Term
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Definition
repeated stimuli within brief period of time have cumulative effect
Ex: stimulate axon twice, two consecutive ESPS, temporal summation occured |
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Term
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Definition
Excitatory Postsynaptic Potential
occurs when sodium ions enter cell.
DEPOLARIZATION |
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Term
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Definition
synaptic inputs from separate locations combine their effects on a neuron.
Ex: pinch two points at once, causes reflex. ESPS from several axons summate their effects on a postsynaptic cell |
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Term
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Definition
| increase negative charge inside the cell, moving it further from the threshold and decreases chance of action potential. |
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Term
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Definition
| hyperpolarization of membrane, synaptic input selectively opens potassium gates and allows for ions to leave cell, allowing for cl- ions to enter. |
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Term
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Definition
Series of action potentials without any synaptic input
can be increased by EPSP and decreased by IPSP |
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Term
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Definition
| Is neurotransmission chemical or electrical? Frog heart experiment. Took fluid from 1 frog’s vagus nerve, placed on other frog’s heart – slowed heart beat, therefore, it’s chemical |
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Term
| What Neurotransmitters are synthesized in the presynaptic terminal? and the soma? |
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Definition
peptides made in soma
other neurotransmitters (non neuro peptide) made in terminal |
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Term
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Definition
Agonist: binds to receptor, like neurotransmitter.
(key fits, turns)
Antagonist: blocks receptors
(key fits in lock, but does not turn it. blocks hole from other keys) |
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Term
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Definition
| neurotransmission attaches to another receptor of another neuron. outside of the cleft. |
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Term
| Ionotropic v.s. Metabotropic receptors |
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Definition
Ionotropic: ions can travel through receptors. require neurotransmitter to bind before they can open. It is the fastest.
Metabotropic: activated by neurotransmitter, no channel involved.
neurotransmitter attaches to the receptor, receptor bends + releases G protein. can attach to an ion channel, react on 2nd messengers, alter metabolic activities, or effect gene transcription factors. THIS IS THE SLOWEST. |
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Term
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Definition
activated by neurotransmitter, no channel involved.
neurotransmitter attaches to the receptor, receptor bends + releases G protein. can attach to an ion channel, react on 2nd messengers, alter metabolic activities, or effect gene transcription factors. THIS IS THE SLOWEST. |
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Term
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Definition
| Ionotropic: ions can travel through receptors. require neurotransmitter to bind before they can open. It is the fastest. |
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Term
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Definition
| too much glutamate, causes apoptosis |
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Term
| 7 events that occur at a synapse |
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Definition
1. synthesis of neurotransmitters
-peptides made in soma, others made in terminal
2. neurotransmitters are transported to the axons and dendrites
3. action potentials travel down axon, causes Calcium+ to enter the cell, which allows for neurotransmitters to be released.
4. neurotransmitters bind to receptors and activates
5. neurotransmitters separate from their receptors, may be converted to inactive chemicals
6. reuptake of neurotransmitter by transporter protein
-recycling of neurotransmitters, keep in cleft. inhibitors stop reuptake.
ex: anti-depressants
7. postysynaptic cells send reverse messages to control further release of neurotransmitters |
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Term
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Definition
| where neurotransmitters are stored |
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Term
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Definition
caused by calcium entering cell after action potential.
- release of neurotransmitter from presynaptic neuron into cleft. |
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Term
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Definition
| protein molecule in a cell or on the surface of a cell to which a substance (such as a hormone, a drug, or an antigen) can bind |
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Term
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Definition
affinity: a reception's strong or weak attraction to a drug
efficacy: a drug's tendency to activate the receptor |
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Term
most common excitatory + inhibitory neurotransmitter
What are the receptors for each of these neurotransmitters called? ( |
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Definition
excitatory: glutamate
---receptor: ionotropic (AMPA, NMDA, kainate), metabotropic (mGlu)
inhibitory: GABA
---receptor: ionic (Gaba), metabotropic
(Gaba-b) |
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Term
| What neurotransmitter do pyramidal neurons synthesize and release? |
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Definition
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Term
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Definition
-slow acting, broad effects
-bind to receptors to alter 2nd messenger systems
-can control release of other hormones
ex: pituitary gland = "master gland," because controls hormone release
Hypothalamus synthesizes: oxytocin (maternal behav, sexual arrousal) and vasioressin (increase water intake in kidneys) |
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Term
| What enzymes break down serotonin, dopamine, and norepinephrine? |
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Definition
MAO (monoamine oxidase) or
COMT (catechol-o-methytransferase) |
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Term
| Pituitary Gland: anterior v.s. posterior |
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Definition
anterior: gland tissue, allows synthesis + release of chemicals
posterior: nevous system tissue |
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Term
| What are the two hormones that are synthesized in the hypothalamus and released by the pituitary gland? |
