Neurotransmitters Flashcards
(24 cards)
What is the gap size range Of a synapse
20-100nm
What is the significance of structure of synapse?
One neurone interact with 100s or thousands of synapses
Can take it information, integrate and transfer and propagate
What are the stages of synaptic transmission
Biosynthesis - packaging and release of neurotransmitter
Receptor action
Inactivation
What is the purpose of the inactivation stage of synaptic transmission
To remove neurotransmitter from synapse and repackage; without this communication cant occur.
What is the significance of glycine neurotransmitter
It’s a ligand; inhibitory neurotransmitter
Work on glycine receptors
What are the types of molecules that can be neurotransmitters?
Amino acids- glycine, glutamate, GABA
Amine- noradrenaline, dopamine
Peptides- opioid peptides
What can neurotransmitter vary in?
Abundance
Speed of effect
What amount of ca2+ is needed for neurotransmitter release
Increase of about 200uM
Explain the concept of quanta synaptic vesicles release
Each SV contain a quanta of about 4K to 10k neurotransmitter molecules.
What is the activation of transmitter release dependent on and what does it require
Calcium
Requires rapid transduction
Describe the process of transmitter release
Membrane depolarisation VGCa CHANNELS open Ca2+ influx Vesicles Fusion Vesicle exocytosis Transmitter release
Explain in detail what happens just before and AFTER release
Before: SVs with neurotransmitter are docked in synaptic zone.
Vesicular and pre-synaptic membrane proteins form and complex with with cytoplasmic proteins and a rapid response to ca2+ entry enable fusion and exocytosis
AFTER
ATP and vesicles are recycled
What are the toxins that inhibit synaptic transmission
Alpha latrotoxin- causes neurotransmitter release until depletion
Botulin toxin- prevent release of ACh and causes flaccid paralysis
Zn2+ endpeptidases- inhibit transmitter relases
Tetanus - causes paralysis
Contrast fast and slow transmission in terms of receptors
Fast - uses ion channel receptors
Slow - uses G protein coupled receptors
What may be effectors in G protein coupled receptors
Channels - Ca2+
Enzymes; maybe adenyly cyclase
Give examples of ion channel-linked receptors
nAChR- NMJ
GluR-CNS
GABAR-CNS
GlyR
Give examples of GPCR
ACh at muscarinic receptors
What are the inhibitory ion channel linked receptor
GABAR and GlyR
Cl- influx
Contrast the two Glutamate receptors
AMPA- fast, rapid onset and desensitisation . Only Na+ can influx
NMDA- slower; needs another input from other neurotransmitter. Ca and Na can both influx
Underlie learning mechanisms
Describe excitatory Glutamate CNS synapse
Glucose to glutamate via TCA
Normal synaptic release and transmission
Glutamate reversibly bind to receptor in post synaptic terminal
Glial cell uptake glutamate and convert it to glutamine by GLUTAMINE SYNTHASE
Presynaotic cell re uptake glutamate via EAATs
What causes seizures
Abnormal cell firing caused by EXCESS glutamate
Describe inhibitory GABA synapse
Glutamate to GABA by glutamic acid decarboxylase
NORMAL synaptic transmission.
GABA binds to GABAR
GABA uptake by GABA reuptake transporter into glial cell
GABA- Succinate SEMIALDEHYDE by GABA transaminase
Describe structure of GABAR and its significance
Pentameric Has alpha(Zn2+ and benzodiazepines bind here) and beta chain(GABA binds here)
Multiple drug binding site in treatment of diseases
Antepileptic
Anxiolytics
Sedative
What are the 1st line therapy drug for epilepsy
Levitrececam vesicle attached proteins
Limatrigine- vvoltage gated sodium channels
