Neurotransmitters Flashcards
What are the 5 criteria of a neurotransmitter
synthesis: must be made in pre-synaptic neuronal storage: presynaptically but not nitrous oxide release: must be released on demand inactivation: must be inactivated
Main classifications of NT
amino acids
biogenic amines
peptides
examples of amino acid NT
glutamate
GABA
Glycine
two classes of biogenic NT
catecholamines: noradrenaline adrenaline dopamine indolamines: serotonin
glutamate
primary excretory NT in the CNS
involved in memory, learning and cell death
postsynaptically via inonotropic receptors
GABA
inhibitory NT in the CNS
acts via chloride channels
Glycine
inhibitory NT in the CNS
but is primary in the spinal cord and brainstem
`What are the three types of glutamate receptors
NMDA -Calcium ions Kainate -sodium and potassium ions AMPA -permeable to cations (calcium, sodium and potassium)
(dys)functions of glutamate
- synaptic plasticity
synapses are strengthened or weakened by feedback mechanisms - excitotoxicity
excessive stimulation of NMDA receptors causes a large influx of calcium ions, can result in cell death
-migraine
Karl Lashleys visual aura, implicated in cortical spreading depression
tell me about the causes epilepsy
excess excitation causes a feedback loop
uncontrolled excitation over expanding areas in the brain
can begin as partial seizures, if they become more uncontrolled, can become gran Mal seizures
What can seizures be treated with
phenytoin
- increases the refractory period between firings in voltage gated sodium channels
benzodiazepines
increase the action go GABA (because its an inhibitory NT)
Benzodiazepines
act on a separate receptor binding site on the GABA receptor subtype than GABA..
This controls the a ability of GABA to open the channel as when its bound the channel can open more frequently.
GABA
Found predominantly in the interneurons of the CNS - modules depending motor information
Acts on ligand gated chloride channels
Inactivated by presynaptic reuptake
Tell me about alcoholism
causes a change in GABA transmission, withdrawal results in convulsive movements and seizures
Can be treated with benzodiazepines and phenytoin
Glycine
second most common inhibitory NT in the CNs
But has major effects in the spinal cord and brainstem
Tell me about tetanus
caused by toxin clostridium tetani
inhibits the release of glycine
-shifts excitation-inhibition balance
mild effects restricted to muscles innervated by cranial nerves
more serious effects include epileptiform fits
treated with anti-toxin and benzodiazepines
dopamine
NT and neuromodulator
involved with pleasure , addition and movement
noradrenaline
sympathetic fight or flight response NT
decrease potentially associated in Parkinson’s and ADHD
Adrenaline
sympathetic
peripheral hormone from adrenal medulla
SYNTHESISED IN THE BOUTON AND INACTIVATED PRINCIPALLY BY RE-UPTAKE
Effects of dopamine
parkinsons
tremor, muscle rigidity due to depleted dopamine in the motor coordination circuits
schizophrenia
over production of dopamine in the mesolimibic system
Addiction
works through pleasure centres of the CNS located in the mesolimbic dopamine system
effects of serotonin
depression and OCD
can be treated with fluoxetine as this is a serotonin reuptake inhibitor
effects of endorphins and encephalins
pain
act on opioid receptors and endogenous ligands , opioids cause the down regulation of opiod receptors in the CNS
leads to opioid tolerance and increased intake
emotional perception:
naloxone can reduce symptoms
acetylcholine - esters
found in both PNS and CNS (neuromuscular junction)
CNS:
-neurons project to the hippocampus and cortex
regions essential for the formation of new memories and learning
Alzheimers disease
associated with dysfunction (reduction/) of ACh in the CNS
Nicotine
acts on nicotinic acetylcholine receptors found in the PNS and the CNS
Anticholinesterases
prevent breakdown of ACh therefore prolonging its activity
Can be therapeutic but also toxic
