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207 Cards in this Set
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neurotransmitters |
Substances released by one neuron that bind to receptors on the target neuron eg. acetylcholine some are referred to as neuromodulators |
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neurohormones |
released by brain or other organs, travel via bloodstream to target neurons eg. epenephrin (adrenal gland) |
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examples of neurotransmitters n the nervous system |
-acetylcholine -dopamine -norepinephrine -serotonin -glutamate -GABA -Anandamide |
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Neurotransmitters -acetylcholine -dopamine -serotonin -epinephrine -glutamate -GABA -Anandamide |
Associated Neurons -cholinergic -dopaminergic -noradrenergic -serotonergic -adrenergic -glutaminergic -GABAergic -cannabinergic |
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Acetylcholine |
-first neurotransmitter discovered (in PNS) -most extensively studied neurotransmitter |
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Cholinergic Neurons |
Dorsolateral Pons -->REM sleep (inlcuding atonia) Basolateral Forebrain--> activates cerebral cortex, facilitates learning Medial Septum--> controls rythms in hippocampus, modulates memory formation |
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Synthesis of Acetylcholine |
Produced by combining the lipid breakdown product choline with acetyl-CoA (made in the mitochondria) |
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Enzymes |
proteins that catalyze a reaction that might normally take a long time to occur -words ending in "ase"--> enzyme -first word or part of word refers to what the enzyme is acting on |
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Two types of ACh Receptors |
-Ionotropic--> Nocotinic AChRs (fast) -Metabotropic --> muscarinic AChRs (slow) |
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Cholinergic Receptors |
-Muscles contain nicotinic AChRs (essential for rapid transmitter action at neuromuscularjunction) -CNS contains both types, though mostly muscarinic AChRs (nicotinic AChRs tend to be found at axoaxonic synapses) |
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Acetylcholinesterase (AChE) |
inactivates ACh after it is released (breaks it into acetate and choline) |
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Choline Re-uptake |
Choline is transported back into the presynaptic terminal for local synthesis of ACh -reuptake is vital because axonal transport of choline from cell body is slow -reuptake has an efficiency of about fifty percent |
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hemicholinium |
drug that inhibits the reuptake of choline |
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acetylcholinesterase |
breaks down acetylcholine into acetate and choline |
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Drugs that affect cholinergic receptors |
-curare -atropine |
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curare |
-blocks nicotinic AChRs (or nAChRs) -had been and still is used by native South American populations -Used to paralyze muscles during surgery |
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Atropine |
-blocks muscarinic AChRs (or mAChRs) -used to treat AChE inhibitors (thus reducing the excess ACh action) -also used to dilate the pupils for eye exams |
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Acetylcholinesterase inhibitors (AChE inhibitors) |
-prolong the effects of ACh released by preventing its breakdown -used as insecticedes -used medically to relieve symptoms of myasthenia gravis (auto immune) -used as biological weapons |
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classification of the monoamine transmitters |
Catecholamines-- dopamine, norepinephrine, epinephrine Indolamines-- serotonin |
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substantia nigra (nigrostriatal) |
to neostriatum, part of basal ganglia (involved in the control of movement |
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VTA (mesolimbic projection) |
to nucleus accumbens (involved in reinforcing effects of drugs of abuse) to amygdala (involved in emotions) to hippocampus (involved in the formation of memories) |
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VTA (mesocortical projection) |
to prefrontal cortex (involved in short term memories, planning, problem solving strategies) |
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Parkinson's disease |
due to the degenerative loss of pigmented neurons, particularly the dopaminergic neurons of the SNc that project to the striatum |
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MAO (monoamine oxidase) |
-destroys excess monamines -MAO-B is specific for dopamine -deprenyl is an MAO-B inhibitor (depression, parkinson's) |
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Reuptake |
transporters are used to remove dopamine from the synaptic cleft and return in to the nerve terminal |
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regulation of dopamine |
-MAO (monoamine oxidase) -reuptake |
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Drugs that affect dopaminergic tranmission |
-monoamine oxidase inhibitors (MAO inhibitors) -Re-uptake inhibitors |
