10 JUNE 2019 Flashcards
so end of ch. 6 start of ch. 7
when is GABA fast acting?
w/ a GABA a receptor
when is GABA slow acting?
w/ a GABA b receptor
what type of response is a GABA amino acid?
inhibitory : generates an IPSP response
what is the most prevalant inhibitory fast-acting amino acid?
GABA
what is the most prevalent excitory fast-acting amino acid?
Glutamate
when is gluatmate fast acting?
w/ AMPA receptor
when is glutamate slow acting?
w/ NMPA receptor
what type of response does glutamate do?
excitory: EPSP repsonse
what two things can serotonin affect?
changes our perceptio of pain
and adjust our arousal levels
what pathology does serontonin affect?
depression - most common anti-depressent drug
what type of fast slow methods does the CNS and PNS have?
CNS has BOTH fast/slow = gas pedal + breaks
PNS has ONLY fast = gas pedal
- to slow you dont press the gas
dopamine affects what four things?
motor activity
cognition
behavior
pleasure
dopamine is associated with what?
addiction
norepinephrine is part of what system?
fight or flight which is the
autonomic - sympathetic system
tell me two things about norepinephrine:
increases attention to sensory information
apart of autonomic - sympathetic system
what does neuroplasticity mean?
the brain can adjust : so it can increase in ability or decrease in ability but there is the ability to change
what are the three big amino acids we need to know?
Acetylcholine
gluatmate
GABA
how many other random proteins do we need to know?
five
what are the five random proteins we need to know?
histamine epinephrine dopamine serotonin peptide
tell me two things about histamine:
it can create an interaction affect
and is part of the neuro inflammatory response
norepinephrine increase what?
attention to sensory information
amines are what?
slow acting neurotransmitters
what are the two types of peptides?
- endogenous opioids
- substance P
endogenous opioids do what?
inhibit perception of pain
substance p can be
a neurotransmitter or modulator
substance p are?
pain pathways
habituation def:
decrease response from a repeated begin stimulus
a short term habituation occur where?
presynaptic facilitation
what two ways can you get a presynaptic facilitation habituation:
1- more presynaptic inhibition
2 - less presynaptic facilitation
name two examples of “pathologies” w/ habituation:
tactile defensiveness
vestibular disorders
a long term habituation occurs where :
post synpatic membrane
how do you get a long term habituation:
you take away the receptors on the membrane so there can no longer be a facilitation response:
down regulates
down regulate def:
less receptitive to AP
how do you down regulate
you INTERALIZE or pull down membrane receptors from the post synaptic terminal making htem
INACTIVE
= flipping the switch permenantly so the lights are off
when you down regulate what happens to potential
it reduces the chance of AP
up regulate def:
increase recepitiveness to neurotransmitters
how do you up regulate?
take receptors inside the cell & stick it up in the membrane = EXTERNALIZE = ACTIVE = unlock the gate to allow ion to flow in
when you up regulate what happens to potential?
increases the chance of an AP
what does myasthentic gravis mean?
muscles dont work BIG time
what are three bad things that happen with MG?
- membrane unfolds
- receptors move closer to the surface
- the amount of acteylchloline receptors decrease
what are the consequences of the bad things in the MG?
the acteylchloline can’t be recycled so the left over proteins gets gobbled up by closer those receptors closer to the surface
what three things do we need to know for neuroplasticity?
1 - habituation
2- experience-dependent plasticity
3 - recovery or maladaptive behavior
what does LTP (long term potentiation do)
converts a silent synapse to an active synapse
