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Margaret Mead
John R. Martin
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About

Master's degree work concentrated on involvement of dopamine on the regulation of body temperature regulation, locomotor activity and stereotypic behavior differences in the spontaneously hypertensive rat and normotensive rat strains (Sprague-Dawley and Wistar Kyoto). An increased sensitivity to dopamine was found in the temperature regulating system suggesting a change dopamine receptor sensitivity in the hypothalamus. Changes in dopamine receptor sensitivity were not present in the mesocorticolimbic system (nucleus accumbens) as no changes in stereotypic behavior was detected nor in locomotor activity indicating no changes in the the nigrostriatal pathway (basal ganglia). PhD work was involved in detecting changes in dopamine receptor sensitivity during the development of tolerance and dependence to opioids. It was found that the mesocorticolimbic dopamine system became supersensitive with an increase in numbers of dopamine receptors during the development of tolerance and dependence and that this increase in sensitivity could be prevented by treatment with lithium, which is known to stabilize dopamine receptors. Postdoctoral work was directed towards determining the effect of central neuropeptide y (NPY) on the regulation of the cardiovascular system. It was found that microinjection of NPY into the posterior hypothalamic nucleus (PHN) of the rat increases blood pressure. This increase in blood pressure was compared to that caused by the microinjection of carbachol into the PHN, which occurs through the activation of muscarinic receptors (the M3 receptor). Also, the microinjection of an amount of NPY into the PHN that has little effect on blood pressure enhances the increase in blood pressure evoked by the microinjection of carbachol into the PHN. In addition, the microinjection of the 5-HT2 receptor agonist DOI into the anterior hypothalamic/preoptic area (AH/PO) increases blood pressure presumably by evoking the release of acetylcholine in the PHN, as this increase is blocked by atropine and the mechanism is the same as that evoked by carbachol given into the PHN. This cholinergic system is apparently activated during pathophysiological conditions, such as hemorrhage, which would be expected to evoke changes in the baroreceptor reflex. The increase in blood pressure evoked by DOI is also modified by the presence of cannabinoid agonists or antagonists in the PHN. Research is ongoing to determine the effect of NPY and cannabinoids on the signal transduction mechanism linked to the stimulation in the PHN of muscarinic M3 receptors.

ORCID ID

http://orcid.org/0000-0002-8280-6088

Reviewer Keywords
psychiatric disorders pain medicine neurology and psychiatric disorders cardiology vasopressin renin angiotensin alderosterone system heart serotonin serotonin agonists neuropeptide y cannabinoids muscarinic autonomic function cardiovascular abnormalities
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My Professional Societies

American Society for Pharmacology and Experimental Therapeutics
Society for Neuroscience
Team-Based Learning Collaborative
International Association of Medical Science Educators
Association of Medical School Pharmacology Chairs
Association of Chairs of Departments of Physiology
Christian Medical and Dental Association