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Monoamine oxidase inhibitors (MAO inhibitors) |
-MAO regulates the production of catecholamines (destroys excess) -MAO inhibitors are used to treat depression -MAO-B is specific for dopamine (e.g. deprenyl) |
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Re-uptake inhibitors |
-blocks re-uptake of dopamine by nerve terminals -e.g. amphetamine, cocaine, methylphenidate |
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Drugs that Affect Dopaminergic transmission |
-L-DOPA -AMPT (methyl tyrosine) -MPTP (methyl phenyl tetrahydropyridene) -resperine |
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L-Dopa
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-used to treat parkinson's disease -crosses blood-brain barrier and enters CNS where it is converted to dopamine |
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AMPT |
-binds to tyrosine hydroxylase -thus it prevents synthesis of L-DOPA and therefor dopamine |
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MPTP |
-contaminant in synthetic Heroin -it's metabolized into MPP+, which destroys dopamine neurons and produces parkinson-like symptoms |
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reserpine |
-prevents sotrage of monoamines in synaptic vesicles -acts by blocking transporters that pump monoamines into vesicles -end result is no transmitter is released |
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Dopamine Receptors |
-DA receptors are metatropic -5 subtypes of DA receptors (D1-D5), D1 and D2 are the most common subtypes -some are autoreceptors (similar to D2) located pre and post synaptic -Apomorphine has multiple effects on DA receptors |
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Postsynaptic (autoreceptors) |
-act to decrease neuron firing (k current) |
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presynaptic (autoreceptors) |
act to suppress tyrosine hydroxylase |
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apomorphine |
-at low doeses it bind presynaptic autoreceptors (decrease DA) -at high doses it acts as an agonist at postynaptic D2 receptors) |
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Schizophrenia |
-serious mental disorder characterized by hallucinations, delusions, and disruption of normal logical thought processes -may involve hyperactivity of dopaminergic neurons (excess) --1. chlorpromazine (D2 antagonist) alleviates hallucinations in schizophrenic patients --2. clozapine (D4 antagonist) also relieves symptoms |
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Noradrenergic Neurons |
Locus coeruleus (located in reticular formation -contains noradrenergic neurons whose acons extend to most of the brain, including thalamus, hypothalamus, limbic, cerebral cortex -activation of LC increases vigilance or attentiveness to environment |
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norepinephrine |
-synthesized from dopamine -synthesis actually occurs inside synaptic vesicles |
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examples of drugs that affect noradrenergic transmission |
1. fusaric acid 2. moclobemide 3. despramine |
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fusaric acid |
-blocks DA-beta-hydroxylase -results in blockade of NE production in vesicles |
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moclobemide |
-blocks MAO-A(which normally destroys excess NE) -results in an increase in NE |
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Desipramine |
-blocks re-uptake of NE (and possibly serotonin) -a tricyclic acid |
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NE Receptors |
-called adrenergic because they respond to both norepinephrine (noradrenalin) and epinephrine (adrenalin)
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adrenergic receptors |
-metabotropic and coupled to G proteins |
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2 types of adrenergic receptors are alpha and beta |
-alpha 1 and alpha 2-->adrenergic (located in CNS and PNS) -beta 1 and beta 2 -->adrenergic (located in CNS and PNS) -beta 3 (located only in PNS) |
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Alpha 1 |
adrenergic (slow depolarizing effect; more responsive to excitatory input) |
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alpha 2 |
adrenergic (slow hyperpolarizing effect) |
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beta 1 and beta 2 |
adrenergic are excitatory (they increase neuronal responsiveness to inputs) beta 1 are mostly on heart muscle wheras beta 2 are mostly on smooth muscle lining bronchioles and arterioles of skeletal muscle |
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serotonin |
-synthesized from the amino acid tryptophan -important in the following --regulation of mood --control of eating, sleep, arousal --regulation of pain (hyperalgesia after injury) --control of dreaming |
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dorsal raphe |
sends 5 HT projections to cortex and basal ganglia |
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medial raphe |
sends 5 HT projections to cortex and dentate gyrus |
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raphe |
crease or seam (the neuclei are found near the midline of the brain stem -the clusters of nuclei that make up the raphe are found in the medulla, pons, and midbrain |
