Midterm 1 Flashcards
G-proteins
- use GTP instead of ATP
- like on/off switches: once activated, ON state can last anywhere from 10s to minutes
Ligand
Molecule that attaches, binds to enzyme or receptor. Neurotransmitters are ligands
Neural integration
Interplay b/w excitatory and inhibitory messages coming from dif neurons to decide whether to activate next neuron or not
Axoaxonic synapse
- attach near axon of another neuron
- cannot start an action potential in next neuron but will influence likeliness of nrtrm release and action potential in next neuron
Autoreceptor
- autoregulatory function
- inhibitory metabotropic receptors
- on every neuron
Classical neurotransmitter
- e.g. glutamate, GABA, dopamine, norepinephrine
- modified amino acids
- synthesized in axon terminal
- dock near entry of Ca2+
- never leave synapse (except neuromodulators)
Metabotropic receptors
- mediate their effect through g-proteins signalling cascade
- can have any effect on cell function which allows for more regulation
Ionotropic receptors
- open ion channels
- have direct and rapid effect by letting in dif ions
Neuropeptides
- more than 70
- only activate metabotropic receptors
- made and packaged in cell body, brought down axon terminal to be released once (they don’t come back like classical nrtrms)
- non-synaptic communication, free to diffuse around
Glutamate
- excitatory, let in Na+ ions
Neuromodulators
- dopamine, norepinephrine, serotonin, acetylcholine
- act on metabotropic receptors
- tend to modulate cell function rather than to cause fast ESPSs or ISPSs
GABA
inhibitory, let in Cl+2 ions
Acetylcholine
- neuromodulator in CNS
- in motor neurons at, muscular junction, acts as primary neurotransmitter activating excitatory ionotropic receptors
- cause muscle contraction
- toxin in black widow’s venom causes massive acetylcholine release
Neurotransmitter clearance
- through enzymatic action
Neostigmine
- breaks enzyme that clears acetylcholine
- acetylcholine stays around much longer causing prolonged muscle contraction
Receptor agonist
inceases directly or indirectly of postsynaptic receptor activity
Receptor antagonist
decreases dir or indir postsynaptic receptor activity
Direct vs indirect agonist/antagonist
direct binds to receptor vs indirect doesn’t
Psychosis
- condition where difficult to tell what’s real and what’s not
- delusions, hallucinations, incoherent speech and behavior
Antipsychotics
- direct dopamine receptors antagonist
- block dopamine D2 receptors: an inhibitory metabotropic receptors
- blocks receptor so more depolarisation
Biased agonism
When ligand causes metabotropic receptor to preferentially activate a certain intracellular g-protein
Competitive binding
When ligand binds to site where nrtrm would normally bind. It competes to take the same spot.
Non-competitive binding
When ligand binds to a different site causing receptor protein to change its behavior (e.g. shape, how well receptor matches with nrtrm)
Non-competitive agonist
Fully or partially activates receptor
- can also be considered antagonist if they reduced slightly effectiveness of nrtrm
Non-competitive antagonist
Always “wins” over normal nrtrm.
Ways to influence receptor activity in psychopharmacology
- giving precursor molecule that enzyme in axon terminal turn into nrtrm, acts as receptor agonist
- antagonist can break down nrtrm-making enzyme
- antagonist can break down nrtrm-packaging enzyme
- can block or activate vesicular release machinery
- through nrtrm clearance: blocking enzymatic deactivation or reuptake, sometimes even reversing nrtrm path
Contralateral
On opposite side
ispilateral
on same side