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David B Menkes

Researcher at University of Auckland

Publications -  160
Citations -  4294

David B Menkes is an academic researcher from University of Auckland. The author has contributed to research in topics: Medicine & MEDLINE. The author has an hindex of 31, co-authored 146 publications receiving 4071 citations. Previous affiliations of David B Menkes include University of Otago & University of Melbourne.

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Receptor Sensitivity and the Mechanism of Action of Antidepressant Treatment: Implications for the Etiology and Therapy of Depression

TL;DR: The effects of long-term antidepressant treatment on biogenic amine metabolism and on various indexes of presynaptic and postsynaptic receptor function are evaluated to provide support for hypotheses of amine receptor abnormalities in depression and indicate the need for expanded studies ofAmine receptor function in patients.
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Behavioral studies following lesions of the mesolimbic and mesostriatal serotonergic pathways.

TL;DR: These experiments suggest that the mesolimbic serotonergic pathway originating in B8 subserves some of the inhibition necessary to dampen behavioral responsivity.
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Efficacy and safety of antidepressants for children and adolescents

TL;DR: Of seven published randomised controlled trials of newer antidepressants for depressed children published in refereed journals, six used a placebo control and the extent to which authors' conclusions were supported by data was analysed.
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Acute tryptophan depletion aggravates premenstrual syndrome.

TL;DR: The dietary technique of acute tryptophan depletion was used to suppress brain serotonin synthesis in 16 women with documented premenstrual syndrome and caused a significant aggravation of pre menstrual symptoms, particularly irritability.
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Guanosine triphosphate activation of brain adenylate cyclase: enhancement by long-term antidepressant treatment.

TL;DR: Activation of adenylate cyclase by a stable guanosine 5'-triphosphate analog was augmented in brain membrane preparations from rats treated on a long-term basis with tricyclic antidepressants or electroconvulsive shock, suggesting a possible mechanism for the changes in sensitivity to various neurotransmitters seen after antidepressant administration.