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Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 4 uppsatser.

Diss. (sammanfattning) Umeå : Umeå universitet, 2005. / Härtill 2 uppsatser.

Thesis--Elangen-Nürnberg. / Copy imperfect: p. 128-129 wanting. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (p. [128]-146).

Thesis--University of Florida. / Description based on print version record. Typescript. Vita. Bibliography: leaves 67-73.

Somatostatin is a neuropeptide found throughout the brain. Several studies have established its anatomical distribution as being quite heterogenous with relatively high concentrations appearing in the limbic and striatal systems. Presently, very little is known about the functions of somatostatin systems in the brain and how they interact with other transmitter systems. The following report is a summary of experiments undertaken to assess the functional and chemical interactions of somatostatin with other neurotransmitter systems. Previous studies have established that the dopaminergic inputs to the basal ganglia are important for locomotor activity and reward. These systems have also been implicated in several mental and neural diseases such as schizophrenia, depression, and Parkinson’s disease. In the first experiment, interactions between dopamine and somatostatin systems were examined using paradigms involving behavioural responses to dopamine agonists. Depletion of somatostatin levels by the drug cysteamine was found to attenuate amphetamine- and apomorphine-mediated motor behaviours but not the reinforcing aspects of amphetamine. The second experiment attempted to further characterize the nature of the dopamine-somatostatin interaction by examining the effects of haloperidol, a dopamine antagonist, on central somatostatin levels. Short term treatment with haloperidol decreased striatal somatostatin levels. Long term treatment (8 months) with haloperidol failed to alter somatostatin levels in the caudate-putamen. Since somatostatin levels appear to be normal in Parkinsonian brains, the effects of MPTP poisoning in mice on central somatostatin levels was also studied to examine the accuracy of this animal model of Parkinson's disease and examine the effects of dopaminergic lesions on somatostatin levels. The results of this experiment indicate that MPTP causes a dose dependent increase in nigral somatostatin levels without altering striatal or cortical levels. These results are in partial disagreement with results obtained from both post-mortem Parkinsonian brains and primates given MPTP, thereby questioning the accuracy of this mouse model of Parkinson's disease. The final experiment examined the effects of the anticonvulsant-antidepressant carbamazepine on central somatostatin levels in the rat. Although the chemical mechanisms responsible for the therapeutic effects of carbamazepine are unknown, previous studies have suggested that its efficacy in the treatment of both manic-depression and epilepsy may be associated with the ability of this drug to reduce the abnormal somatostatin levels observed in these diseases. In this experiment, neither acute, chronic, nor withdrawal from chronic treatment with carbamazepine were found to alter the levels of somatostatin in rats. The lack of effects of carbamazepine on basal somatostatin levels may indicate somatostatin cells are susceptible to carbamazepine only under pathological situations. Together, these results are discussed in the context of recent observations of abnormal somatostatin levels in several diseases of the central nervous system and provide some insight into the interactions and functions of somatostatin systems in the normal and abnormal brain. / Medicine, Faculty of / Graduate

Thesis (Ph. D.)--University of Wisconsin--Madison, 1938. / Typescript. Includes abstract and vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references: leaves [100-102].

Thesis (Ph.D.)--University of Wyoming, 2008. / Title from PDF title page (viewed on August 6, 2009). Includes bibliographical references.

Thesis (Ph.D.)--University of Minnesota, 1998. / Includes bibliographical references. Also available on the World Wide Web as a PDF file.

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