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blue = lecture

green = textbook

yellow = article

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ionotropic vs metabotropic NT receptor types

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ionotropic vs metabotropic NT receptor types

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ionotropic vs metabotropic receptor:

glutamate

AMPA, kainate, NMDA

metabotropic (8 subtypes)

acetylcholine

nicotinic ACh (many)

muscarinic ACh (5 subtypes)

GABA

GABAA and GABAC

GABAB

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ionotropic receptors

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metabotropic receptors (2 types: GPCRs and RTKs)

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2 types of GPCRs - heterotrimeric and monomeric

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2 types of GPCRs - heterotrimeric and monomeric

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things that happen in the intracellular side

heterotrimeric: receptor in the membrane, activates a G proteins (group of 3 proteins) on the inside of the membrane, then move about

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type of ionotropic

when receptor binds to the two separate pieces, it brings the two protein together, and then when they're together they can be phosphylated

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doesn't have to be g-protein, it can be any of the second messengers

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main excitatory neuron

when glutamate is bound to the NMDA receptor, it allows Na and Ca to pass

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nAChR (ionotropic ACh receptor) vs mAChRs

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nAChR (ionotropic ACh receptor) vs mAChRs

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nicotinic acetylcholin receptor

nonselective cation channel

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short-term plasticity

seconds to a few minutes

long-term plasticity

use it or lose it

immature to mature spine density

at least 30 minutes, hours or days

facilitation, potentiation --> long term potentiation (LTP)

increase in synaptic strength

depression, depotentiation --> long term depression (LTD)

decrease ins synaptic strength

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siphon: tube-like structure that water flows though, helps locomotion, feeding, respiration, reproduction; part of mantle

gills

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involuntary, defense, reflex/response

2-component reflex that happens in response to a stimulus applied to siphon or mantel (siphon or gill reflex)

behaviors we can study: habituation, dishabituation, sensitization

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lead to changes in circuit function

lead to changed in behavioral plasticity

short term (affecting NT release)

long term require changes in gene expression or new protein synthesis

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a persistent strengthening of synapses based on recent patterns of activity

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activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus

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LTP and LTD occur at synapses in many parts of the brain

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LTP and LTD occur at synapses in many parts of the brain

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hippocampus

cerebral cortex: visual, somatosensory, motor, prefrontal

amygdala

cerebellum

thalamus

striatum

nucleus accumbens

ventral tegmental area

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high fast frequency (fast influx of Ca)

has to be at least 30 mins to a couple days

LTP is reversible, and can be saturated

3 steps

1. induction

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properties of LTP at a CA1 pyramidal neuron receiving synaptic inputs from the 2 independent sets of Schaffer collateral axons

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NMDA receptor channels can open only during depolarization of the synaptic neuron from its normal resting potential

on the right, that's the initiation of LTP

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NMDA receptors are required for LTP

mechanisms responsible for long-lasting changes in synaptic transmission during LTP

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caused by slow low frequency

LTD is below control after the action potential

abt 15 mins long to several hours

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long-term synaptic depression in hippocampus

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long-term synaptic depression in hippocampus

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bc they're channels, they open rapidly

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bind a ligand, and can't form ion permeant pore

affect ion channels indirectly --> this requires TIME

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LTD suppors learning and LTP supports unlearning

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LTD suppors learning and LTP supports unlearning

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NMJ = endplate is where motoneuron axon contacts a skeletal muscle fiber expressing nAChRs

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NMJ = endplate is where motoneuron axon contacts a skeletal muscle fiber expressing nAChRs

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on all skeletal muscle, mediates communication btwn a motoneuron axon and a skeletal muscle fibers

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in all autonomic ganglia, mediates communication btwn an autonomic preganglionic neuron and ganglionic neuron

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in the brain and mediates communication btwn two central atoms

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GABA receptor, the receptor changes conformation that is permeable to Cl ions

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all ionotropic receptor are all EPSPs or IPSPs

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all ionotropic receptor are all EPSPs or IPSPs

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step 1 the NT turning on the effector protein

then the effector protein turns on the second messenger

second messenger effects another effector protein or releasing something

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habituation: they get used to a stimuli and have a less response to the same stimiiuli

dishabituation:

sensitization: make them rly sensitive to a stimulus

if you touch their gill/mantle and pair it with an electric shock, next time you just touch the gill/mantle, they'll think the shock is coming and have a rly strong rxn

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less communication to motor neurons