In Memoriam: Alan Neil Epstein, July 29, 1932-January 9, 1992
Alan Epstein was taken from us suddenly and well before his time when he was struck by a bus in Cancun, Mexico, just before attending the winter Developmental Psychobiology meetings. He is survived by his wife, Fifi, his three children, Lise, Mark, and Ruth, two grandchildren, Philip and Rachel, and scores of colleagues, friends, and present and former students. We all profoundly feel his loss and miss him deeply. Alan’s contributions to the fields of biological psychology, neurosciences, ingestive behavior, and development were singular. With James Sprague and later Adrian Morrison, he edited Progress in Psychobiology and Physiological Psychology (P4), an enormously influential series of monographs that spanned the Reprint requests should be sent to Dr. E. M. Blass; Psychology and Nutritional Sciences, 220 Uris Hall, Cornell University, Ithaca, NY 14853-7601, U.S.A. Received for publication 21 April 1992 Accepted at Wiley 15 May 1992
Developmental Psychobiology 25(5):313-3 17 (1992) 0 1992 by John Wiley & Sons, Inc.
CCC 0012-1630/92/050313-05$04.00
314
BLASS
entire domain of biopsychology from visual psychophysics to activity, nutrition, and growth, to catecholamines and recovery of function. As an editor, Alan was without peer-he got the best out of his contributors, sharpened their ideas, and improved their communication. His background as editor of the undergraduate Hopkins newspaper, The Newsletter, stood him in good stead for his adult task. He edited two chapters that I wrote-one for P4 with Ted Hall and Marty Teicher and one for an AAAS symposium on thirst. In both instances, he was a delight to work with, serious-but with humor and grace. As always, I learned a lot from him and this helped me enormously in editing Volumes 8 and 9 of the Handbook of Behavioral Neurobiology. His editing alone would have made him an important player in the field of Behavioral Neurosciences. In fact, it was the most modest of his contributions. His two major professional legacies were as a bench scientist and as a teacher and mentor. As a scientist, Alan had a “green thumb.” He had the great talent of being able to articulate an empirical question and devise a technique-always simple and accessible-to provide an answer. His medical training at Hopkins provided a keen awareness for symptoms that travelled together, their recovery, and residual deficits. His clinical eye recognized this as a syndrome so that I I years after Anand and Brobeck wrote of a profound aphagia in rats with lateral hypothalamic lesions, Teitelbaum and Epstein (1962) documented the Lateral Hypothalamic Syndrome. This was a remarkably important breakthrough for Psychobiology because it emphasized in a systematic and evaluative way a cluster of profound deficits and the recovery of complex motivational acts. More than that, however, the precise documentation of recovery has provided a frame of reference for the succeeding rounds of analyses on hypothalamic function and its disruption by neurochemical lesions. It was the recognition of a syndrome that provided a clear target against which deficits caused by other means and in other locations in the basal forebrain could be evaluated. In parallel with the central analysis, Alan started a decade-long project on the control of food and water intake in the absence of olfactory or gustatory stimulation. Alan devised a rat-sized version of the nasogastric tube that he well knew from rounds in internal medicine. Certain diagnostic procedures required threading a tube through the naso-pharynx into the esophagus. In a powerful series of studies, Epstein with Teitelbaum and later Snowdon demonstrated that long-term homeostasis could be sustained in neurologically intact rats chronically self feeding through the nasogastric tube in the absence of olfactory and gustatory stimulation. Body weight was defended, caloric density and dilution was compensated for, as were preloads of different density. The role of the vagus in control of gastric emptying and its relation to ingestion was established. Alan’s laboratory was multifaceted and busy. One difficulty experienced by rats with lateral hypothalamic lesions was salivary insufficiency and this led to analyses, with Kissileff, into the contribution of saliva as a lubricant for feeding and with Hainsworth and Stricker on the use of saliva in a thermoregulatory capacity. This last series of studies is a major and meticulous analysis of behaviorphysiology synergism in the rat’s defense of core temperature against heat stress that has not received the attention that it deserves. I arrived in Alan’s lab in 1969, at a very felicitous moment because Alan’s attention was turning again to stimulating the brain directly with substances that the brain naturally receives. He had earlier devised a simple and inexpensive
EPSTEIN MEMORIAM
315
