The increased locomotor activity induced by systemic injections of d-amphetamine or scopolamine in rats was studied in Digiscan Animal Activity Monitors. This multifactorial analysis of locomotion demonstrated that activity measures of horizontal (ambulatory), vertical (rearing), stereotypic, and rotational behaviors differed depending on dose and drug. The topographies of these activity variables may be unique for the dopaminergic and cholinergic systems underlying hyperactivity. These results are a first step toward a needed increase in the sophistication of behavioral pharmacological techniques, allowing for the development of specific activity prints for different classes of psychoactive agents.

Most investigators have found a decrease in emotional defecation in rats given neuroleptics in novel environments, supporting their action as a major tranquilizer. We have found, however, that in rats a profound increase in emotional defecation can result from neuroleptic administration in well habituated environments, such as the homecage. Anticholinergics are known to be effective in treating the side effects associated with neuroleptic administration in humans. Therefore the present study determined the effects of anticholinergic treatment in this animal model. In male rats, defecation was measured for a 1-h test period in their homecage following various doses of the central and peripheral anticholinergics, scopolamine, and n-methylscopolamine, respectively. A decrease in fecal excretions and an attenuation of haloperidol-induced defecation was found following administration of scopolamine. n-Methylscopolamine reduced defecation at all doses. When n-methylscopolamine was combined with haloperidol, both fecal mass and number decreased significantly. Since both anticholinergic agents reduced haloperidol-induced defecation it is suggested that their effectiveness is mediated through peripheral mechanisms.

The neuroleptic haloperidol was found to produce increased defecation in laboratory rats when tested in well habituated environments. It is well known that haloperidol induces catalepsy through antagonism of striatal dopaminergic receptor mechanisms. When another cataleptic agent, morphine, was tested, no significant increases in defectation were detected. Another study focused on the possible role of peripheral dopamine receptor sites within the gastrointestinal tract on neuroleptic-induced defecation. When the peripheral dopamine receptor antagonist domperidone was tested, no significant differences in fecal elimination were recorded. Thus, it appeared that the cataleptic state per se, or the peripheral effects of haloperidol did not seem to be responsible for the increased defecation. Defection is often used as an index of emotionality. The fact that this measure increased following administration of a major tranquilizer suggested the need to study more directly the relationship of this phenomenon of defecation with the affective state of the animal. In a control study it was found that the antianxiety agent benzodiazepam did not by itself influence defecation. However, those animals which were pre-injected with diazepam followed by haloperidol did not show increased defecation. Thus under certain circumstances, normal rats given haloperidol show "emotional defecation" which seems to reflect increased anxiety. This finding may serve as a basis for the development of an animal model for some of the atypical side effects of major tranquilizers, such as akathisia, dysphoria, and neuroleptic anxiety syndrome.

No abstract