In recent years we have been involved in determining the stimulus for thirst and sodium appetite during hypovolemia, the contribution of angiotensin to thirst, the role of central catecholaminergic neurons in mediating the nonspecific aspects of motivation, and the possible contribution of certain brain areas in the specific control of motivated ingested behavior.
The aims of the proposed research are to continue to make progress along these lines. More specifically, (a) the dipsogenic effects of angiotensin during hypotension and hypertension will be compared, to determine whether drinking is induced only when blood pressure is elevated. The physiological basis of sodium appetite will be explored (b) by determining the possible role of various endocrine systems in mediating the rapid induction of sodium appetite that we have recently observed to ccur when rats maintained on sodium-deficient diet are made hypovolemic. Central factors involved in the specific control of thirst will be investigated in two ways: (c) studies of the excitation of thirst will proceed from analyses of drinking behavior in rats with lesions of brain tissue surrounding the anteroventral third ventricle, a region of apparent significance in the control of thirst; (d) studies of possible central inhibitory mechanisms will proceed from analyses of the polydipsia that we have recently observed to ccur in rats after brain lesions are made just dorsal to this diencephalic area. Finally, (e) nonspecific factors in the control of thirst will be investiated by determining the effect of dehydration on activity in central dopaminergic neurons. It is the ultimate goal of these studies not only to obtain some basic information about the physiological mechanisms which underlie thirst and sodium appetite, but also to obtain insights into the basic processes by which all motivation is mediated. In this regard, we have developed a model of brain function which we believe has considerable relevance for problems related to mental health and cerebral dysfunction.
| Stricker, Edward M (2016) 2015 Distinguished career award: Reflections on a career in science. Physiol Behav 162:196-200 |
| Bykowski, Michael R; Smith, James C; Stricker, Edward M (2007) Regulation of NaCl solution intake and gastric emptying in adrenalectomized rats. Physiol Behav 92:781-9 |
| Smith, Carrie A; Curtis, Kathleen S; Smith, James C et al. (2007) Presystemic influences on thirst, salt appetite, and vasopressin secretion in the hypovolemic rat. Am J Physiol Regul Integr Comp Physiol 292:R2089-99 |
| Stricker, Edward M; Hoffmann, Myriam L (2007) Presystemic signals in the control of thirst, salt appetite, and vasopressin secretion. Physiol Behav 91:404-12 |
| Stricker, Edward M; Bushey, Michael A; Hoffmann, Myriam L et al. (2007) Inhibition of NaCl appetite when DOCA-treated rats drink saline. Am J Physiol Regul Integr Comp Physiol 292:R652-62 |
| Hoffmann, Myriam L; DenBleyker, Megan; Smith, James C et al. (2006) Inhibition of thirst when dehydrated rats drink water or saline. Am J Physiol Regul Integr Comp Physiol 290:R1199-207 |
| Manesh, Reza; Hoffmann, Myriam L; Stricker, Edward M (2006) Water ingestion by rats fed a high-salt diet may be mediated, in part, by visceral osmoreceptors. Am J Physiol Regul Integr Comp Physiol 290:R1742-9 |
| Stricker, Edward M; Hoffmann, Myriam L; Riccardi, Christiana J et al. (2003) Increased water intake by rats maintained on high NaCl diet: analysis of ingestive behavior. Physiol Behav 79:621-31 |
| Stocker, Sean D; Smith, Carrie A; Kimbrough, Celeste M et al. (2003) Elevated dietary salt suppresses renin secretion but not thirst evoked by arterial hypotension in rats. Am J Physiol Regul Integr Comp Physiol 284:R1521-8 |
| Stricker, Edward M; Sved, Alan F (2002) Controls of vasopressin secretion and thirst: similarities and dissimilarities in signals. Physiol Behav 77:731-6 |
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