cannula that could be implanted into the brain and kept patent for the animal’s lifetime. He and I provided evidence for thirst osmoreceptors in the preoptic area. The really influential studies, however, came from his collaboration with James Fitzsimons and Barbara Simons (Rolls) who demonstrated that picogram injections of angiotension decapeptide (AII) into the brain would cause copious drinking. This was advanced by Johnson and Epstein’s demonstration that A11 had to gain access to the ventricular space-that the A11 receptors were not on the brain-side of the ventricles but on the ventricular side. Shortly thereafter, Simpson and Epstein demonstrated that A11 injections into the subfornical organ (SFO) that resides in the ventricular space caused drinking. Preventing ventricular flow into the SFO eliminated drinking to intraventicular A11 injection. The developmental studies with which many of the members of this Society are familiar have had a long history. Alan’s first report in 1970’onthe vital role of saliva in suckling demonstrated that saliva formed a sealant on the nipple to provide the suction necessary for the infant to hold the nipple and exert negative pressure for milk withdrawal to occur. Alan’s developmental interests remained active. In 1976, Wirth and Epstein, for the first time, demonstrated the newborn’s ability to behaviorally adjust to dehydration by drinking from a continuous flow. This study set the stage for Hall’s analyses of independent ingestion. There was a lively interest in suckling determinants as well. Houpt and Epstein provided evidence for gastric control over intake and a more detailed analysis by Lorenz Ellis and Epstein in 1982 made a stronger case for upper GI fill as a determinant of intake, but not nipple attachment (Alan and I disagreed on that one-but more on that later). Epstein was interested in the time course of development of hydrational controls as reflected in his studies on angiotension induced drinking (Misantone, Ellis & Epstein; Leshem & Epstein) on alpha- and beta-adrenergic anorexia, and on dehydration induced anorexia (Leshem & Epstein, 1988). As part of his professional lifetime dedication to mechanisms of salt appetite, which I will discuss directly, Alan also studied its ontogeny. Karen Moe demonstrated a protracted tolerance to and preference for very concentrated NaCl solutions until 10 days of age. This striking finding when better understood will provide insights into sodium balance, gustation, and their integration in homeostatis and motivation. And there was the remarkable demonstration by Sakai, Frankmann, Fine, & Epstein on the potentiating effect of prior salt depletion and repletion in later salt ingestion in need-free rats. This was an enormous phenomenon and Alan saw its potential. But his first love was salt appetite. It was the intellectual subject of his imprinting. When an undergraduate with Eliot Stellar at Hopkins, Alan and Eliot published an important article in The Journal of Comparative and Physiological Psychology on “The Control of Salt Preference in the Adrenalectomized Rat.” His interest in this issue gained new momentum with the discovery that angiotension provoked a salt appetite independent of and in addition to one for water. These findings unleashed a sustained attack on the hormonal determinants of sodium appetite, with an important progress report from his laboratory and the international efforts supported by the McCarther Foundation just recently appearing in Volume 10 of the Handbook of Behavioral Neurobiology, edited by Ed Stricker. Thus, we have all suffered the loss of a preeminent behavioral neuroscientistneuroendocrinologist. His work was always characterized by its meticulousness and thoroughness. He attacked the big issues and his findings have been so solid
316
BLASS
and important and stated with such clarity that others have been able to build upon them. His enthusiasm for science and his generosity as a colleague were infectious and often galvanized scientific enterprises that lay dormant. My own recollections, I think, are representative of those of us who had the good fortune of working in Alan’s laboratory and being a friend. It may sound corny, but he sought the truth. Alan was a person of the highest principles and he acted on them professionally and personally. He was incredibly strong willed and determined which, in combination with his basic intelligence, made him a great audience when he agreed with you and a worthy and stimulating adversary when he disagreed with you, which was often. We were equally stubborn in our hold on the truth. Our arguments were always impassioned and exhausted us both. They always ended with a smile or a laugh. Alan created an atmosphere in the lab that 1, and others, have tried to emulate. When you were with him, you received his undivided attention. He worked incredibly hard to bring out the best in each of us-he recognized each of our strengths and weaknesses and drew from the first to shore up the latter. He was generous in his praise and clear and direct when we displeased-you always knew where you stood-and you always stood, you were never put down. He filled the lab-he had a sense of himself and of us as his extended family. He was always in the lab observing