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Synthesis of Serotonin (or 5HT) |
PCPA (p-chlorophenylalanine)--blocks tryptophan hydroxylase and thus serotonin production MAO-A (monoamine oxidase A)--inactivates excess serotonin, ultimately converted into 5 HIAA (measurable metabolite)(5hydroxyindoleacetic acid) |
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serotonin receptors |
-5HT receptors are metabotropic (except 5HT3 is an ionotropic CL- channel) -At least 9 different subtypes of 5 HT receptors -5HT3 are important in nausea and vomiting (antagonists help in chemo patients) |
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autoreceptor |
receptor on its own axon terminal that responds to the neurotransmitter released by the same axon (a negative feedback mechanism) |
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drugs that affect serotonin |
-5HT reuptake inhibitors -fenfluramine -ecstacy |
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5HT re-uptake inhibitors (SRIs or SSRIs) |
useful in treating certain mental disorders (these drugs act by prolonging the action of serotonin at synapses) eg fluoxetine (prozac)--depression and anxiety disorders |
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fenfluramine |
has been used as an appetite suppressant (in combination with phenteramine which acts on catecholamines to counteract the drowsiness caused by fenfluramine) |
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5HT2A agonists |
cause hallucinations eg LSD is though to exert behavioural effects as an agonist of 5HT2A receptors in the forebrain |
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ecstacy (MDMA) |
(methylenedioxymethamphetamine) causes release of serotonin, norepinephrine, and to a lesser extent dopamine (agonistic effect) MDMA damages serotonergic neurons |
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Amino Acid Neurotransmitters |
excitatory and inhibitory 1. the excitatory neurotransmitter is glutamate (in brain and spinal cord) 2. the inhibitory neurotransmitter is GABA (in brain) or Glycine (in spinal cord and lower brain) |
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Glutamate (principle excitatory transmitter) |
-4 receptor subtypes (3 ionotropic and 1 metabotropic) -caffeine -msg |
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4 receptor subtypes (3 ionotropic and 1 metabotropic) |
-AMPA receptor (ionotropic is the most common (Na+ influx). these ionotropic receptors bind glutamate and open ion channel, even when the cell is at rest. -NMDA receptor (ionotropic) is also common but these require depolarization because they are blocked by Mg2+ when neuron is at rest |
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caffeine |
increases glutamate indirectly by blocking adenosine receptors which normally inhibit glutamate release |
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MSG (monosodium glutamate) |
binds glutamate receptors and can produce tingling, burning, ringing in the ears, loss of sensation |
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6 NMDAR binding sites |
1. glutamate (natural agonist) 2. glycine (co-agonist required for glutamate to have any effect on NMDARs) 3. MG2+ (binds inside channel and blocks) 4. Zn2+ (decreases activity) 5. polyamine (increases activity) 6. PCP (blocks channel) --Thus, the NMDA receptor is a voltage and neurotransmitter dependent ion channel |
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GABA (major inhibitory transmitter in brain) |
-2 main receptor subtypes (1 ionotropic and 1 metabotropic) |
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Glycine (inhibitory transmitter in cord and lower brain) |
-ionotropic receptors (Cl- influx causes IPSPs) -strychnine is an antagonist (convulsions via excess/ uncontrolled excitatory drive) |
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GABA receptors |
-enzyme GAD (glutamic acid decarboxylase) converts glutamic acid to GABA... GAD is inhibited by allylglycine (thus blocking GABA synthesis) -GABA receptor subtypes |
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GABA receptor subtypes |
-GABA(A) -GABA(B) |
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GABA(A) |
-ionotropic -opens Cl- channel, causing Cl- influx and hyperpolarization |
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GABA(B) |
-metabotropic (coupled to G-proteins) -causes K+ efflux and thus hyperpolarization -Baclofen is an agonist (relaxes muscles) |
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GABA(A) receptor's 5 binding sites |
-GABA (natural agonist) -benzodiazepine (indirect agonist) -barbiturate (indirect agonist) -steriod (indirect agonist) -picrotoxin (indirect agonist) |
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GABA (natural agonist) |
muscimol and bicuculline are direct agonists |
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benzodiazapine (indirect agonist) |
anxiolytic drugs (diazepam or valium) tranquilizers, promote sleap, reduce seizure activity, relax muscles. --beta CCM may be a natural ligand for benzodiazepine binding site. this is an inverse agonist and thus produces fear, tension, and anxiety. it may be part of our fight or flight danger system. |
