Chlorpromazine dopaminergic receptor

The answer is d. (Hardman, pp 407-4122) Haloperidol is a butyro phenone derivative with the same mechanism of action as the phe-nothiazines, that is, blockade of dopaminergic receptors. It is more selective for D2 receptors. Haloperidol is more potent on a weight basis than the phenothiazines, but produces a higher incidence of extrapyra-midal reactions than does chlorpromazine. 

Relative affinity of clozapine, chlorpromazine and haloperidol at Dn and D2 dopaminergic receptors... 

Qll Other neuroleptic agents include phenothiazines, such as chlorpromazine, promazin and thioridazine, and thioxanthines, such as flupenthixol. The non-specific blockade of dopaminergic receptors afforded by these drugs leads to development of side effects, such as endocrine dysfunction and extrapyramidal motor symptoms. The unwanted antagonism of motor tracts results in extrapyramidal side effects, such as Parkinsonism and tardive dyskinesia. The latter is associated with involuntary movements of the face, limbs and trunk. Chronic neuroleptic therapy can inhibit the release of GABA. This in turn leads to changes in mobility. 

In 1943, the best antidote that Hofmann could come up with was milk, but milk is a no more effective antidote to LSD than it is against insomnia. By 1980, it was clear that chlorpromazine, the phenothiazine antipsychotic that began the psychopharmacologic revolution in psychiatry in 1955, could ameliorate LSD psychosis as well as schizophrenia. And this closes the dopamine circle. Because chlorpromazine blocks dopamine receptors, its therapeutic efficacy in LSD psychosis gives further credence to our hypothesis of its dopaminergic mediation. 

The release of prolactin from the adenohypophysis is a centrally mediated event involving the dopaminergic neurons. Stimulation of these neurons blocks prolactin production, whereas blockade of dopaminergic function causes lactation. Chlorpromazine, which blocks dopamine receptors ... 

The discovery that the first antipsychotic drugs in the early 1950s, such as chlorpromazine, work in vitro by blocking dopamine receptors led to the hypothesis that schizophrenia was the result of excessive dopaminergic neurotransmission (54, 55). Supporting this hypothesis, dmgs that enhance dopamine action (e.g., cocaine, amphetamines, and L-DOPA) worsen the symptoms of schizophrenia. However, it is clear that 1) not all patients respond to neuroleptic treatment and 2) not all symptoms are reversed by the medication. 

Not understood. It is known that chlorpromazine can inhibit adrenergic and dopaminergic activity, which could explain some part of the antagonism of the amfetamines, the euphoriant effects of which are said to be mediated by central dopamine receptors. 

Fig. 6 shows that BC-PL are able to affect in men prolactin secretion and spinal lumbar HVA suggesting an effect on dopaminergic system also in humans. Phospholipids induce a decrease of serum prolactim and an increase of HVA in the lumbar spinal fluid. Serum prolactin is believed to be under the inhibitory control of DA along the hypothalamic pituitary axis (Me Leod Lehmeyrer, 1974), while lumbar HVA may be indicative of DA turnover (Curzon, 1975). Furthermore, BC-PL reverse the chlorpromazine effect on serum prolactim. The effect of phenothiazines on prolactin secretion seems to depend on a block of dopamine receptors and it is counteracted by the administration of L-dopa and of dopamine agonists (Frantz et al., 1972). 

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