Neurotransmitters and functions Flashcards
Epinephrine: which molecule does it increase
Increases cAMP
How is epin made?
From norep with enzyme PMNT
Norep has to be released into cytosol out of vesicle, converted, then returned to vesicles
effects of epinephrine
Bronchodilation
Stim. heart and CNS
FIGHT OR FLIGHT
NE and E bind to adrenergic receptors, what are these?
alpha 1: smooth muscle CONTRACTION
alpha 2: PREsynaptic receptor causing NEG. FEEDBACK (inhibits neurotransm. release)
beta 1: Increase CO, renin, ghrelin (stomach)
beta 2: varied
beta 3: lipolysis in adipose tissue
serotonin
raphe nuclei
serotonin functions
mood, emotional behaviour, sleep aggression control of food intake pain cognition thermoregulation memory
antidepressants and serotonin
increase serotonin levels in synapse:
MAO inhib
blocking SERT for reuptake into presynaptic cell
psychedelics and serotonin
stim Serotonin 2A
hallucinations
antiemetics and serotonin
INHIBITS serotonin 3 recep in gut
inhibits nausea and vomiting
antimigraine drugs and serotonin
STIM Serotonin 1D
Catecholamines
dopamine
norepinephrine
epinephrine
made from tyrosine (tyrosine hydroxylase is rate-limiting step)
how are levels decreased (cats)
reuptake via Na-dependent channels
chemical in between dopamine and tyrosine
L-dopa
4 pathways involved with dopamine
- Niagrostriatal-movement
- Mesolimbic-starts in ventral tegmental area to nucleus accumbens, amygdala and hippocampus of limbic system-MOTIVATION AND DESIRE
- mesocortical-starts in ventral tegmental area and ends in frontal lobe cerebral cortex
- Tuberinfundibular-arcuate nucleus (hypothal.) to post. pit
Mesolimbic
Motivation and desire
disorders: ADHD, Addiction (reward path), schizo, depression
Mesocortical
Motivation in cognition and sensation
Conscious emotion
Disorders: ADHD, Schizo
Tuberinfundibular
regulation of prolactin release
Cocaine and dopamine
blocks reuptake by transporter
meth
reverses the action of the
transporter, which then actively pumps out more
dopamine
anything that messes with dopamine system is ADDICTIVE
norepinephrine
release: lat tegmental area in pons, medulla
locus coeruleus: pons
to neocortex and cerebellum with previous things
norepinephrine function
VIGILANCE/AROUSAL= MOMMY
how is it made (norep)
transported from cytosol to vesicle (dopamine) via VMAT2
there dopamine can be converted into norep because enzyme only present in vesicles
Norep and disease
Depression (partially)
• Apathy (lack of arousal)
– Attention Deficit Hyperactivity Disorder (partially)
• Reduced focus
Norep and drugs
– Cocaine
– Methylphenidate (Ritalin)
– Amphetamines (Adderal / “Speed”)
– Methamphetamine (“Tik”, “Crystal Meth”)
Antidepressants
• Tricyclic Antidepressants (Desipramine)
• Selective Serotonin Norepinephrine Reuptake Inhibitors (Cymbalta)
• Norepinephrine Reuptake Inhibitors (Stattera)
ACh
released from basal forebrain, motor neurons, neurons of ANS
projects to cerebral cortex and hippocampus
nicotinic and muscarinic receptors
ACh function
arousal
wakefulness
learning
memory
reversal potential for glutamate channels AMPA and NMDA
0mV
which ionotropic glutamate receptor also involves Ca
NMDA
why are NMDA receptors special?
NMDA receptors only open at depolarized potentials due to the Mg2+ block. • Ie NMDA receptors only open when the cell is already depolarised • NMDA receptors are permeable to Ca2+ • Ca2+ can activate enzymes / 2nd messengers • Important for learning and memory (Long Term Potentiation)
what enters the vesicles: glutamate or glutamine (in reuptake process)
glutamine
which cells are involved in the reuptake of glutamate and release (conversion of glut to glutamine)
glial cell: astrocytes
which neurotransmitter is associated with excitotoxicity during cerebral ischaemia
glutamate-excess activation of NMDA so Ca2 enters
GABA
inhibitory
ionotropic receptors: Cl-
metabotropic: presynaptic vesicles, K efflux so hyperpolarisation
Target site for:
• Alcohol
• Benzodiazepines
• Most General Anaesthetics
how is GABA made
glutamate decarboxylase (carboxyl group from glutamate removed)
