Amphetamine and tranylcypromine are structurally related chemical isomers with pharmacologically distinctive activity profiles. Since they are equimolar and structurally similar they may be used to assess the pharmacologically distinctive activity profiles. Since they are equimolar and structurally similar they may be used to assess the pharmacological specificity of a proposed animal model of depression. Adult male Sprague-Dawley rats were exposed to a chronic stress regimen or remained undisturbed. They were then acutely stressed with white noise. The monoamine oxidase inhibitor tranylcypromine was effective in restoring otherwise reduced stress elicited open field activity in chronically stressed rats. Amphetamine did not resemble tranylcypromine or other antidepressants, and produced a variety of effects at least some of which indicated a potential increase rather than reduction in depression consequent to chronic administration.

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We have previously demonstrated that adult male Sprague-Dawley rats which are chronically maintained upon a schedule of intracranial reward (ICS) show elevated rates of response after a mild tail pinch. Both dopamine and opiates have been implicated in the mediation of other stress induced behavioral alterations, and may therefore also possibly be involved in the ICS effect. The present report replicated the initial finding of tail pinch induced facilitation of ICS, and further demonstrated that while opiate blockade failed to affect the ICS response dopaminergic blockage in fact inhibited it. These findings suggest neuropharmacological specificity for stress related behavioral change, and further implicate dopamine in stress responses.

In the first experiment, adult male Swiss-Webster mice were systemically injected with a standard dose of morphine. Compared to the influence of vehicle, the motor activity of morphine-injected mice was increased. Neither phenytoin sodium nor carbamazepine alone facilitated motor activity, but pretreatment with both drugs further facilitated the increased motor activity produced by morphine. In a second experiment, mice were injected centrally with a long-acting analog of leu-enkephalin. It also increased motor activity in comparison with vehicle. Again, both phenytoin sodium and carbamazepine further facilitated this response. Both experiments suggest a facilitatory interaction between some aspects of these anticonvulsants and opiate-induced motor activity.

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