Neuropharm Flashcards
NT abnormality in mood disorders
depleted Noradenaline
What NTs are deficient in depression?
Serotonin, dopamine, noradrenaline, GABA
What NTs are in excess in depression?
ACh, substance P
What hormones are in excess in depression?
Corticotrophin releasing hormone (from hypothalamus) which results in raised cortisol secretion from adrenals via ACTH from anterior pituitary
Name of reward pathway
Mesolimbic dopaminergic system
Monoamines
Serotonin, dopamine, noradrenaline
Mechanism of tricyclics
Inhibits reuptake of noradrenaline and serotonin
SE of tricyclics
Dry mouth, blurred vision, urinary retention, constipation
Drowsiness, wt gain
Cardiotoxic and decreased seizure threshold
Tricyclic examples
imipramine, amitriptyline
SSRI examples
Fluoxetine, citalopram, sertraline
SSRI SEs
Sweating, nausea, headache, vivid dreams, hyponatraemia in elderly, worsened anxiety, increase suicide risk in under 25yrs
Monoamine oxidase inhibitors action
Stop metabolism of serotonin
SE of MOAs
Malignant hypertension and headache when eat cheese because can’t metabolise tyramine
MOA example
Phenelzine
SNRI examples
Duloxetine, Venlafaxine, mirtazapine
SE of Lithium
Hypothyroidism, tremor, polyuria
Toxic if dehydrated
Lithium toxicity
Ataxia, course tremor, drowsy, d+v
What is the main excitatory NT in the CNS?
Glutamate
What effect does glutamate release have on post synaptic neurone?
Glutamate activates post synaptic ionotropic receptors to increase cation uptake (Na+)
This causes depolarisation and excitation and pass on of AP
Creates the excitatory postsynaptic potential (e.p.s.p)
What is the main inhibitory NT in the CNS?
GABA and glycine
What effect does GABA or glycine release have on post synaptic neurone?
Increases anion (Cl-) uptake into post-synaptic neurone Negative uptake makes cell hyper polarise and not pass on the AP This creates the inhibitory postsynaptic potential
