Neurotransmitters Flashcards
Criteria for NETs
present in pre synaptic terminals
released in response to stimulation
able to interact with postsynaptic receptors
rapidly removed from synapse
needs mechanisms for: synthesis/storage, release, receptors, transmitter removal
5 steps in trasmission
synthesis storage release postsynaptic effects inactivation
Characteristics of transmitters
- amino acids and amine NETs are?
- peptide NETs are?
small molecules, stored and released from synaptic vesicles, many activate both types of receptor
large molecules, stored in secretory granules, only activate G-coupled proteins
Dale’s principle - one NET per neuron
how is it disproved?
many peptide-contained neurons have both peptide NET and aa or amine NET
Synthesis of non- peptides
Glu and Gly abundant in all cells
Ach, GABA and amines - synthesis localised to axon terminal by specific enzymes
all packaged into secretory vesciles
Glutamate
inhibitory/ excitatory?
- what receptors do they bind to?
most common excitatory transmitter in CNS
binds to various receptors, particularly NMDA and AMPA receptors important in fast transmission (Glutamate binding to AMPA = Na+ and K+currents producing an EPSP)
NMDA receptors often co-exist with AMPA – they have voltage-dependent MG2+ block (to stop ions going through)= need to be indirectly activated by another transmitter
GABA inhibitory/ excitatory? channels name? what is converted into gaba and by what enzyme? Too much causes? too little causes?
inhibitory NET (most common in brain) produces IPSPs via GABA-gated chloride channels(found commonly in striatum and cortex) GLutamate converted into GABA via enzyme(Glutamic acid decarboxylase GAD) Too much = coma too little = serizure
Presynaptic inhibition
disinhibition?
Anxiolytic drugs?
Opiates? - synthesis, distribution(3 main receptors), mode of action
1 neuron suppresses the action of another (release GABA to inhibit neuron)
disinhibition = inhibiting inhibition
Anxiolytic drugs = anxiety dissolving
- GABA receptor can also bind other chemicals that can modulate/ stimulate its GABA response
Opiates - act via the endogenous opaite system
synthesis - peptides, made in RER and packaged into secretory granules
distribution - opiate receptors: 3 main types
-Mu - Kappa - Sigma
mode of action:
opiate receptors are ‘G-coupled = act as modulators
therapeutic uses= analgesia- reduces perception of pain, intestinal disorders - reduces diarrhoea(decreases dehydration), antitussive - cough suppressant
BUT NEGATIVES=
tolerance builds up, analgesic and euphoric effects linked, analgesia and dependence linked, relieves dull visceral pain better than sharp pain
Opiates effect on: spine periaqueductal grey amygdala frontal cortex brain stem (medulla)
Effect on:
spine = block pain signal
periaqueductal grey - regulates sensation of ‘pain’
amygdala - regulates emotion
frontal cortex - cog. aspects
Brain stem (medulla) - depress respiration and cough reflex
Common features of the diffuse modulatory systems of the brain
hosepipe effect?
enpassent?
effects over large areas of brain
core nuclei in centre of brain (often brain stem)
neurons may contact large no.s of postsynaptic neurons
‘hosepipe effect’ = spraying over large area of brain
enpassent = swelling and then moving along
Acteylcholine widespread or not? Where is it found? associated with what functions? if lost what is caused? Acetyl CoA + choline = ? (and enzyme used?)
widespread, distribution including: autonomic nerves, neuromuscular junction, basal forebrain, hippocampus
associated with: memory, sleep, co-ordination, mood
lost in Alzheimers
Acetyl CoA + choline —-> ACh + CoA (enzyme = ChAT)
ACh —> Acetic acid + choline (enzyme = acetylcholinesterase)
Life cycle of ACh - how can we interfere? (3 ways)
Prevent releaseeg. botulism
AChE inhibitors eg. nerve gas
Block receptors – nicotinic recpetors blocked by curare, and muscartinic by atropine
What are catecholamine systems?
synthesis?
regions of nervous system associated with movement, mood, attention, visceral function (dopamine system and noradrenaline system)
tyrosine–>dopa –>dopamine –>norepinephrine–>epinephrine
(Enzymes in order: Tyrosine hydroxylase (TH), decarboxylase(dopa), dopamine B-hydroxylase (DBH), phentoamine N-methyltransterase(PNMT)
Parkinsons disease: who does it affect? symptoms? pathology? theory? drugs and treatment?
v common disease, affects 1 in 200 over 70yrs
tremor, rigid, akinesia, postural changes, slurred speech
pathology: substantia nigra affected –>nigrostriatal pathway (nigra to striatum)
theory = striatum inhibits motor function, D2 receptors inhibits cells in striatum (decreases inhibition action), if inhibition is lost = get increase in inhibition of motor control
Drugs and DA neurotransmission
L-dopa increases DA
storage = reserpine destroys vesicular stores = parkinsons
release = amphetamine = increases DA release
reuptake = cocaine blocks reuptake so increase DA
receptors = D2 agonists - treatment, D2 antagonists induce parkinsons