techniques, developing paradigms, encouraging, and adjusting. It seemed that we were always eating and always talking about science or books or the Phillies or politics. Alan used to congratulate me on my own lab and students. He was so happy that David Olton and I were able to recreate at Hopkins the excitement that he knew with Stellar. It was a great source of joy for me that he took this pride-I once told him in this, as in many other things, he was the model-and he was. His reach extended beyond the lab and touched us deeply. He and I travelled together to Washington to participate in the first Pentagon March. You learn a lot about people under those circumstances. I learned about his deep hurt and outrage at a Government that betrayed his ideals in this terrible war. It all came to a head when we worked our way up to the Pentagon wall protected by soldiers with rifles and fixed bayonets. Just as we got there-and the crowd was peaceful-we heard the orders to fire tear gas. Alan and I ran clear of the conflagration and when we stopped, and I finished venting my anger at the scene, Alan simply said we as citizens have been violated by the Government and we did not speak again till we got to the bus. My last recollection was the day of his memorial service in Philadelphia of Alan’s family and friends gathering to pay an immediate tribute four days after his death. At least 500 people came-many spoke-they relived little and big incidents of his life as a father and grandfather, as an undergraduate, a teacher and colleague, but mainly as a friend: a complex man who filled a wonderful space. I felt then and I still do-it is hard to imagine life being the same withnl*+G-
References Blass, E. M., & Epstein, A. N. (1971). A lateral preoptic osrnosensitive zone for thirst in the rat. Journal of Comparative and Physiological Psychology, 76, 378-394. Epstein, A. N. (1991). Prospectus: Thirst and salt appetite. In E. M. Stricker (Ed.), Neurobioiogy of food andfluid intake (I@, (pp. 489-512). New York: Plenum.
EPSTEIN MEMORIAM
3 17
Epstein, A. N., Fitzsimons, J. T., & Simons, B. J. (1970). Drinking induced by injection of angiotensin into the brain of the rat. Journal of Physiology (London), 210, 457-475. Epstein, A. N., & Stellar, E. (1955). The control of salt preference in the adenalectomized rat. Journal of Comparative and Physiological Psychology, 48, 167-172. Epstein, A. N., & Teitelbaum, P. (1962). Regulation of food intake in the absence of taste, smell and other oropharyngeal sensations. Journal of Comparative and Physiological Psychology, 55, 753-795. Hainsworth, F. R., & Epstein, A. N. (1966). Severe impairment of heat-induced saliva-spreading in rats recovered from lateral hypothalamic lesions. Science, 153, 1255-1257. Hainsworth, F. R., Stricker, E. M., & Epstein, A. N. (1968). The water metabolism of the rat in the heat: Dehydration and drinking. American Journal of Physiology, 214, 983-989. Houpt, K. A., & Epstein, A. N. (1973). The ontogeny of the controls of food intake in the rat: GI fill and glucoprivation. American Journal of Physiology, 225, 58-66. Johnson, A. K., & Epstein, A. N. (1975). The cerebral ventricles as the avenue for the dipsogenic action of intracranial angiotensin. Brain Research, 86, 399-418. Kissileff, H. R., & Epstein, A. N. (1969). Exaggerated prandial drinking in the recovered lateral rat without saliva. Journal of Comparatiue and Physiological Psychology, 67, 301-308. Leshem, M., Boggan, B., & Epstein, A. N. (1988). The ontogeny of drinking evoked by activation of brain angiotensin in the rat pup. Developmental Psychobiology, 21(1), 63-75. Leshem, M., & Epstein, A. N. (1989). Ontogeny of renin-induced salt appetite in the rat pup. Developmental Psychobiology, 22(5), 437-445. Lora-Vilchis, M. C., Chambert, G., Rodriquez-Zendejas, A. M., Soto-Mora, L. M., Russek, M., & Epstein, A. N. (1988). Ontogeny of alpha and beta adrenergic anorexia in rats. American Journal of Physiology, 255, R908-R913. Misantone, L. J., Ellis, S. E., & Epstein, A. N. (1980). Development of angiotensin-induced drinking in the rat. Brain Research, 186, 195-202. Moe, K. E. (1986). The ontogeny of salt preference in rats. Developmental Psychobiology, 19, 185-196. Sakai, R. R., Frankmann, S. P., Fine, W. B., & Epstein, A. N . (1989). Prior episodes of sodium depletion increase the need-free sodium intake of the rat. Behauioral Neuroscience, 103(1), 186- 192. Simpson, J. B., Epstein, A. N., & Camardo, J. S. (1978). Localization of dipsogenic receptors for angiotensin in the subfornical organ. Journal of Comparative and Physiological Psychology, 92, 768-795. Snowdon, C. T., & Epstein, A. N. (1970). Oral and intragastric feeding in vagotomized rats. Journal of Comparative and Physiological Psychology, 71, 59-67. Teitelbaum, P., & Epstein, A. N. (1962). The lateral hypothalamic syndrome: Recovery of feeding and drinking following lesions in the lateral hypothalamus. Psychological Review, 69, 74-90. Wirth, J. R., & Epstein, A. N. (1976). The ontogeny of thirst in the infant rat. American Journal of Physiology, 230, 188-198.
