane 7 times Coupled to G protein |
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Gs protein |
has as subunit. activates AC Synthesizes cAMP GTPase activity of as subunit turns off complex. opens L-type Ca++ channels directlysecond messenger - kinase phosphorylates channel |
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Cholera Toxin importance in G-protein ID |
ADP ribose to as subunit as loss of GTPase activity GTP remains bound as stays active |
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Pertussis Toxin importance in G-protein ID |
ADP ribose ai subunit blocks Gi activation. unable to inhibit AC function |
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Causes for down regulation of G protein linked receptors |
extended exposure to agonist uncoupling of receptor and g-protein |
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Gi protein |
muscarinic aCh receptor functions via Gi protein ai subunit, inhibits AC inhibits cAMP production By subunit opens K channels, hyper polarizes cell |
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Gt protein (transducer) |
at subunit activates cGMP PDE in photoreceptors This decreases cGMP, hydrolyzes cGMP, closes cGMP gated ion channels |
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Gq protein |
aq subunit activates phospholipase C-B |
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Neurotrophins |
Neurotrophins are a family of proteins that induce the survival, development, and function of neurons. NGF and BDNF |
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Activation of Enzyme receptor Tyrosine Kinase |
1. Growth factor binds to receptor 2. dimerizes receptor 3. Each Tyrosine kinase phosphorylates the other = dimer with two phosphorylated growth factors on cytoplasmic side 4. Activates catalytic main 5. Get formation of intracellular signal protein complex (binds phosphate group at the site on receptor) |
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PI 3 Kinase/Akt |
tyrosine kinase receptor pathway PI 3 kinase phosphorylates PIP2 > PIP3 Activates serine/threonine kinase Akt phosphorylates proteins, including BAD, which induces apoptosis. This inhibits apoptosis |
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phosphatase |
dephosphorylates. Can turn response off serine or threonine |
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Nitric Oxide Synthetase |
activated by Ca++ and calmodulin in cerebellar cortex, cerebral cortex, hippocampus, and striatum Makes NO |
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NO |
Nitric oxide activates soluble GC (binds to heme moiety) diffuses between cells volatile gas second messenger |
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cGMP Mechanism of action |
cGMP dependent protein kinase OR direct effect on ion channels (cGMP gated ion channels in photoreceptor cells) activates/inhibits PDEs |
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Recoverin |
recovery from light to dark
Ca++ sensitive inactive with high Ca++ Active with+ Activates GC increases cGMP channel opens Increase Na/Ca flux depolarization r |
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Divergence |
same transmitter, diff cellular response |
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convergence |
different transmitter, same cellular response |
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Free receptors |
unmyelinated nerve ending terminal branches
nociceptors thermoreceptors |
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encapsulated receptors |
based on structure surrounded by connective tissue |
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Somatic Receptor Function |
1. Stimuli to skin deforms nerve endings 2. changes ionic permeability of receptor membrane 3. generates depolarizing current 4. triggers AP |
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phasic receptor |
fires then is quiet conveys information about changes in stimuli adapting receptor responds maximally but transiently |
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tonic receptor |
slowly adapting sustained discharges keeps firing as long as stimuli continues info about persistence of stimuli |
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Meissner's corpuscles |
found in glabrous skin elongated connective tissue capsule sensitive to low frequency vibrations sense textured objects |
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Pacinian corpuscles |
subcutaneous tissue and interosseous membrane onion like capsule discrimination of fine surface textures produces vibration detects vibrations transmitted to skeleton |
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Merkel's disks |
slowly adapting
dense in fingertips, lips, external genitalia saucer shaped ending producers light pressure, discrimination of shapes, edges, rough textures |
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Ruffini's corpuscle |
spindle shaped capsular (leafy) deep in skin, tendons sensitive to cutaneous stretching role in proprioception slow adapting |
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Proprioception |
continous info about position of limbs and other body parts i.e. intrafusal spindle fibers |
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stretch reflex |
a physical response to the extension of a muscle causes a contraction, thereby stopping a stretch. This mechanism, which occurs in two major stages, serves to prevent injury. |
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ARAS |
Ascending Reticular Activating System -reactivation of large regions of cerebral cortex inputs from: all sensory systems, cranial nerves |
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Limbic system/RF importance in pain |
alterting/arousal to pain |
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Thalamus importance in pain |
discrimination/location of pain |
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Hypothalamus/Medulla importance in pain |
coping response to pain: fight or flight Release of stress hormones |
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Cortex importance in pain |
higher order pain integration |
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A-delta nociceptors |
myelinated (20 m/s) Respond to: intense mechanical stimuli mechanothermal stimuli |
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C fiber nociceptors |
unmyelinated. Slow, dull pain. |
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Evidence of specialized pain neurons, not just greater discharge of normal neurons |
heat pain. heat threshold, not pain |
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First pain |
sharp pain mediated by A-delta |
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Second pain |
delayed, longer lasting pain Mediated by C fibers |
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Hyperalgesia |
increased pain sensitivity at damaged tissue area why? |
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Referred pain |
pain is referred to site that is not source of pain visceral pain angina pain related to cardiac stress |
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Phantom limbs
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region anesthetized presents sensation |
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Sclera |
Outer layer, forms cornea |
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Iris |
opposing muscles control size of pupil |
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ciliary body |
ring of muscles regulating lens |
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ciliary process |
produces aqueous humor in front chamber of eye
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vitreous humor |
80% of fluid of the eye between lens and retina maintains eye shape has phagocytic cells |
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distant objects (lens) |
lens is thin = less refractive power |
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close objects (lens) |
lens is thicker = more refractive power |
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retina |
