synaptic plasticity

neurobiology test 2

three mechanisms that a synapse can monitor their action

1. glia,

2. autoreceptors, and

3. retrograde signaling

plasticity

comes from ancient greek, that which can be mulded

plasticity refers to the ability

to alter the neural connections of the brain as a result of experience: the learning process

synaptic plasticty is only

one form of neural plasticity

feedback at synapses can be through

autoreceptors, glial receptors, or retergrograde signals

endocannabinoids

a type of retrograde signal

autoreceptors

located in the presynaptic membrane and respond to NT released by PREsynaptic terminal.

autoreceptors are typically

ligand gated metatropic receptors

Autoreceptors provide negative

feedback to decrease NT release by the presynaptic terminal

examples of autoreceptors

Dopamine (DA), serotonin (5-ht) norepinephrine and glutamate neurons

glial cells are

uniquely placed to mediate synaptic plasticity

retrograde signaling via endocannabinoids is NOT a

autoreceptor

retrograde signaling via endocannabinoids is

a signal released by the postsynaptic neuron

cannabinoid receptors are

metabotropic

presyptic neuron of a retrograde signal neuro is usually

GABAergic or glutamatergic

endocannabinoids usually act on

CB1 receptor to reduce the opening of presynaptic voltage-gated calcium channels

what does the CB1 receptor effect when blocked

the opening of voltage gated calcium channels

calcium signaling for endocannabinoid release can

come from internal stores

some patterns of stimulation of the presynaptic motor neuron can result in

a decrease in the size of EPSPs recorded in the muscle fiber

pattern of NT release detected by mACH receptors on schwann cells

creates feeback onto terminal to cause less NT release for each AP

a reduction in synaptic activity is important to minimize

synaptic fatigue and the rundown of NT

aplysia study showed

gill withdrawl reflex could learn, neuromodulators made the process faster

the modification of the gill withdrawal reflex depends on input from

serotonin modulatory interneuron l29

serotonin modulatory interneuron l29 does what?

forms a synapse onto the terminal of the sensory neuron

what is the result of the serotonin modulator

a stronger reaction by the muslces as a result of the sensory MN synapse change

the mechanism for sensitization is

presynaptic facilitation

presynaptic facilitation works by

decreasing k+ conductance via PKA acting on voltage-gated k+ channels

How does decreasing K+ conductance increase glutamate release

causes a decrease in k+ conductance in the sensory neuron terminal (fewer k channels open) and causes synpase growth

what are the effects of decreased k+ conductance in the sensory terminal

less k+ efflux, slower falling phase, less/no undershoot, bigger AP

hippocampus

temporal lobe, needed for learning, spatial and sort term memory

LTP can be studied in the

ca3 to ca1 synapse

long term potentiation is

a lasting potentiation of the EPSP

LTP can be induced with a

strong depolarization of input 1

tetanic stimulation

high frequency

LTP in the hippocampus requires what two things

1. a strong depolarization of the pistsynaptic (ca1 neuron)

2. at the same time as presynaptic activity

hebbian plasticity

if it fires together, it wires together

NMDA receptors can be

essential for LTP

NMDA receptors only allow calcium influx when

bound by glutmate, glycine, and depolarized

increased effectiveness of AMPA receptors can

be a mechanism underlying LTP in hippocampus

Increase in number of AMPA receptirs in the postsynaptic membrane is

another mechanism underlying various types of LTP in hippocampus

can retrograde signaling be involved in LTP

yes

cannabinoid recptors are

metabotropic

synaptic plasticity is

directly involved in learning

LTP can

last a really long time (

LTP can be mediated by

structural changes

LTP can cause what to grow bigger

dendritic spines

why do dendritric spines grow in response to LTP

To fit more AMPA receptors