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barbiturate (indirect agonist) |
-low doses have a calming effect -rarely uses as an anesthetic due to small therapeutic index (easy to OD) |
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Other neurotransmitters/ neuromodulators |
-peptides -lipids -nucleosides -soluble gases |
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peptides |
-2 or more amino acids linked together -includes various endogenous opioids -substance P is thought to be the primary neurotransmitter signaling pain |
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lipids |
-can transmit between or within cells -eg anandamide- endogenous cannabinoid receptor ligand (THC in marijuana binds to the same receptors); altered mood and sensory perception as well as memory and motor impairments |
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nucleosides |
-sugar + purine (A and G) or pyrimidine (C and T) base eg adenosine (ribose + adenine) coupled to G proteins which open K + channels, thuse causing IPSPs (thus it's inhibitory) - caffeine blocks adenosine receptors and thus is excitatory |
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Soluble Gases |
- nitric oxcide or NO (NOS converts argenine to NO; blocked by L-NAME) -carbon monoxide or CO -diffuse out of the cell and activate neighboring cells to produce cGMP |
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Development of the Human Brain |
Relative Brain Size -at birth: 350 g -1 year: 1000 g -adult: 1200 g |
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neurogenesis |
declines significantly by week 20 and is nearly complete by 5 months, but it does continue throughout life in some regions |
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Neurotrophic factors |
-EGF -bFGF -PDGF |
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EGF |
(epidermal growth factor) -stem to progenitor |
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bFGF |
(basic fibroblast growth factor) -progenitor to neuroblast |
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PDGF |
(platelet derived growth factor) -progenitor to glioblast (specificallly oligodendrocyte) |
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Processes involved in neuron production |
-proliferation -migration -differentiation and maturation -myelination -synaptogenesis |
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proliferation |
-production of new cells (primitive glia and neurons) -stem cells continue to divide |
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migration |
-occurs inside out |
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differentiation and maturation |
-formation of acons the dendrites (transplantation depends upon age) |
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myelination |
-continues gradually over many years |
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synaptogenesis |
-formation of synaptic connections (requires extra cholesterol from glia) -continues throughout life |
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growth cones
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extend out as acons seek targets |
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tropic molecules |
guide acons; produced by targets (e.g. netrins) |
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trophic molecules |
support survival of cells and axons once target is reached (neurotrophins, e.g. NGF, BDNF) |
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Synapse Pruning (Elimination) |
synaptic connections are plastic |
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environmental enrichment |
-increases dendrite complexity -increases number of synapses |
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Regrowth of Axons |
-can occur as long as the soma or cell body is intact. -rate is usually about 1 mm/day in PNS (in CNS, axons usually regenerate only 1-2 mm total, thus paralysis due to spinal cord injury is usually permanent) -in PNS, axon regrowth follows myelin sheath back to target |
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Regrowth in PNS may not be perfect |
if a motor neuron's acon is cut (not crushed), segments may not align and axon may synapse on wrong target muscle |
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Amphetamine |
causes DA release from existing axon terminals |
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apomorphine |
stimulates DA receptors (an appropriately high dose was used) |
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3 kinds of muscle |
1. skeletal muscle 2. smooth muscle 3. cardiac muscle |
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skeletal muscle
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-striated appearance -attached to bones and cartilage -moves bones -under somatic n.s. control |
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smooth muscle |
-smooth or non-striated appearance -lines blood vessels and various organs -under autonomic n.s. control |
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cardiac muscle |
-striated appearance -found only in heart |
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Skeletal muscle |
-attach to bone or cartilage via tendons -made up of cells (muscle fibers) -each muscle fiver contains contractile proteins --actin-thin filaments --mysin- thick filaments -the filaments overlap |