part of CNS pigmented layer supports photoreceptors |
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Major neuronal pathway of the eye |
photoreceptor cell to bipolar cell to ganglion cell to optic nerve |
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photoreceptor cells |
light sensitive cells; pigmented end is near pigmented endothelial layer of the eye Contains membranous disks with photopigment Rods and cones changes MP |
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Major Neuronal pathway of the eye (in depth) |
Receptor cells form synaptic connection with bipolar cells (or horizontal cells) Bipolar cell synapses with the dendritic processes of the ganglion cells Larger axons from ganglion cells form the optic nerve |
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Horizontal and Amacrine Cells |
cell bodies in inner nuclear layer primarily lateral interactions btw receptors, horizontal, and bipolar cells important in sensitivity to luminance/contrast over wide range of light intensities |
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Compare and contrast Rods and Cones |
Rods have low resolution and high light sensitivity; cones are opposite
Rods can respond to a single photon; Cones require 100s of photons for response Cones do not saturate at high levels of illumination, rods do. Cones adapt to changes in current about 4x faster than rods Rods and Cones linked to ganglion cells along same pathway BUT early links with ganglion cells are different - Rod bipolar cells contact ganglion cells - Cone bipolar cells synapse with amacrine cells Cone bipolar have both direct and indirect connections to ganglion cells Rods are highly convergent (i.e. many rod cells contact a bipolar, many bipolar contact a given amacrine cell = better detector of light). Cones are less convergent. (one cone cell connected to one bipolar cell. Better spatial resolution, but poor light sensitivity) Higher density of rods than cones loss of cone function has profound effects on vision, while loss of rods only eliminates night vision |
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Scotopic vision |
rod mediated vision lowest level of light (only rods) |
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Photooptic vision |
light conditions in which rods no longer contribute to vision Only cones are active light saturates rods |
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Mesopic vision |
levels of light in which both cones and rods contribute to vision |
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Fovea |
a small depression (1.2 mm) in the retina of the eye where visual acuity is highest. The center of the field of vision is focused in this region, where retinal cones are particularly concentrated 200 fold increase in cone density (also smaller cones) |
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Foveola |
- Very small central area of the fovea (30 micrometers) - no rod cells - high density of cone cells - blood vessels are displaced and cellular layers reduce light scatter - moving just 6˚ from center reduces acuity by 75% + why we move our eyes and head so frequently |
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For best night vision, how should you look at an object? |
Don't look directly at the object. Night vision is best when field of vision not centered on fovea, because need rod cells to see in dark |
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Short cones |
blue wavelength |
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Medium cones |
green wavelength |
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Long cones |
red wavelength |
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Is each type of cone cell excited by a photon of a specific wavelength? |
Nah fam. We have different photopigments, but doesn't discriminate wavelengths. The change in MP of a cone cell can be found by looking at responses in ganglion cells We don't know how |
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What is color perception? |
The represented relative levels of activity of the three sets of cones, each with different absorption spectra only 3 colors can blend to make most of colors we see |
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Dichromacy |
only 2 colors needed to represent color vision color blindness inherited, recessive, sex-linked |
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Protanopia |
all color from green + blue |
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Deuteranopia |
only blue and red light |
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Anomalous trichromats
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use all 3 light sources, but need more of a certain light to match colors |
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Protanomalous trichromats |
all colors with 3 light sources but need more red to match color
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Deuteranomalous trichromats |
need more green |
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Photopigment genes |
genes encoding pigments. Red and green encoding genes have high sequence homology. Located close together on X chromosome |
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Horizontal cells |
enable lateral interactions between photoreceptors and bipolar cells, thought to maintain casual system's sensitivity to contrast. |
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Amacrine cell processes |
postsynaptic process go to bipolar cell terminals presynaptic process goes to dendrites of ganglion cells Different subclasses make distinct contributions to visual function One type changes the persistent response from bipolar cells to brief transient response in ganglion cells Other type conveys info from rod photoreceptor cell to ganglion cell |
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Why does light pass through non-light sensitive cells of retina first? |
Functional relationship between the pigmented epithelium and photoreceptor outer layer. Since pigmented disks must be replaced every 12 days, pigmented disks are formed at inner segment of photoreceptor cell. These move toward tip of outer segment to be shed. The tip separates from the photoreceptor cell and is engulfed by epithelium and phagocytosed. Also plays important role in regenerating and recycling photopigment. |
seems counterintuitive |
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How are photoreceptor cells functionally different from regular cells? |
in most, stimuli depolarizes MP, AP is produced, NT is released. There are no action potentials in photoreceptor cells, only graded potentials, which correspond to rate of NT release. Why no APs? short signal distance Light stimulus hyperpolarizes the membrane. This is how NT is released. Changes in luminance alters NT release. |
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Photopigment |
retinal. Pigment changes conformation under light/dark conditions.
11-cis retinal isomer conformation is bound to opsin. When light,pigment is bleached and becomes trans retinal isomer and dissociates from opsin retinal + opsin = rhodopsin |
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Phototransduction of Retinal/Opsin |
1. Photon is absorbed by retinal 2. Retinal changes shape from cis to trans isomer 3. Retinal dissociates from opsin 4. Opsin is activated. 5. Opsin activates Gt protein transducer. 6. at of Gt protein activates cGMP PDE 7. cGMP PED hydrolyzes cGMP = lowers cGMP 8. Fewer cGMP to bed cGMP gated Na channels 9. Membrane hyperepolarizes, prevents NT release |
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Light adaptation |
increase light, sensitivity decreases
In light, decreased Ca results in increased GC because activates recoverin which activates GC Increases cGMP levels |
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Circadian rhythm |
body clock based on light |
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melanopsin |
similar structure to rhodopsin non-image forming function regulates circadian rhythm |
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