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Dopamine neuroleptic drug

Figure 7.8 Dopamine and motor function. When nigrostriatal dopamine activity is normal so is motor function. Any reduction in this DA activity, as in Parkinson s disease, results in reduced motor activity, i.e. akinesia. By contrast, too much DA activity, as in Huntington s Chorea, produces abnormal motor function, i.e. dyskinesia. The latter may be controlled by neuroleptic drugs (DA antagonists) but they can swing the balance in DA activity sufficiently to produce akinesia (Parkinsonism). DA agonists (and levodopa) may overcome akinesia but can induce DA overactivity and dyskinesia (peak dose effect) (see Chapter 15)... Figure 7.8 Dopamine and motor function. When nigrostriatal dopamine activity is normal so is motor function. Any reduction in this DA activity, as in Parkinson s disease, results in reduced motor activity, i.e. akinesia. By contrast, too much DA activity, as in Huntington s Chorea, produces abnormal motor function, i.e. dyskinesia. The latter may be controlled by neuroleptic drugs (DA antagonists) but they can swing the balance in DA activity sufficiently to produce akinesia (Parkinsonism). DA agonists (and levodopa) may overcome akinesia but can induce DA overactivity and dyskinesia (peak dose effect) (see Chapter 15)...
Dailey, JW (1992) Typical and atypical neuroleptic drug effects on dopamine and other neurotransmitter functions in rodents. PhD thesis, University of London, p. 125. [Pg.160]

Dopamine A few studies have examined the dopaminergic effects of LSD. The affinity of LSD for D2 receptors is similar to its affinity for 5-HT2 sites, and it has a slightly lower affininty for D1 receptors (Watts et al. 1995). LSD has partial agonist effects at D2 receptors as seen in the inhibition of prolactin release (Giacomelli et al. 1998). Neuroleptic drugs are also used clinically to terminate an LSD experience. Thus, the effects of LSD on dopaminergic function may contribute to its hallucinogeinc effects. [Pg.350]

Neuroleptic drugs are used in the treatment of psychosis, such as schizophrenia they are generally antagonist ligands of dopamine at the central nervous system level. " Indications and therapeutic effects of the various families of neuroleptics result from two factors. The first one is the specifity of the ligand toward the different types of dopaminergic receptors, which are unequally distributed in the... [Pg.300]

Peroutka, S.J. and Snyder, S.H. (1980) Relationship of neuroleptic drug effects at brain dopamine, serotonin, a-adrenergic, and histamine receptors to clinical potency. Am Psychiatry 137 1518-1522. [Pg.339]

It is an atypical neuroleptic drug. It interferes with binding of dopamine at D1 and D2 receptors in CNS. It produces few ex-trapyramidal symptoms. [Pg.98]

In summary, treatments for tardive dyskinesia include cessation of the neuroleptic switching to a novel agent cholinergic agents and dopamine depleting drugs, such as reserpine or tetrabenazine. [Pg.84]

Dopamine is a major neurotransmitter which acts on multiple receptors. It can activate both a and 3 adrenoceptors in addition to acting on specific dopamine receptors. These are widely distributed throughout the CNS and are also present in the renal tubules and renal and mesentric blood vessels, and many dopaminergic drugs are used in the treatment of Parkinson s disease, psychiatric disorders, as antiemetics, and for renal protection. Neuroleptic drugs, such as haloperidol and droperidol, are dopamine receptor antagonists. [Pg.28]

The hypothetical link between dopamine and schizophrenia was forged by two reciprocally related findings. The first was that potent dopamine agonist stimulants like d-amphetamine and cocaine could cause a psychosis that was schizophrenia-like, in that it had auditory hallucinations and paranoia. The second was that the neuroleptic drugs that were effective in reversing both schizophrenia and stimulant-induced psychosis were dopamine blockers. Moreover, the antipsychotic potency of the neuroleptics was proportional to their binding affinity to the D2 receptor. [Pg.235]

While there is extensive experimental evidence showing that all clinically effective neuroleptic drugs block dopamine receptors, and a general agreement that blockade of the D2 receptors in the mesocortical regions is particularly important for antipsychotic activity, only with the advent of... [Pg.266]

Laborit in the early 1950s is credited with the observation that chlorpromazine had a "calming effect in disturbed schizophrenic patients and since that time psychopharmacologists have sought to explain the mechanism of action of neuroleptic drugs. Carlsson and Linquist in 1963 demonstrated a link between the therapeutic effects of the phenothiazine neuroleptics and an inhibition of dopamine receptor function. This led to... [Pg.268]

There is no doubt that dopamine-sensitive adenylate cyclase (D site) is not involved in the antipsychotic effect of neuroleptic drugs. [Pg.23]

Dopamine agonists produce a decrease of brain DOPAC and HVA concentrations, which can be antagonized by neuroleptic drugs (107, 108). ... [Pg.132]

Neuroleptic drugs are believed to be effective in schizophrenia and psychosis by interfering with the function of neurotransmitters in the brain. The most popular neurotransmitter candidate is dopamine, although others have been proposed sporadically. The drugs are thought to exert their main effect on the dopamine system by blocking transmission at D2 (Dopamine 2) receptors (there are several known... [Pg.64]

The fact that the theory was stimulated by observed actions of neuroleptic drugs on dopamine is clearly demonstrated in these early... [Pg.72]


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