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skeletal muscle |
-striated appearance due to arrangement of actin and myosin -actin filaments (thin) are attached to proteins that form the z-line -myosin filaments (thick) are found between rows of actin |
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sliding filament theory of muscle contraction |
-during contraction, the following events occur 1. actin filaments slide along each mysin filament (from both ends) 2. z-lines get closer together (because actin is attached to z-line) 3. result is that the muscle shortens |
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neuromuscular junction and muscle contraction |
-motor neurons innervate skeletal muscle fibers at a special region called the motor endplate -the motor endplate contains ACh receptors (mostly nicotinic) -one motor neuron can innervate multiple muscle fibers (motor unite= motor neuron plus the muscle fivers it innervates) -muscles used for very fine (discrete) movements have smaller motor units. -muscles used for posture have larger motor units |
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red muscle |
-high concentration of myglobin (carries oxygen) -relies heavily on oxidation to produce ATP -engages in heavy activity without fatiguing -used for slow, sustained movements e.g. chicken or turkey legs |
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white muscle |
-low concentraion of myoglobin -quickly goes into oxygen debt during contraction -fatigues quickly -used for rapid contractions in short bursts eg chicken or turkey breasts |
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human movement colours |
-sprinting uses white -hiking/walking uses red |
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antagonistic muscles |
flexion and extension |
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isotonic contraction |
muscle shortens eg legs, produces the movement when carrying heavy box |
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isometric contraction |
muscle length stays same eg back and arm muscles contract when holding or carrying heavy box |
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reflexes |
-rapid movements mediated by either brain stem nuclei or the spinal cord -very important (protect body, basic life support) -vary in complexity and number of synapses: --simple (withdrawal or flexion reflex) --complex (postural, involving many different muscles) |
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three reflexes seen in infants |
-grasping -babinski -rooting |
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the babinski reflex |
in children and adults it's diagnostof of CNS |
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positive babinski |
-fanning of toes with stroking bottom of foot -always seen in infants less that 6 months due to lack of descending inhibition |
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negative babinski |
-curling of toes with stroking bottom of foot -seen in older infants and all healthy people -results from descending inhibition |
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withdrawal reflex |
-simple reflex involving only a few synapses between the sensory (afferent) neuron and the motor (efferent) neuron -involves one or more interneurons between the sensory and motor neuron |
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2 types of motor neurons |
-alpha motor neurons -gamma motor neurons |
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alpha motor neurons |
-larger diameter -faster conduction time -innervate extrafusal muscle fibers |
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gamma motor neurons |
-smaller diameter -slower conduction time -innervate intrafusal muscle fibers -important for enabling muscle spindle to provide a readout of muscle length |
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extrafusal fibers |
run the length of the muscle |
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intrafusal fibers |
do not run the length of the muscle and are located within the muscle spindle |
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muscle spindle |
a few intrafusal fibers joined to a nuclear bag (inside the nuclear bag is a stretch receptor called the annulospiral receptor) |
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axons from annulospiral receptor |
terminate onto motor neurons in spinal cord --thus, stretching a muscle activates the annulospiral receptor which then stimulates extrafusal fibers |
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annulospiral receptor |
Muscle Spindle - vital for maintaining muscle tone |
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problem inherent in the stretch reflex |
-contraction of one muscle would produce contraction of antagonist muscle -the simple bending of the arm by biceps contraction (agonist) would cause the arm to straighten due to activation of the stretch reflex of triceps (antagonist) muscle |
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reciprocal innervation |
(discovered by sherrington) with this, the axons of motor neurons that synapse on a muscle also branch and activate interneurons that inhibit motor neurons that synapse on the antagonist muscles |
