Biochemistry and Biological Psychiatry. Department of Psychiatry 1 st Faculty of Medicine Charles University, Prague Head: Prof. MUDr. Jiří Raboch, DrSc. Introduction.
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Department of Psychiatry
1st Faculty of Medicine
Charles University, Prague
Head: Prof. MUDr. Jiří Raboch, DrSc.
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.
AR – adrenoceptor
G – G protein
PI-PLC – phosphoinositide specific phospholipase C
IP3 – inositoltriphosphate
DG – diacylglycerol
CaM – calmodulin
AC – adenylyl cyclase
PKC – protein kinase C
Biological models of schizophrenia can be divided into three related classes:
Multifactorial-polygenic threshold model:
Schizophrenia is the result of a combined effect of multiple genes interacting with variety of environmental factors; i.e. several or many genes, each of small effect, combine additively with the effects of non-inherited factors. The liability to schizophrenia is linked to one end of the distribution of a continuous trait, and there may be a threshold for the clinical expression of the disease.
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.
Genetic and no genetic risk factors that may have impacted on the developing brain during prenatal and perinatal life - pregnancy and birth complications (PBCs):
According to the classical dopamine hypothesis of schizophrenia, 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. MAOI act as antidepressants by blocking of enzyme MAO, thus allowing presynaptic accumulation of monoamine neurotransmitters. Tricyclic antidepressants act as antidepressants by blocking membrane transporters ensuring reuptake of 5-HT or NE, thus causing increased extracellular neurotransmitter concentrations.
A deficit in central indolaminergic 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 indoleaminergic transmission, act as a proximate cause for affective disorders and determine their quality, catecholaminergic transmission being elevated in mania and diminished in depression.
The common final result of chronic treatment by majority of antidepressants is the down-regulation or up-regulation of postsynaptic or presynaptic receptors. The delay of clinical response corresponds with these receptor alterations, hence many receptor hypotheses of affective disorders were formulated and tested.
Receptor catecholamine hypothesis:
Classical norepinephrine receptor hypothesis:
Molecular and cellular theory of depression:
Laboratory survey methods in psychiatry coincide with internal and neurological methods: