Amphetamine Smuggling Thesis


Amphetamine Smuggling Thesis

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Excerpts from Amphetamine Smuggling Thesis

However, other types of evidence suggest a dopaminergic basis for amphetamine-induced psychosis. On the basis of neurophysiologic evidence, it would appear that DA mediates the euphoria and the acute paranoid psychosis in abusers as well as the activation of schizophrenia, since all are more sensitive to d-amphetamine. The fact that the ability of neuroleptic drugs to antagonize the effects of amphetamine in man and stereotyped behavior in laboratory animals correlates with clinical potency is further evidence that these effects of amphetamine are due to increased DA. There is additional evidence that DA is relevant to the psychotomimetic effects of amphetamine. As we have indicated, it is well established that the neuroleptics are potent antidotes both to human amphetamine psychosis and to the amphetamine effects upon primate behavior. The reasons for concluding that neuroleptic blockade indicates a dopaminergic mechanism for amphetamine psychosis have been reviewed by these authors and by Snyder and will not be repeated here. However, the neuroleptic drugs also have antiadrenergic properties, albeit weaker than their anti-DA effects. The recent report that pimozide, formerly thought to be a neuroleptic specific for DA blockade, is a potent inhibitor of a NE-stimulated adenylate cyclase, a possible NE receptor, has prompted the speculation that NE blockade may be relevant to antipsychotic effects. Nevertheless, the evidence in favor of an anti-DA mechanism for the neuroleptics is very strong and does support the contention that increased DA is the mechanism of amphetamine psychosis. This conclusion is also strengthened by the report that the α-adrenergic blocker, phenoxybenzamine, and the β-blocker, propranolol, did not inhibit the euphoriant effects of high‐ dose amphetamine in detoxified amphetamine addicts. Their finding that AMPT pretreatment blocked the amphetamine effect is consistent with either a DA or a NE hypothesis. The report by Janowsky et al. that methylphenidate, which is more potent as a central DA releaser than a NE releaser, can activate schizophrenia more potently than d-amphetamine, supports the idea that activation of psychosis was due to DA rather than NE.

The finding that amphetamine stimulates brain DA turnover in man —as demontrated by an increased CSF HVA after probenecid without an increase in CSF 3-methoxy-4-hydroxy-phenyl glycol (MHPG), the major metabolite of NE—suggests that amphetamine has a more potent effect on brain DA than NE. However, this does not specifically link the increased DA turnover to the central effects of amphetamine.

All evidence considered, it is reasonable to conclude that increased DA plays a significant role in the induction of euphoria, an acute paranoid state, and an exacerbation of schizophrenia by amphetamine.

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