lecture 12 modulation Flashcards
things that can cause synaptic strength to change
diseases (myasthenia gravis, startle disease)
drugs (therapeutic, recreational)
prior or ongoing activity (experience changes thoughts and actions by altering synaptic function
what mechanisms lead to altered synaptic strength
addition or loss of synaptic connection
(can take hours to occur)
growth or shrinkage of synapse
(synaptic current directly proportional to number of open receptors)
rapid change in synaptic efficacy with no structural change
(no new proteins)
how to measure synaptic strength between 2 neurons
1) stimulate axon with electricity
2) fires action potential
3) releases neurotransmitters
4) epsp detected by recording electrode in post synaptic cell
how is facilitation different from temporal summation
facilitation piggybacks but the amplitude gets bigger every time and the second one starts after the first has gone back to rest (presynaptic because it relies on residual calcium)
vs
temporal summation where the epsps piggyback on top of each other and the next one starts before the first one has ended (postsynaptic because it relies on open lgic)
spatial summation
several weaker signals from different locations vs temporal several weak signals from one source that add up
facilitation increases quantal content why
the residual calcium hypothesis- ca enters to trigger neurotransmitter release then is removed
when second stimulus arrives soon after the first, new ca enters before the initial pulse is fully removed
this causes smaller synaptic potentials with repetitive stimulation
short term depression
ionotropic receptors
fast, ion channels
metabotropic receptors
slower, ligand gated, can activate a g proteins
g protein coupled receptors steps
1) binding of neurotransmitter to the extracellular receptor protein
2) activation of g proteins
3) activation of effector systems
secondary messengers
the activated proteins are enzymes that generate small molecules (second messengers like cyclic amp)
camp activates protein kinase a (pka) which phosphorylates proteins by adding phosphate groups and changes the properties of the proteins so it can activate other proteins
the 3 general second messenger systems that interact with specific g proteins
increases camp (gs)
decreases camp (gi/go)
stimulates phospholipase c, dag, ip3, pkc
opiate receptors are…
GPCRs and the ligands are small peptides called enkephalins and endorphins
pain modulation by opiate receptors
drg cells sense pain
spinal interneuron releases enkephalin
enkephalin binds GPCR
g protein (go) inhibits VGca channel
less neurotransmitter release when activated (weaker pain signals w opioid receptor activation)
aplysia
giant sea slug that has simple nervous system and large neurons, stereotyped behaviors