Biomedical subjects

M. Didriksen

Publications and source records attributed to M. Didriksen.

3 recordsLinked to original sources

PubMed1995

The effect of risperidone on schedule-induced polydipsia.

The effects of risperidone on the acquisition of schedule-induced polydipsia in rats were investigated in a chronic dose regime followed by seven days of withdrawal. Risperidone dose-dependently suppressed water intake and number of panel pushes. Drinking efficiency and free water intake in home cages were unchanged. By comparing the effects of risperidone in the present paper with the effects of different-neuroleptics in the same procedure from an earlier study, it appears that the effect of risperidone is intermediary to that of the 'typical' and 'atypical' neuroleptics. It may be concluded that risperidone acts as an atypical neuroleptic compound; however, increasing the dose only two-fold will cause EPS.

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PubMed1994

The effects of amphetamine, phencyclidine, dopaminergic antagonists and atypical neuroleptics on schedule-induced polydipsia (SIP) are distinguishable.

The effects of amphetamine, phencyclidine, dopaminergic blockers and atypical neuroleptics on the acquisition of schedule-induced polydipsia in rats were compared in a chronic dose regime followed by 7 days of withdrawal. All compounds suppressed water intake. However, different mechanisms were responsible. The antidopaminergic compounds inhibited the initiation of drinking, as the temporal pattern of licking was shifted to the right. Phencyclidine inhibited the maintenance of drinking as the number of licks/ml water consumed was increased. The suppressing effect of amphetamine may have been due to the reduction of high rates of licking and/or a competition between licking and locomotor or other amphetamine-induced activities. The number of panel entries were increased by amphetamine and phencyclidine. The typical antidopaminergic compounds decreased the number of panel pushes, whereas the atypical antidopaminergic compounds were without effect on this parameter. In conclusion, it was possible to differentiate between the types of compounds investigated by comparing their effects on water intake, panel pressing, drinking efficiency and the temporal patterns of licking and panel pressing.

Journal Article↗

PubMed1993

The attenuation of schedule-induced polydipsia by dopamine blockers is not an expression of extrapyramidal side effect liability.

The effects of scopolamine and diazepam on attenuation of schedule-induced polydipsia (SIP) produced by a dopamine D1 antagonist, SCH 23390, a dopamine D2 antagonist, raclopride, and a mixed D1/D2 antagonist, cis(Z)-flupentixol, were examined in a chronic dose regime, followed by 7 days of withdrawal. Scopolamine potentiated the effect of SCH 23390, but did not alter the effects of raclopride of flupentixol. Diazepam reversed the effect of flupentixol, suppressed the reversal of the SCH 23390-treated group to control level after withdrawal, and was without effect of the raclopride-treated group. It is concluded that the suppression of SIP behaviour induced by the dopamine blockers is not due to the induction of extrapyramidal side effects. However, it cannot be excluded that the effects of SCH 23390 and flupentixol may be mediated through the motoric dopamine system, as they inhibited the initiation of drinking behaviour.

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