Neurotransmitters & Pharmacology Flashcards by J A

4 features of Synaptic Transmission

Rapid timescale
Diversity
Plasticity
Learning and memory

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what are protien molecules called on dendrites

spine

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function of cell body/soma

Information reception
then integration of the information
lastly
Rapid transfer (action potential)

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function of spine

increase the surface area of recipet of information recipt

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what sort of trasmition happen in an action potential

electrical (AP)
chemical(nuerotrasmiter)
Electrical (AP)

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can nuerotrasmition happen anywhere else other than synapse

nope

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what are the post synaptic clefts

dendrite or soma

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Synaptic transmission: 3 stages

Biosynthesis, packaging and release of neurotransmitter (●)
Receptor action( bind to receptor on postsynaptic receptor)
Inactivation(happens on the postsynaptic region)

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3 types of nuerotrasnmitter

Amino acids
Amines
Neuropeptides

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Recap: synaptic transmission – essential features

Restricted to specialised structures - the synapses

Calcium is essential - transmitter release requires an increase in intracellular Ca2+ (200 M)

Transmission is fast - within ms

Synaptic vesicles (SVs) provide the source of neurotransmitter (4,000-10,000 molecules per SV)

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transduction

is the transmission of molecular signals from a cell’s exterior to its interior

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where are the synaptic vesciles docked

synaptic zone

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how do nuerotransmitter enter vescicles

they have protien pumps

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after being docked onto the pre synaptic membrane what happens

theyre primed
to release the nt
then fuse

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what do the Special proteins on the vesicle and presynaptic membrane enable

enable fusion & exocytosis

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what are they called on vesicles

vesicular protien
mediate the action of exocytosis of nt
improtnant in docking

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Vesicular proteins are targets for

neurotoxins

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what is Alpha latrotoxin

from black widow spider

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function

stimulates transmitter release to depletion of presynaptic termial

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what do the victims suffer from

muscular paralysis

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function of Zn2+-dependent endopeptidases

inhibit transmitter release

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example using tetanus toxin

causes spasms & paralysis

by inhibiting GABA and glycine release

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another example using BOTULINUM TOXIN

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causes flaccid paralysis

paralyisis due to muscle relaxation

structure of BOTULINUM TOXIN

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bi chain (2 chain)

how does it work

first part binds to nerve terminal (cholernergic) 2nd chain penetrates the cholonergic nerve terminal and intercats with vesicular proteins cleaves peptide bond thus inactivating them so you no longer get docking fusion or relase of transmiter

how is vesicle docking and a rapid response to Ca2+ entry leading to membrane fusion and exocytosis enabled

Protein complex formation between vesicle, membrane and cytoplasmic proteins

is the transmitter release require energy

yes

Ion channel-linked receptors | mediate what sort of trasnmittion

``` FAST response (msecs) Mediate all fast excitatory and inhibitory transmission ```

exitotory signal is produced by what

opening of sodium ion channel (glutamate receptors) | leads to depolarisation of post synaptic terminal

and ihnibitory

chlorine( GABA) leads to hyperpolarisation of postsynaptic terminal

G-protein-coupled receptors | mediate what action

SLOW response (secs/mins)

what are the effectors

enzymes or channels

what happens upon binding to the gpc receptor

g protien binds to a receptor inside the cell (adenyl cyclase) produces sencond messenger like cAMP ehich causes effect to enzymes or channel

examples of Ion channel-linked receptors

CNS- Glutamate,GABA | NMJ-ACh at nicotinic receptors (nuermo muscular junction)

G-protein-coupled receptors | examples

CNS and PNS: ACh at muscarinic receptors dopamine noradrenaline serotonin

Ion channel-linked receptors have how many subunits | and what do they allow

5 | → distinct functional properties

what does a excitatory nurotranssmitter receptor cause

an excitory postsynaptic potential | EPSP

what does an Inhibitory neurotransmitter receptor | cause

inhibitory postsynaptic potential (IPSP)

what is the main Excitatory trasmitter in brain

Glutamate

and Inhibitory t in brain

GABA

2 examples of Glutamate receptors

AMPA RECEPTORS | NMDA RECEPTORS

AMPA RECEPTORS mediate

Majority of FAST excitatory synapses Rapid onset, offset and desensitisation permeable to na

NMDA RECEPTORS | mediate

Slow component of excitatory transmission | Serve as coincidence detectors which underlie learning mechanisms

NMDA RECEPTORS permeable to

na and ca

how is glutamate synthesised

from glucose via TCA cycle & transamination

what happens once glutamate is exocyotsed

Glutamate reversibly binds postsynaptic receptors

how is it inactivated

Rapid uptake of glutamate | reloaded in vesicles and used again

how are they uptaken in glial cell and where are they

glial cell surround synapses | 3. Rapid uptake of glutamate by excitatory amino acid transporters (EAATs)

what happens in the glial cell

4. Glutamate enzymatically modified by glutamine synthetase to glutamine in glial cells

by what enzyme

glutamine sythesase

what happens to the glutamine

in is pumped into presynaptic teminal and used to make more glutamate

what is the process called

glutamate glutimine cycle

what happens when too (uncintrolled) much glutamate release

spiking in the Electroencephalography (EEG) (measures electrical activity in the brain)

what happens if too much glutumate in synapse

Abnormal cell firing leads to seizures associated with excess GLUTAMATE in the synapse

what happens as the glutamate is comming bac =k down to normal level

converted to glutamine but takes lomger to come back down to normal level

Neurotransmitters & Pharmacology Flashcards

(55 cards)