Flashcards in 11/5 Synaptic Communication Deck (53)
What is an electrical synapse?
it is a synapse through a gap junction!
what are the characteristics of a electrical synapse?
very rapid and unidirectional or biderectional communication.
where would we see electrical synapses?
in embryonic nervous tissue, some brain regions and the HEART!
What is a chemical synapse?
specialized for the release and reception of neurotransmitters.
what are the two parts of a chemical synapse?
the Axon terminal of the presynaptic neuron (with synaptic vesicles) and the receptor region on the postsynaptic neuron.
Why would I care about chemical synapse as a doctor?
many diseases come from problems in these synapses.
what is the sequence of chemical synapse?
1. Action potential arives at axon; 2. voltage-gated Ca channels open and Ca enters the axon terminal; 3. Ca entry causes neurotransmitter-containing synaptic vesicles to release their contents by exocytosis; 4. Neurotransmiter diffuses across the synaptic cleft and bind to specific receptors on the postsynaptic membrane. 5. binding of neurotransmitter opens ion channels, resulting in graded potentials. 6. neurotransmitter effects are terminated by reuptake through transport protiens, enzymatic degredation or diffusion away from the synapse.
what are some of the steps needed to form the presynaptic vesicles?
tranmitter uptake and dock the vesicle, use snap and syntaxin etc. then with synaptic brrevin 1/2, snap-25, and syntaxin 1 open the vesicle and release the transmitter. the end of the story is that the vesicles are docked and controlled very tightly!
activity dependent decrease in transmitter release
synaptic depression -- where we "use up" the vesicles and don't make more fast enough!
causes of synaptic depression
vesicle depletion and modulation of Ca channels
Activity dependent increase in transmitter release
synaptic facilitation due to an rapid build up of Ca at the junction due to a short burst of high activity!
what is the time scale for a chemical synapse and why is it that scale
very short a few milliseconds, since you have degradation by enzymes of the signal, reuptake by astrocytes or axon terminal, and diffusion away from the synaptic cleft.
why would be not have electrical synapses in the brain
hard to turn off, hard to control the dirrection, and strength at the synapse etc.
What is a autoimmune disorder that tartets presynaptic Ca2+ channels at the NMJ?
what is the result of Lambert Eaton syndrom?
certain cancers may cause it and see progressive weakness, eye movement deficits, autonomic deficits: dizziness, dry mouth.
where are the Ca channels in the synapse?
they are in the pre-synaptic axon just outside the area where the transmitter is released
Autoimmune disorder targeting nicotinic Ach receptors at NMJ
what are the symptoms of Myesthenia Gravis?
eye movement deficits, ptosis, progressive weakness.
How can we determine the different diagnosis of Myesthenia Gravis and Lambert eaton?
L-E gives buildup of muscle contraction after repeated stimulation or exercise due to accumulation of presynaptic Ca2+ (synaptic facilitation). Does not occur with my. Gravis
What is the treatment of Both L-E and my. Gravis?
Ach-esterase inhibitors such as neostigmine.
why would a K+ channel blocker help with L-E?
it will make the AP longer by making the repolarization take longer and this will alow more Ca in and make up for the loss of channels
Neurotransmitter that is released at neuromuscular junctions and at some ANS neurons and some CNS neurons
what ANS neurons use Ach?
they are used by the pre-synaptic sympathetic and the pre and post synaptic parasympathetic
what is the enzyme that makes Ach?
what degrades Ach?
enzyme Acetylcholinesterase (AchE)
What are the name of synapses that use Ach?
Neurotoxins that target cholinergic synapses
Curare; Sarin, VX, etc. Insecticides; Botulinum toxin
blocks nicotinic Ach receptors at NMJ! antidote is Neostigmine
Potent acetylcholinesterase inhibitors
Sarin, VX etc. and treat with atropine
why would you not see a re-build of strength with repeated use in my. Gravis?
the receptor is not present, and so a build up of Ca will not cause a return in synaptic function!
which type of drug would treat both lambert eaton and myesthenia gravis?
a Ach-esterase inhibitor
neostigmine, insecticides, malathion, parathion etc. same class as sarin etc.
how does botulinum toxin work to become the most potent toxic substance known?
it works to stop synapse by cleaving SNARE protiens and stopping the vesicles from binding! and it has a crazy high affinity for the receptor in the vesicles of the synapse
what can you use botulinum toxin for?
face muscle paralysis; spasm, dystonias, hyperphidrosis, chronic migraine.
What does Ach signaling do in the brain?
involved in attention and arousal and in memory (damaged in alzhiemers)
what does nicotine do?
it targets the Ach or cholinergic signaling specifically!
what are some amino acid neurotransmitters?
GABA; Glycine; Glutamate
the major inhibitory neurotransmitter in brain
enhance GABA-receptor activation
a major inhibitory neurotransmitter in spinal cord
The major excitatory neurotransmitter in brain
Where does GABA come from?
glutamate to GABA with enzyme GAD
What is the class of neurotransmitters that are based on amines
What are the subclasses of amine based (biogenic amines) signals in neurons
Catacholamines and indolamines
dopamine, norepinephrine (NE), and epinephrine
What are the neurotransmitters that are involved in reward, arousal, and motor systems?
Dopamine and NE !
what is the connection between biogenic amines and depression?
most anti-depresents seem to support the biogenic amines such as dopamine and serotonin that seem to be involved in the reward, arousal, and motor systems.
what are the neurotransmitters that are known to be involved in sleep/wake cycles,, and emotions?
biognnic amines: Indolamins: serotonin and histamine!
What are the Indolamine class of biogenic amines
serotonin, and histamine
how do anti-depresents usually work
target the way that the transmitter is removed from the synapse i.e. block how seritonin uptake and/or neuro-epinephrin uptake
what does an amphetamine do?
it binds to the pre-synaptic vesicle and causes a release of dopamine at the synapse through the transporters that usually take up dopamine!
how does Cocaine work?
it blocks the DA transporter that would reuptake dopamine to the pre-synaptic vesicel and therefore it give a high level of dopamine!!