Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

47 Cards in this Set

  • Front
  • Back
what is the time scale for fast and slow synaptic transission, neuromodulation, and neurotrophic effects?
fast - msec
slow - 100s of msec to sec
neuromodulation - minutes to hours
trophic effects - hours to days
neuromodulators are usually ___
metabotropic receptors are involved in ___ synaptic transmission
the effects of ____ receptors are indirect
metabotropic / GCPR
neurotrophic factors act through ___ receptors
structural differences between ionotropic and metabotropic receptors?
5 subunits each with 4 TMD's
4 subunits each with 3 TMD's (glutamate)
these form a pore

one serpentine GPCR (7 TMD)
what NT has just ionotropic receptors?
which NT's have just metabotropic receptors?
dopamine, norepinephrine, and all neuropeptides
sensory receptors are in the category of ____ receptors
what is densensitization?
the decrease of the response to an agonist event though the agonist is still present (bound??)
when would the relative amounts of the agonist and antagonist matter in determining effect?
with a competitive antagonist
glutamate ionotropic receptors structure
4 subunits with 3 TMD's and a pore loop
all other ionotropic receptor structure
5 subunits with 4 TMD's
how is the diversity of ionotropic receptors with regards to desentization, regulation, agonists and antagonists, and selectivity achieved?
with different combinations of subunits
2 receptors for glutamate differ in their amount of desentization. how is this accomplished?
by different combinations of subunits
GABA and glycine are ____ NT's and their receptors are permeable to ____
inhibitory; Cl
Glutamate, Ach, and serotonin are ____ NT's and their receptors are permeable to ____
excitatory; Na, K, sometimes Ca
how are muscle Ach receptors different from those in the brain?
muscle 2a,b,g,d
brain -just a and b. some are homopentamers of alpha
which subunits of AchR bind Ach
all ionotropic glutamate receptors are permeable to __ and ___, and some are also permeable to ___
Na, K; Ca
3 types of ionotropic glutamate receptors
NMDA, AMPA, Kainate
difference b/t NMDA and AMPA glutamate receptors?
NMDA is blocked by a Mg ion at RMP. with depolarization AND glutamate, it can open. NMDA is permeable to calcium. its dual requirement for opening makes it important in learning and memory.

AMPA is not blocked at RMP and is not Ca permeable
picrotoxin and biculline are antagonists of ___ receptor
GABA (GABAa receptor)
___ is the predominant GABA receptor in the brain. ___ is only in the retina
why are allosteric binding sites on the GABAa receptor important?
they allow affects from drugs like barbituates, benzodiazepines, steroids, convulsants (biculline), and ethanol to modulate inhibitory current in the brain and spinal cord
benzodiezapines - effect and mech?
potentiate GABA binding at GABA receptors, have anti-anxiety and muscle relaxing properties
blocks glycine receptors. (major inhibitory NT of the spinal cord) causes muscle spasms
co-agonist for NMDA receptor?
cholera toxin
prevents GalphaS from hydrolyzing GTP. this keeps it in active form.
pertussis toxin
prevents Galphabetagamma bound to GDP from releasing GDP. this keeps the G protein from becoming activated again.
how can a GPCR modulate the release of NT?
there is autoregulation at presynaptic nerve terminals. there are alpha-2 adrenergic receptors (GPCR) that inactivate calcium channels preventing further release of NT.

presynaptic autoreceptors
how can metabotropic NT receptors produce the longest effects?
by modulating gene expression

e.g. modulating enzymes, etc, and changing the synthesis of NT's
what implication does a variety of metabotropic receptor subtypes have for drug design?
the same NT can have different affects in different cells. a drug may have side effects because of this
Alzheimer's is associated with which NT?
glycine receptors are blocked by ___
what is slow channel syndrome?
a mutation in muscle AchR causes the channel to stay open too long. these people have prolonged AP's which results in muscle problems
what is startle disease / stiff baby syndrome?
mutation in glycine receptor causes exaggerated startle reflex
benzodiazepines and barbituates act at __ receptor
GABA. they are agonists and increase inhibition
Enhancement of ___ is a highly effective method for treating some types of anxiety and epilepsy.
the ____ receptor is implicated in excitotoxicity and stroke
how can glutamate play a role in stroke?
ischemic neurons release glutamate
glutamate binds to NMDA receptors on other neurons and causes them to fire, taking in large amounts of Na and Ca.
these neurons die (excitotoxicity) and they then release glutamate
toxic cascade
cocaine blocks reuptake of ___ which plays a role in the ____ system of the brain
amphetamine causes the _____ to run in reverse resulting in ____ release
dopamine transporter
ritalin blocks ____
dopamine and norepinephrine transporters, keeping them in the synapse longer for greater affect
MAO inhibitors function as ___ and block degredation of ___

serotonin, norepinephrine, and dopamine
what is serotonin syndrome?
a side effect of too much serotonin. SSRI or drugs (ecstasy) can cause this happy drunk feeling, lots of other shit, and then death
MDMA acts causes release of ___ and inhibits reuptake