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what if the muscle is contracting too vigorously? |
if this happens, gogli tendon organ reflex is activated |
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Gogli Tendon Organ (GTO) |
-stretch receptor found in the tendon -provides feedback to nervous system about muscle contraction -GTO fires when stretched -GTO axons synapse onto inhibitory spinal cord neurons -result of GTO activation is inhibition of the motor neuron -prevents damage to muscle as a result of excess contraction |
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Sir Charles Scott Sherrington (1884-1935) |
-studied many kinds of reflexes -discovered reciprocal innervation -introduced the term synapse -Principle of the common path--> motor neuron is final common path for all movement -Principle of the integrative action of neurons -->allneurons in the body work together to produce smooth, precice movements. -->the crossed extensor reflex is an excellent example |
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crossed extensor reflex |
-withdrawal reflex activated by sensory neuron synapsing onto interneuron, which excites motor neurons of the ipsilateral flexor -interneuron also crosses over and synapses onto and excites the motor neurons of the contralateral extensor |
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upper motor neurons |
-above level of spinal cord motor neurons -cortical neurons |
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lower motor neurons |
-spinal cord motor neurons -those in ventral horn of spinal cord |
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contemporary classication scheme
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-the lateral group or system (fine or directed movements)-->lateral corticospinal tract (dorsolateral tract) -the medial group or system (automatic or postural movements)--> anterior corticospinal tract (ventromedial tract). -->basal ganglia and cerebellum |
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the lateral (pyramidal motor system) |
-originates in the primary motor cortex -axons of these upper motor neurons project downward--through internal capsule--through medullary pyramids (hence name)--main branch crosses over at pyramidal decussation in medulla and descends through the contralateral spinal cord forming the lateral corticospinal tract |
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lateral corticospinal tract |
-fine, directed motor control -hands, fingers, feet, teos -synapse directly onto motor neurons or indirectly via interneurons |
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effects of damage to cortospinal tract |
-initial loss of muscle tone (atonia)--transient flaccid paralysis immediately upon damage -hyperactive deep tendon reflexes (myotactic)--hyperreflexia -appearance of the babinski sign (positive babinski)--a positive babinski may have be seen during sleep or intoxication, and in infants <6mo. |
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apraxia |
produced from damage to the premotor or supplementary motor cortex or to parts of the parietal or temporal cortex |
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apraxia without action |
difficulty carrying out purposeful movements, in the abscense of paralysis or muscle weakness |
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apraxias are classified according to the systems affected |
-limb apraxia--movements (parietal lobe damage) -oral apraxia--speech (broca's area damage) -apraxic agraphia--writing (left parietal lobe damage if right handed) -constructional apraxia--drawing or construction (parietal lobe damage) |
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posterior association cortex |
involved with perceptions |
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frontal association cortex |
involved with plans for movement |
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mirror neurons |
activated by -movement -observing movements |
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muscular dystrophy |
(muscle wasting) -30 different types, Duchenne's MD is the most common -about 1in3-4000, typically between ages of 2 &6 -due to defect in gene that encodes dystrophin -more common in boys (due to gene on x chromosomes) |
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myasthenia gravis |
(degeneration of acetylcholine receptors at NMJ) -results from an autoimmune response against AChRs -treated with immonusuppressants or thymectomy -treated with anticholinesterases (acetylcholinesterase inhibitors) -may also try plasmapheresis (filter the AchR-attacking antibodies from the patients blood) |
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amyotrophic lateral sclerosis of ALS |
(lou gehrig's disease, motor neuron generation) -degeneration of motor neurons in brain and spinal cord -progresses from muscle weakness to muscle wasting -no treatment -5-6000 new cases each year, typically between ages 40 and 70 |
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the medial (extrapyramidal motor system) |
-coordinates gross movements and postural adjustments -develops before the pyramidal (lateral) system -develops at different times |
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cerebellum |
-receives sensory information from all sensory systems and cortex -it must know what every muscle in the body is doing at every moment -ballistic movements, learned movements |
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basal ganglia |
-relays infor to and from cerebral cortex -numerous structures work together to coordinate gross movements |
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the cerebellum and movement |
-important for rapid coordination of movements -important for ballistic movements -receives information from all senses and cerebral cortex -must know what every muscle is doing at any given time in order to properly coordinate rapid movements |
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damage in cerebellum |
-ataxia-->inability to walk in a coordinated manner -disequilibrium--> loss of balance |
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basal ganglia |
a cluster of neuronal structures concerned with the production of movement |
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stiatum |
(caudate, putamen) -receives information from cerebral cortex -sends that information to globus pallidus -caudate--process of cognitive information -putamen--relays motor signals |
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globus pallidus |
sends information back to cortex via thalamus |
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substantia nigra |
produces DA and projects to caudate and putamen |
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subthalamic nucleus (STN) |
sends projections to and receives projections from the globus pallidus |
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damage to the basil ganglia |
(movement disorders result from this) -tics -choreas -huntington's disease -parkinson's disease |
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tics |
brief, involuntary contractions of specific muscles |
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choreas |
involuntary movements of head, arms, legs |
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huntington's disease |
-uncontrolled tics and choreas early, dementia later -disruption of gene on chromosome 4 (excess CAG repeat) resulting in a n abnormal huntington (HTT) protein (with an elongated string of glutamine residues on it). the Htt mutation ultimately leads to death of GABAergic inhibitory neurons in the putamen (part of the striatum) |
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parkinson's disease |
-temor, loss of balance, rigidity (hard to initiate movement) -caused by loss of dopaminergic neurons in substantia nigra |
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relationship between CAG repeats and Age of onset |
-CAG codes for glutamine -11-24 CAG repeats is normal ->36 is linked to huntington disease |
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treatments for parkinson's disease |
-pharmacological treatments -destructive surgical treatments -nondestructive surgical treatments -restorative surgical treatments |
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phormacological treatments |
-L-DOPA crosses blood-brain barrier and is converted to dopamine -glutamte antagonists reduce hyperactivity of glutamate in subthalamic nucleus |
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destructive surgical treatments |
-thalamotomy- surgical cut in ventral thalamus -pallidotomy--surgical cut through the globus pallidus *both are thought to interfere with excitatory messages that produce symptoms and both reduce the rigidity and tremors (improving posture, gait, locomotion *less common than deep brain stimulation |
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nondestructive surgical treatments |
subthalamic nucleus (STN) stimulation reduces symptoms *also called deep brain stimulation |
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restorative surgical treatments |
stem cell implantations- injection of stem cells that will become DA-producing cells -use of embryonic cells raises serious ethical issue -use of adult stem cells aboud ethical issue gene therapy-- intoduction of a gene that would rescue function |
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electromagnetic radiation, vibration, sound |
many stimuli are transmitted as waves |
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the electromagnetic spectrum |
1. wavelength (nm, 1nm =10^-9m) 2. frequency (Hz, Hertz, cycles per s) 3. amplitude (dB, decibels, range: 0-160) |
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wavelength |
~280-760 nm is visible to humans |
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electromagnetic radiation (eg lightwaves) |
relationship between velocity (v), frequency (f), and wavelength (w) v=fw |
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adaptation |
decrease in the firing rate in response to a continuous stimulus (odor perception decreases as you get used to it) |
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anatomy of the eye |
-cornea -aqueous humor -pupil -lens -vitreous humor -retina -optic nerve -optic axis -fovea centralis -optic disk -sclera |
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cornea |
transparent covering in front of eye, curvature aids in focusing light |
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aqueous humor |
fluid behind cornea |
