Biochemistry and Biological Psychiatry ass. prof. Zdeněk Fišar , CSc. Department of Psychiatry 1 st Faculty of Medicine Charles University, Prague Head: prof. MUDr. Jiří Raboch, DrSc. Biochemistry and B iological P sychiatry
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Biochemistry and Biological Psychiatry
ass. prof. Zdeněk Fišar, CSc.
Department of Psychiatry
1st Faculty of Medicine
Charles University, Prague
Head: prof. MUDr. Jiří Raboch, DrSc.
1. Educational portal of our faculty:
(section Psychiatry, Psychology, Sexuology)
2. Direct links:
(presentation of lectures from psychiatry)
(teaching material from biological psychiatry)
The neurons are the brain cells that are responsible for intracellular and intercellular signalling.
Action potential is large and rapidly reversible fluctuation in the membrane potential, that propagate along the axon.
At the end of axon there are many nerve endings (synaptic terminals, presynaptic parts, synaptic buttons, knobs). Nerve ending form an integral parts of synapse.
Synapse mediates the signal transmission from one neuron to another.
Nicotinic acetylcholine receptor is made of 5 subunits, 2 of which (shown in orange) bind acetylcholine (red).
GABAA receptor, nicotonic acetylcholine receptors, ionotropic glutamate receptors, etc.
AR – adrenoceptor
G – G protein
PI-PLC – phosphoinositide specific phospholipase C
IP3 – inositoltriphosphate
DG – diacylglycerol
CaM – calmodulin
AC – adenylyl cyclase
PKC – protein kinase C
Biochemical hypotheses of mental disorders are based on the study of mechanisms of action of psychotropic drugs at the level of:
Biological models of schizophrenia can be divided into four related classes:
Multifactorial-polygenic threshold model:
A substantial group of patients, who receive diagnosis of schizophrenia in adult life, have experienced a disturbance of the orderly development of the brain decades before the symptomatic phase of the illness.
Psychotic symptoms are related to dopaminergic hyperactivity in the brain. Hyperactivity of dopaminergic systems during schizophrenia is result of increased sensitivity and density of dopamine D2 receptors. This increased activity can be localized in specific brain regions.
Depression was due to a deficiency of monoamine neurotransmitters, norepinephrine and serotonin.
Advanced monoamine theory: serotonin or norepinephrine levels in the brain are regulated by MAO-A activity mainly. However, specific symptoms of depression or mania are related to changes in the activity of monoamine transporters in specific brain regions. So, both MAO-A activity and density of transporters are included in the pathophysiology of affective disorders.
A deficit in central serotonergic transmission permits affective disorder, but is insufficient for its cause; changes in central catecholaminergic transmission, when they occur in the context of a deficit in serotonergic transmission, act as a proximate cause for affective disorders and determine their quality (catecholaminergic transmission being elevated in mania and diminished in depression).
Receptor catecholamine hypothesis:
Classical norepinephrine receptor hypothesis:
Neurotrophic hypothesis(molecular and cellular theory) of depression:
Duman et al. 1997
Nestler et al. 2002