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Very rare adverse effects of olanzapine (that are necessarily causally related), occurring less than 0.01%, include: Agranulocytosis, a potentially fatal drop in white blood cell count, basically an exaggerated form of leukopaenia. Thrombocytopaenia. A drop in blood platelet counts which are involved in blood clotting.
Olanzapine, sold under the brand name Zyprexa among others, is an atypical antipsychotic primarily used to treat schizophrenia and bipolar disorder. [13] It is also sometimes used off-label for treatment of chemotherapy-induced nausea and vomiting [14] and as an appetite stimulant. [15]
Antipsychotic drugs such as haloperidol and chlorpromazine tend to block dopamine D 2 receptors in the dopaminergic pathways of the brain. This means that dopamine released in these pathways has less effect. Excess release of dopamine in the mesolimbic pathway has been linked to psychotic experiences. Decreased dopamine release in the ...
Dopamine receptor flow chart. Dopamine receptors are all G protein–coupled receptors, and are divided into two classes based on which G-protein they are coupled to. [1] The D 1-like class of dopamine receptors is coupled to Gα s/olf and stimulates adenylate cyclase production, whereas the D 2-like class is coupled to Gα i/o and thus inhibits adenylate cyclase production.
Dopamine receptors are a class of G protein-coupled receptors that are prominent in the vertebrate central nervous system (CNS) and are implicated in many neurological processes, including motivational and incentive salience, cognition, memory, learning, and fine motor control, as well as modulation of neuroendocrine signaling.
Dopamine released at this site inhibits the secretion of prolactin from anterior pituitary gland lactotrophs by binding to dopamine receptor D2. Some antipsychotic drugs block dopamine in the tuberoinfundibular pathway, which can cause an increase in the amount of prolactin in the blood (hyperprolactinemia).
The dopamine neurons of the dopaminergic pathways synthesize and release the neurotransmitter dopamine. [2] [3] Enzymes tyrosine hydroxylase and dopa decarboxylase are required for dopamine synthesis. [4] These enzymes are both produced in the cell bodies of dopamine neurons. Dopamine is stored in the cytoplasm and vesicles in axon terminals.
The excess dopamine resulting from inhibition of the dopamine β-hydroxylase enzyme increases unpleasant symptoms such as anxiety, higher blood pressure, and restlessness. Disulfiram is not an anticraving agent, because it does not decrease craving for drugs. Instead, positive punishment from its unpleasant effects deters drug consumption. [23]