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Definition
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Term
| What are the four stages of pharmacokinetics for a drug? |
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Definition
1. Absorption: how drug absorbs into bloodstream
2. Distribution
3. Metabolism
4. Elimination |
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Term
| What three properties must a drug possess in order for it to cross the blood brain barrier? |
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Definition
-uncharged
-small
-lipid solluble |
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Term
| What role does the liver play in pharmacokinetics? |
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Definition
| liver helps break down drug (metabolism) |
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Term
| four types of tolerance to drug effects. |
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Definition
Cross-tolerance: be tolerant to 1 drug, be tolerant to other drugs in same class
drug dispositional tolerance (pharmacokinetic): minimize drugs affects, need more
Pharmacodynamic (cellular): conditioned tolerance
behavioral tolerance: not apparent physical affects of drug
ex: functional alcoholic |
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Term
| drug effects v.s. drug actions |
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Definition
drug effects: behavioral effects of drug
drug actions: physiological actions through which drugs are produced |
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Term
| How do drugs affect Dopamine transmission? |
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Definition
-dopamine synthesized by Dopa (AMPT reduces dopamine release)
-L-dopa increases dopamine release
-MAO breaks down dopamine, increase dopamine release
-amphetamine: increases release of dopamine into synaptic cleft
cocaine, nicotine, block reuptake
(antagonist) |
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Term
| Dopamine in the Nucleus Accumbens? |
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Definition
more dopamine released in NAC = increase reward
Gaba is inhibitory -> increase gaba, decrease reward
increase in da -> decrease in activity of GABA, results in increase in reward effects
Release of glutamate increases activity of GABA and inhibits/decreases rewarding effects
reduce glutamate => reward effects
-block glutamate receptors
ex: PCP |
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Term
| What effects do psychostimulants have? |
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Definition
Psychostimulants: decrease appetitie, increase B.P. and other autonomic processes. give "high" feeling, increase alertness and mood
increase dopamine in NAC |
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Term
| What are two methods used for cocaine administration? What are the different preparation methods of cocaine for each form of administration? |
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Definition
Freebasing: dissolved in water, add ammonia and ether
Cocaine HCl: injection, drink it, "salt" form
Crack cocaine: cocaine, baking soda, and heat. inhale vapors |
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Term
| What are the mechanisms of action for cocaine? |
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Definition
blocks reuptake of Dopamine, norepinephrine, and serotonin.
rewarding effects: Da, Da2 receptor stimulation in NAC |
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Term
| Name a few drugs classified as amphetamines |
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Definition
| Benzedrine, Dexedrine, methamphetamines, ecstasy |
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Term
| What are the mechanisms of action of amphetamine (e.g., d-amphetamine)? |
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Definition
| Interferes with Dopamine storage, reverses uptake transporter for doapmine |
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Term
| What are the neurotoxic effects of MDMA? |
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Definition
euphoria, increase energy, increase socialness
stimulated dopamine release at low doses, serotonin at high doses
destroys serotonin synapses |
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Term
| What are the two most common ways of tobacco usage? Which is most efficient for getting nicotine absorbed into the blood stream? |
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Definition
Nicotine vaporized at 800 degrees Celsius, enters lungs on particles
smoking is more effective than chewing |
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Term
| How does nicotine produce its rewarding effects? |
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Definition
| binds to nicotinic receptors, bound by acetylcholine. NAC -> rewarding efffects |
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Term
What are the effects of caffeine at low doses and at high doses?
How does caffeine produce these effects? |
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Definition
low doses: increase energy, alertness, etc
high doses: tensions and anxiety
blocks adrenodine receptors (sleep) |
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Term
| What is the active ingredient in marijuana? |
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Definition
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Term
| What is the mechanism of action for marijuana’s reinforcing effects? |
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Definition
| act at cannabinoid receptors, increase dopamine release in NAC, decrease level of leptin (appetitite suppressing hormone) |
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Term
What is the principle ingredient in opium?
Name a few synthetic opiates.
How do opiates produce rewarding effects? |
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Definition
-from poppy plant
-morphine, heroin, methadone
-mu, delta, and kappa receptors, increase dopamine release in NAC |
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Term
Which form of the alcohols is safe to consume?
what is the elimination rate for alcohol? |
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Definition
-distilled alcohol and ethanol
-10ml/hour |
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Term
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Definition
-nausea, headache, intense thirst, fatigue
-cause: residual acetyldehyde, gastric irritation, excess fluid loss, rebound for sugar drop |
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Term
| Type I v.s. Type II alcoholism |
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Definition
Type 1: develop alcohol problems gradually
Type II: rapid onset, before age 25, most have relatives with alcohol problems |
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Term
| What is Antabuse (disulfiram) and how does it work? |
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Definition
inhibits acetaldehyde, causes a build up
-get very sick when drinking
used for alcoholism |
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Term
What is a neuromuscular junction?