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pupil |
opening in center of iris |
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lens |
transparent structure that focuses images on retina -controlled by ciliary muscles (smooth muscle) -when image is far away, the lens flattens (gets thinner/weaker) -when image is close, the lens shortens (gets fatter/stronger) -process of lens changing shape is accommodation -presbyopia is age-related loss in lens elasticity (need reading glasses) |
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vitreous humor |
clear gelatinous liquid inside main part of eyeball |
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retina |
interior lining of the back of the eye -contains photoreceptors (rods and cones) |
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optic nerve |
carries visual signal from retina into the brain |
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optic axis |
imaginary straight line through eye to fovea centralis |
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fovea centralis |
-cones only (no rods in fovea!) -the highest density of rods is in the area right next to the fovea (rods decrease in density with distance from fovea) |
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optic disk |
-where optic nerve exits -blind spot |
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sclera |
tough outer white covering |
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rods |
respond best to dim light -1 kind of rod -more numerous than cones (~120 million rods) -dispersed throughout the retina -insensitive to detail; peripheral vision -extremely sensitive to light (best in dim light )-- scotopic or dark vision |
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cones |
respond best to bright light (color) -3 different kinds of cones -less numerous than rods (~5 million cones) -concentrated in fovea centralis (macula) -fine detail -less sensitive to light (best in bright light)-- photopic or light vision |
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visual receptors |
-outer segment- photopigments --eg rhodopsin (rods) --photopigments absorb photons (light) --2 pars: protein opsin and lipid retinal --11cisretinal (benifits of vitamin A) --bleached after absorption of photons --unbleached after removal of lilght (called dark adaptation) -inner segment- nucleas and organelles |
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bleaching of photopigments |
rods-very sensitive to light (thus sensitive to bleaching)-->photpigments bleach faster and more completely than cones cones-less sensitive to light-->photpiments bleach more slowly -->if light is bright enough, even cones will bleach (sun reflecting off snow is blinding) |
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dark adaptaion |
unbleaching note. when a photoreceptor absorbs light, it is bleached (unresponsive to light). following removal of light, recovery (unbleaching) occurs and photoreceptor is ready to respond to light once again |
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5 layers of cells in the retina (listed from the back or outer layer of the eye) |
1.visual receptors 2. horizontal cells 3. bipolar cells 4. amacrine cells 5. ganglion cells |
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visual receptors |
located near the back outer layer of retina, just in front of the pigment epithelium. they absorb photons (light waves) |
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bipolar cells |
transfer generator potentials from visual receptors to ganglion cells |
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ganglion cells |
located just behind the vitreous humor and fire action potentials. their axons from the optic nerve |
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pigment epithelium |
back layer of cells that contains blood vessels that nourish the retina and also serves to absorb stray photons (thus minimizing distortion) |
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3 main layers of the retina |
-photoreceptor layer -bipolar cell layer -ganglion cell layer |
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visual receptors |
in the dark, rods and cones are depolarized and release inhibitory transmitter onto bipolar cells (hyperpolarizing them). light closes ion channels that are permeable to Na+ results in hyperpolarization of visual receptors and less transmitter release, thus depolarizing bipolar cells |
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bipolar cells |
transmit between visual receptors and ganglion cells (releases excitatory transmitter glutamate onto and activates ganglion cells) |
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ganglion cells |
just behind the bitreous humor and fire action potentials. their axons form the optic nerve |
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summary of the effects of light stimulation |
-normally the visual receptor is depolarized and inhibiting the bipolar cell -light hyperpolarizes the visual receptor (rods or cones) which then depolarizes the bipolar cell -depolarization of the bipolar cell causes depolarization of the ganglion cells -depolarization of the ganglion cell causes it to fire more action potentions **net result is that light shining on the photoreceptor excites the ganglion cells |
