Behavioral evidence for supersensitivity after chronic administration of haloperidol, clozapine, and thioridazine
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Cited by (95)
Rationale and neurobiological effects of treatment with antipsychotics in patients with chronic schizophrenia considering dopamine supersensitivity
2021, Behavioural Brain ResearchCitation Excerpt :A study reported that clozapine, like aripiprazole, did not cause DRD2 up-regulation at cell levels [154]. On the other hand, several animal models showed behavioral supersensitivity caused by clozapine [155,156]. Past studies have shown that clozapine greatly improved tardive dyskinesia which was caused by previous medications [157].
Continuous versus extended antipsychotic dosing in schizophrenia: Less is more
2021, Behavioural Brain ResearchCitation Excerpt :This exaggerated response is the most commonly used index of antipsychotic-induced dopamine supersensitivity in laboratory rodents. In rats, antipsychotic-induced dopamine supersensitivity produces robust sensitization to the psychomotor-activating effects of dopamine agonists, but also to their reward-enhancing effects [39,40,43–49]. Antipsychotic-evoked dopamine supersensitivity is often studied in otherwise neurologically intact animals, but it can also be seen in well-established animal models of schizophrenia symptoms [45].
5-HT<inf>2</inf> receptors modulate the expression of antipsychotic-induced dopamine supersensitivity
2015, European NeuropsychopharmacologyCitation Excerpt :However, amphetamine-induced locomotion permits an accessible and rapid assessment of dopamine function following antipsychotic treatment. In parallel, other studies have shown that antipsychotic-induced dopamine supersensitivity is also characterized by an enhanced ability of the direct dopamine receptor agonist apomorphine to stimulate both horizontal locomotor activity and stereotyped behaviour (Asper et al., 1973; Clow et al., 1979; Gianutsos et al., 1974; Montanaro et al., 1982; Sayers et al., 1975; Smith and Davis, 1975, 1976). Finally, a question raised by our findings is whether treatment with an atypical antipsychotic would induce similar alterations in 5-HT2 receptor density and function.
Parallels between behavioral and neurochemical variability in the rat vacuous chewing movement model of tardive dyskinesia
2012, Behavioural Brain ResearchCitation Excerpt :While variability is not explicitly discussed in those studies, the standard error reported by Burt et al. [87] for increased binding after 3 weeks of the low dose of haloperidol is 8% of the mean (i.e. the standard deviation would be 18% of the mean), and standard errors for stimulant behavioral sensitization appear to be similarly small [16,17], a far cry from the extreme variability observed in both tardive dyskinesia and vacuous chewing movements. Both behavioral sensitization to stimulants [90–92] and receptor upregulation [86] reverse within a few weeks after neuroleptic withdrawal. Moreover, D2 receptor supersensitivity and vacuous chewing movements have often been found to be dissociable.
T-type calcium channel antagonism produces antipsychotic-like effects and reduces stimulant-induced glutamate release in the nucleus accumbens of rats
2012, NeuropharmacologyCitation Excerpt :On day 21 animals were given vehicle or TTA-A2 60 min prior to saline or amphetamine and locomotor activity was evaluated. These groups allowed us to determine whether 20 days pre-treatment with TTA-A2 resulted in desensitization of the ability of TTA-A2 to attenuate amphetamine-induced psychomotor activity, as well as whether prior treatment with TTA-A2 sensitized the amphetamine response, as has been observed with haloperidol and other clinically approved antipsychotics (Rebec et al., 1982; Samaha et al., 2007; Smith and Davis, 1975, 1976). As a positive control, a sixth group of animals was treated with haloperidol (0.2 mg/kg) for 20 consecutive days and on day 21 received amphetamine (without haloperidol) to confirm the sensitized amphetamine response.