The present study investigated the neural mechanisms by which environmental stimuli guide conditioned behaviors in the amphetamine conditioned place preference (CPP) paradigm. Systemically injected D1 and D2 dopamine antagonists blocked both acquisition and expression of the CPP: the selective D1 antagonist more effectively blocked expression than the D2 antagonists. The site of action of the antagonists on expression was the nucleus accumbens. Systemically injected reserpine, but not intra-accumbens a-MPT microinjections, also blocked the expression of the amphetamine CPP. Pre-conditioning and post-conditioning electrolytic or excitotoxic lesions of the lateral amygdaloid nucleus impaired the CPP. It was concluded that the effect of conditioned incentive stimuli is mediated by a neural system which involves the reserpine-sensitive dopamine pool and the D1 dopamine receptor in the nucleus accumbens and the lateral amygdaloid nucleus.

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There has been a great deal of research investigating drug combinations which can increase analgesia. A number of studies have been conducted with one particular combination--opioids combined with the amphetamine drugs. Despite the existing literature, this combination is rarely used in clinical practice. One purpose of this thesis is to review the literature pertaining to the opioid-amphetamine combination. Another purpose of this thesis is to investigate whether dextroamphetamine sulfate ($ circler$Dexedrine) can potentiate morphine sulfate analgesia in rats in the formalin test (Experiment 1). To investigate whether these results can be generalized to another psychostimulant, methylphenidate hydrochloride ($ circler$Ritalin) is used in Experiment 2. Methylphenidate has been chosen instead of another amphetamine drug because it is currently being used in clinical studies without supporting evidence from animal studies. The results of the two experiments indicate that low doses of d-amphetamine and methylphenidate can potentiate the analgesic effects of morphine.

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A series of experiments was carried out to clarify the effects of morphine (0.3 - 10 mg/kg) on intracranial self-stimulation (ICS) and to compare these with the effects of the stimulant amphetamine on this behavior. It was shown that the enhancement of ICS by morphine requires repeated drug exposure, is prevented by pre-exposure to the drug in a non-ICS context, is mimicked by administration of vehicle, and is not reliably reversed by naloxone. In contrast, facilitation of ICS by amphetamine was immediate and remained stable over repeated days of testing. It was concluded that ICS facilitation induced by morphine, but not by amphetamine, is largely the outcome of a learned association between the drug effect and the ICS procedure, and does not appear to be a direct, opiate receptor-mediated effect. Finally, 6-OHDA lesions of ventral tegmental dopamine neurons were shown to block the facilitation of ICS by morphine but not by amphetamine. These lesions were also shown to delay the development of tolerance to morphine-induced catalepsy.

This study examined the contributions of different brain areas to several of the behavior effects of amphetamine. The drug was micro-injected into each of six discreet brain sites in rats and the effects on behavior were examined. Amphetamine's rewarding effects were studied using the conditioned place preference (CPP) paradigm. Animals that had received injections into the nucleus accumbens showed a CPP, suggesting a rewarding effect of the drug. No effect was produced by injections into the medial frontal cortex, medial or lateral parts of the caudate nucleus, amygdala or the region around the area postrema. A conditioned taste aversion (CTA) towards a flavour that had been paired with the drug was produced by injections into the region around the area postrema, but not from the other sites. Anorexia and adipsia were both producted only by injections into the nucleus accumbens and amygdala. In the open field, increased activity was produced by intra-accumbens amphetamine injections, with smaller effects from the medial frontal cortex and medial caudate. Stereotyped behavior was not produced by any intra-cranial injection. The CPP, anorexia, adipsia and increase in activity that were produced by the intra-accumbens injections were interpreted as suggesting that the drug had stimulated approach behavior towards all stimuli, as if they had all become rewarding. The observation of a CPP from the accumbens and a CTA from the region around the area postrema suggests that the rewarding and apparently aversive effects of systemically injected amphetamine result from actions of the drug on different neuroanatomical substrates. Other hypotheses of the behavioral function of the neural substrates of the observed effects are presented.

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