Behavioral profile of amisulpride in agonistic encounters between male mice

Amisulpride is a substituted benzamide derivative that acts as a selective dopamine D2/D3 receptor antagonist. Although the anti‐aggressive properties of neuroleptic drugs are well known, the effects of amisulpride on agonistic interactions have not been explored, and there are no studies comparing acute and subchronic effects of this compound on aggression in rodents. In this study, we examined the action of amisulpride (5–25 mg/kg, i.p), administered acutely or subchronically for 10 days, on agonistic behavior elicited by isolation in male mice. Individually housed mice were exposed to anosmic "standard opponents" 30 min after drug administration, and the encounters were videotaped and evaluated using an ethologically based analysis. After acute treatment, amisulpride (5–20 mg/kg) exhibited an ethopharmacological profile characterized by a marked decrease of offensive behaviors (threat and attack) without an impairment of motor activity. By contrast, the anti‐aggressive action of the highest dose used (25 mg/kg) was accompanied by a weak increase of immobility. Body care was also significantly enhanced after treatment with the drug (20 and 25 mg/kg), emphasizing the involvement of dopaminergic receptors in this behavior. After subchronic treatment, no tolerance to amisulpride anti‐aggressive activity was observed. Overall, this behavioral profile is similar to that observed by other atypical neuroleptics. Aggr. Behav. 25:225–232, 1999. © 1999 Wiley‐Liss, Inc.     

Decreasing Neuroleptic Doses in Older Adults with Schizophrenia

This prospective study of 27 older adults, residing in long-term care facilities, examined the effects of reducing neuroleptic medications to the point of controlling symptoms and reducing side effects. Schizophrenia is a challenging health care condition that leads to delusions, hallucinations, disorganized speech, and a host of other symptoms. Unfortunately, medications control many of the symptoms but cause unwanted side effects unless monitored closely and regulated to each person's needs. This study addresses six research questions related to the reduction of neuroleptic medications. Study findings related to neuroleptic medication dose reduction were encouraging. Additionally, the findings strongly suggest that health care providers working with older adults with the diagnosis of schizophrenia would benefit from planned educational programs about behavior, observations, and medications.     

Pharmacological manipulations of brain catecholamines and the aggressive behavior induced by marihuana in REM-sleep-deprived rats

A marihuana extract, apomorphine, and amphetamine provoked in rats previously deprived of REM sleep for 96 hr an upright position with the animals pawing each other as in fighting. Nondeprived rats injected with the drugs did not show this aggressive behavior. The marihuana-treated animals also bit vigorously a rod introduced into the cage, a fact not observed with the apomorphine-treated rats. These data suggest that the marihuana aggressiveness could at least partially be mediated through the brain catecholamines. Haloperidol, chlorpromazine, α-methyl-p-tyrosine, and reserpine decreased the marihuana aggressiveness of the deprived rats. Increase of dopamine concentration by previous treatment with Dopa potentiated aggressiveness. Blockade of norepinephrine synthesis by FLA-63 was ineffective in reducing marihuana aggressiveness in the REM-sleep-deprived rats. Actually, in these animals aggressiveness appreared even without the marihuana injection. Phenoxybenzamine partially blocked marihuana aggressiveness but also severely depressed the rats. However, 20 mg/kg alone succeeded in provoking aggressiveness in the deprived rats. It is suggested that in rats with neural excitability heightened by previous REM-sleep deprivation dopamine facilitates aggressive behavior, an effect inhibited by porepinephrine. This hypothesis would imply that marihuana induces aggressiveness in REM-sleep-deprived rats by inhibiting, through an as yet unknown mechanism, the central norepinephrine system.