In skeletal muscles, what neurotransmitter is released from neuromuscular junctions? |
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Definition
Neuromuscular junction: point where motor neuron meets muscle fiber
-releases acetylcholine, causes muscles to contract |
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Term
| prefrontal cortex, premotor cortex, supplementary motor cortex and primary motor cortex. Sort out the roles in these regions play in eliciting a motor response. |
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Definition
Prefrontal cortex: beginning of motor signal; responds to sensory info and plans movements accordingly
Premotor cortex: Preparations for movement
Supplementary motor cortex: preparation for rapid series of movements
primary motor cortex: precentral gyrus ~ elicits movement |
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Term
| Lateral v.s. medial corticospinal tract |
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Definition
Lateral: movements of extemities
-pyramidal tract
-opposite sides control each other, cross over in basal ganglia (contralateral control)
Medial: controls trunk muscles, posture, bending, standing, walking |
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Term
How do the basal ganglia “select” a movement?
What is the feedback pathway from cortex to the basal ganglia and then back to cortex? |
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Definition
-receives cortex info
-info routed to motor and prefrontal cortex
-selects movements that should be activated
-takes away inhibitors |
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Term
| What are the three classes of motor symptoms in Parkinson’s disease? |
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Definition
-Bradgkinesia: abnormal movement, loss of voluntary movement
-rigidity: resistance to passive movement
-tremors: rhythmic involuntary movement |
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Term
| Cognitive effects of Parkinson's Disease |
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Definition
-slow on cognitive tasks, such as imagining events or actions even when they dont have to do anything
-depressed, memory and reasoning deficits |
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Term
| What brain structures and pathways are damaged in Parkinson’s disease? |
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Definition
| lose 70-80% of dopamine neurons in substantia nigra (BASAL GANGLIA) |
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Term
| How do older antipsychotic drugs cause Parkinson’s-like symptoms? |
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Definition
EXTRAPYRAMIDAL SIDE EFFECTS (EPS)
-Da transmission blocked, block receptors
too much dopamine, but block D2 receptors in NAC -> increase effects |
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Term
| What is the primary treatment for Parkinson’s disease and what is a serious side effects of this treatment? |
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Definition
| L-dopa: increase dopamine release; increase psychosis |
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Term
| Environmental Neurotoxicity |
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Definition
| study of how environment can damage nervous system |
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Term
| How do substances damage nervous system? |
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Definition
Neuronopathy - damage neurons
Axonopathy - damage axons
myelinopathy - myelin damage
transmission toxicities - interferes with neurotransmission |
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Term
| What are the neurotoxicological effects of sarin? When does death occur? |
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Definition
acetylcholinesterase inhibitor;
no muscle control -> restriction, inability to breathe
survivors: weakness, fatigue, blurry vision, cognition difficulties, PTSD |
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Term
| What are the symptoms, pathology, and life expectancy of Huntington’s Disease? |
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Definition
-brain damage in basal ganglia
-symptoms: jerky arm movements, facial twitch, tremors, writhing movements
-age onset: 30-50
-death within 15-20 years
Huntingtin gene - mutation leads to disease |
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Term
| What are the symptoms, pathology, and life expectancy of ALS? |
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Definition
Lou Gehrig's disease
symptoms: muscle weakness + atrophy, dofficulty breathing
life expectancy: 3-5 years
pathology: damage to motor neurons, overstimulated by glutamate; too much calcium enters cell and causes apoptosis |
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Term
| What are the symptoms and pathology of myasthenia gravis? |
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Definition
autoimmune disease
-immune system forms antibodies that attack acetylcholine receptors at neuromuscular junctions
-causes muscles to become fatigued, impairs movement |
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Term
Acetylcholine
-location of cell bodies
-target regions of pathways
-the steps in synthesis
-the receptor names |
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Definition
-cell bodies located in basal forebrain
-Target regions: cortex, hippocampus, basal ganglia
Receptors
Nicotinic: ionotropic, alpha + beta subunits
Muscanic: metabotropic; m1-m5
Acetyl Co A + Choline -> Acetylcholine |
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Term
Dopamine
-location of cell bodies
-target regions of pathways
-the steps in synthesis
-the receptor names |
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Definition
-soma in ventral tegmental (reward pathway) + substantia nigra (goes to basal ganglia - movement)
-target regions: basal ganglia + cortex
-receptors: D1-D5
Tyrosine -> Dopac -> Dopamine |
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Term
Norepinephrine + Epinephrine
-location of cell bodies
-target regions of pathways
-the steps in synthesis
-the receptor names |
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Definition
-soma in locus coerulus (stress rxn)
-target areas: thalamus, amygdala, cortex
receptors: adrenoceptors; alpha, beta
Tyrosine -> Dopac -> Dopamine -> Norepinephrine -> Epinephrine |
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Term
Serotonin
-location of cell bodies
-target regions of pathways
-the steps in synthesis
-the receptor names |
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Definition
-soma in Raphe Nucleus
-target regions: all throughout brain
-5-HT receptors
Tryptophan -> 5-HTP (5-hydroxytryptophan) -> 5-HT (hydroxytryptotamine) |
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Term
| what prevents extra GABA and glutamate from leaving cleft? |
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Definition
| Astrocytes break them down |
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