Ch. 3-6 Flashcards
what is the final step in synaptic transmission
clear the synapse and re-set
Little pores in the axon that vaccum back up the neurotransmitter. Helps get everything ready for the next signal
re-uptake transporter
disassemble neurotransmitter to clear synapse space
enzymes
synapse from axon to soma
axosomatic
synapse from axon to dendrite
axodendritic
synapse from one axon to another axon
axoaxonic
2 kinds of potentials that can happen on the postsynaptic (receiving) membrane
EPSP and IPSP
excitatory postsynaptic potential. Depolarizing. Na+ or Ca++ into cell. “Facilitation” of nerve communication
EPSP
inhibitory postsynaptic potential. Hyperpolarizing. Cl- into cell. “Inhibition” of nerve communication
IPSP
2 types of presynaptic potentials
presynaptic facilitation and presynaptic inhibition
causes an enhancement of Ca++ influx and facilitates neurotransmitter release
presynaptic facillitation
causes a reduction of Ca++ influx and inhibits neurotransmitter
presynaptic inhibition
modality that operates on the presynaptic inhibition principle
TENS unit
what causes an IPSP
hyperpolarization, Cl- coming into cell, a ligand channel that lets Cl- in
Where is a neurotransmitter released
into synaptic cleft
What does a neurotransmitter act upon
synaptic receptors
Types of neurotransmitters
fast acting, slow acting
what type of effect does a fast acting neurotransmitter have on the postsynaptic membrane
direct, quick, short-lived response
what type of effect does a slow acting neurotransmitter have on the postsynaptic membrane
indirect (from inside cell), slow, longer-lived response (tends to stay open longer)
what makes a neurotransmitter fast or slow acting
the type of receptor it binds to
a substance, other than a neurotransmitter, released by a neuron and transmitting information to other neurons, altering their activities. CAN AFFECT MANY NEURONS
neuromodulator
where does a neuromodulator act
at a distance from the synaptic cleft
what type of onset does a neuromodulator have
slow, longer response
BIG 3 IMPORTANT LIGANDS
Acetylcholine, Glutamate, and GABA
Neurotransmitter of the neuromuscular junction. Excitatory ligand that is fast acting at the PNS
Acetylcholine
Most prevalent fast acting excitatory neurotransmitter in the CNS (can also be slow acting)
Glutamate
Most prevalent fast acting inhibitory neurotransmitter in the CNS (can also be slow acting)
GABA
3 kinds of synaptic receptors
directly open ion channels (fast), indirectly open ion channels (slow), and activate intracellular events (slow )
how does a synaptic receptor indirectly open an ion channel
neurotransmitter binds to receptor and energizes G protein, a piece of the G protein breaks off and opens the gate from the inside and holds it open as long as it as energy
how the second messenger system works (synaptic receptor that activates intracellular events)
ligand (first messenger) binds to G-protein receptor, G-protein is activated. G-protein turns on the machine and produces a product (second messenger) that affects the cell function from the inside
receptor protein is pulled down inside the cell and the membrane is closed over it to inactivate it
internalization
receptor protein stays in the membrane but gets denatured so it no longer can do what it used to do
inactivation
receptor protein is brought to the surface of the membrane
externalization
ligands which are not released by the presynaptic terminal but still bind post synaptic receptors and cause action on the postsynaptic membrane
agonist
example of an agonist
nicotine
on or ligand that diminishes the effect of a neurotransmitter at a synapse
antagonist
2 ways an antagonist reduces the effect of a neurotransmitter
- preventing it from getting out 2. blocking it’s receptors
example of an antagonist
Botox
how does Botox work
acts at the presynaptic terminal by inactivating the calcium channels on the presynaptic terminal so calcium can’t get in and neurotransmitter doesn’t get shoved out. Muscle won’t contract
pathology associated with acetylcholine receptors where they have trouble contracting and sustaining a muscle contraction
Myasthenia Gravis
What is 1 tx of MG
prescription drug that contains an anti cholinesterase that “turns off” the esterase (things that eat Ach) in order to prolong the time the Ach is in the synaptic cleft. Increase the chances that Ach will bind to a receptor. Promotes stronger, longer muscle contractions
drug that turns off the re-uptake transporter, keeping serotonin in the synapse and increasing the chances it will bind and cause an effect on the post synaptic membrane
Selective Serotonin Reuptake Inhibitor (SSRI)
a decrease in response to a repeated, benign stimulus
habituation
short term habituation of the nervous system
not releasing as much neurotransmitter so you get less of a response
long term habituation of the nervous system
internalize receptors on the post synaptic membrane
2 ways you can turn down the response of a repeated, benign stimulus
short term and long term habituation
Example of how you can use habituation by creating a systematic program of touch
tactile defensiveness
Example of how you can use habituation by creating a program of head movements
vestibular disorders
Long-term change in the synapse that makes signaling stronger
LTP long-term potentiation
The extension of habituation. Structural change at the synapse that turns down the signaling. It’s an adaptation or conversion of silent synapses.
LTD long-term depression
The foundation of declarative learning and procedural learning
long-term potentiation
turning down the strength of synaptic connections
long term depression
importance of astrocytes
Can store and release both calcium and glutamate, which are essential for remodeling the synapse
how does cellular recovery occur after axonal injury in the periphery (2 ways nervous system tries to repair itself in the peripheral )
collateral sprouting and regenerative sprouting
intact surviving neurons send out a new branch to innervate target tissue that have lost their innervation
collateral sprouting
Where the intact end (proximal end) of a neuron regrows where it used to be
regenerative sprouting
if regenerative sprouting doesn’t work, what happens
collateral sprouting