Neurotransmitters Flashcards
Discuss the 3 main steps done by 3 sucessive neurons in synaptic transmission?
1 transmitter released form 1st cell, 2 synapic activation of segond cell, signal intergration and conduction by 2nd cell
Quickly describe the mophology of a neuron
Dendrites with spine of them, leading to soma, then 1 axon that can split at nerve ending/terminals
How long is the delay between arrival in one cell and axon of the arrival to the next?
About 2ms
List the 3 main categories of neurotransmitter? How fast do they go and how abundant are they?
Amino acids (glut, GABA, gly-fast), Amines (Noradrenaline, dopamine-slow), and neuropeptides (opoids-slow) Abundance usually sits between mM and nM
Explain the main ion interaction and mechanism of neurotransmitter release, and what happens after
The neurotransmitters are stored in the vesicle near the synaptic membrane. When localised depolarisation (AP) comes in (as Na in and K out), Ca2+ comes in-Ca binds vesicule and leads to release -then acts on receptors, leading to ion uptake by the second cell
After, Transmitter is re-uptaken by the cell, sourrounding glial cells
Na/K balance remade with Na/k transporter
Explain how vesicle docking contributes to extremly fast release
Stnapic vesicles filled with neurotransmitters have docking proteins on the outside-primed and ready. Only release when Ca2+ comes in, allowing complex between docking protein and synaptic membrane prots-already there
Give exemples of toxins that target docking proteins?
tetanus toxin, Botulinum toxins target the docking proteins and their interaction with membrane-paralysis
Black widow Latrotoxin stimulates release and leads to depeletion
Explain what 2 different types post synaptic are found in the body, general things they bind and how they effect the cell
Can be FAST ion channels-upon binding ligan, open and allow selective entry of a specific ions. in CNS-Glu and GABA, NMJ AcetylCholine
GCPR-SLOW but major-use cAMP, PLC or more after-CNS and PNS ACh muscarinic receptrs, dopamin, noradrnamine
Explain hwo glutamate and GABA excite the cell
Glutamate to glutamate receptor, a Na+ ion channel-as glu binds, rapid intake leads to depolarisation and activation potential. Glutamate mediates most exciation
GABA binds GABAR, a Cl- ion channel-rapid intake leading to hyperpolarisation-cell becomes harder to excitate
List the 2 main forms of Glutamate receptors
AMPA recepors are the na channels-act FAST and are on most excitory synapses, rapid onset, offset and desensitisation
NMDA receptors allow both Na and Ca to ente. SLOW. Ca2+ modifies AMPA receptor and increases AMPA response, and number of receptor
Explain where gluta,ate comes from and what happens to glutamate after binding its receptors
Glu is easily available as product of metabolism (TCA and aKeto)
After bind GluR (AMPA and NMDA), glu is left in the clef-reeuptaken by close glial cells or neuron by Excitory amino acid transporter EAAT
In the neurone, it can be reuses and packages again
In glial cells, glutamine synthase converts it to glutamine, where it can be uses as AA or fuel
Explain how GABA is made and what happens to it after it binds it receptors
GABA comes from glutamate-Glutamic acid decarboxylase (GAD) makes it
Packaged, released to GABAaR-then reuptaken by glial cells and neuron by transporter GAT
In neuron it can be repackaged
Or in both, GABA transaminate makes it into Succinate semialdehyde-then to TCA
Explain the rapid structure of the GABA receptor and why it is important to Epilepsy treatment
GABAr is a pentameric Cl ion channel-importantly can bind many drugs
because epilepsy is uncontrolled exitation of neuron, GABA is a main target to reduce that
barbituates can bind GABAR and increase opening amount per GABA-more ion intake
Benzodiazepines increase the frequency of opening with GABA
ethanol and some steroids also act on GABA
All this leads to increased hyperpolarsisation and reduced chance of over activation of neurones
Also targets for epilepsy are GAT (tiagabrin) and GABA (Vigatrin)T, to increase local concentration of GABA