ELLIOTT M. BLASS Psychology and Nutritional Sciences Cornell University Ithaca, N Y
Alan Epstein was taken from us suddenly and well before his time when he was struck by a bus in Cancun, Mexico, just before attending the winter Developmental Psychobiology meetings. He is survived by his wife, Fifi, his three children, Lise, Mark, and Ruth, two grandchildren, Philip and Rachel, and scores of colleagues, friends, and present and former students. We all profoundly feel his loss and miss him deeply. Alan’s contributions to the fields of biological psychology, neurosciences, ingestive behavior, and development were singular. With James Sprague and later Adrian Morrison, he edited Progress in Psychobiology and Physiological Psychology (P4), an enormously influential series of monographs that spanned the Reprint requests should be sent to Dr. E. M. Blass; Psychology and Nutritional Sciences, 220 Uris Hall, Cornell University, Ithaca, NY 14853-7601, U.S.A. Received for publication 21 April 1992 Accepted at Wiley 15 May 1992
Developmental Psychobiology 25(5):313-3 17 (1992) 0 1992 by John Wiley & Sons, Inc.
CCC 0012-1630/92/050313-05$04.00
314
BLASS
entire domain of biopsychology from visual psychophysics to activity, nutrition, and growth, to catecholamines and recovery of function. As an editor, Alan was without peer-he got the best out of his contributors, sharpened their ideas, and improved their communication. His background as editor of the undergraduate Hopkins newspaper, The Newsletter, stood him in good stead for his adult task. He edited two chapters that I wrote-one for P4 with Ted Hall and Marty Teicher and one for an AAAS symposium on thirst. In both instances, he was a delight to work with, serious-but with humor and grace. As always, I learned a lot from him and this helped me enormously in editing Volumes 8 and 9 of the Handbook of Behavioral Neurobiology. His editing alone would have made him an important player in the field of Behavioral Neurosciences. In fact, it was the most modest of his contributions. His two major professional legacies were as a bench scientist and as a teacher and mentor. As a scientist, Alan had a “green thumb.” He had the great talent of being able to articulate an empirical question and devise a technique-always simple and accessible-to provide an answer. His medical training at Hopkins provided a keen awareness for symptoms that travelled together, their recovery, and residual deficits. His clinical eye recognized this as a syndrome so that I I years after Anand and Brobeck wrote of a profound aphagia in rats with lateral hypothalamic lesions, Teitelbaum and Epstein (1962) documented the Lateral Hypothalamic Syndrome. This was a remarkably important breakthrough for Psychobiology because it emphasized in a systematic and evaluative way a cluster of profound deficits and the recovery of complex motivational acts. More than that, however, the precise documentation of recovery has provided a frame of reference for the succeeding rounds of analyses on hypothalamic function and its disruption by neurochemical lesions. It was the recognition of a syndrome that provided a clear target against which deficits caused by other means and in other locations in the basal forebrain could be evaluated. In parallel with the central analysis, Alan started a decade-long project on the control of food and water intake in the absence of olfactory or gustatory stimulation. Alan devised a rat-sized version of the nasogastric tube that he well knew from rounds in internal medicine. Certain diagnostic procedures required threading a tube through the naso-pharynx into the esophagus. In a powerful series of studies, Epstein with Teitelbaum and later Snowdon demonstrated that long-term homeostasis could be sustained in neurologically intact rats chronically self feeding through the nasogastric tube in the absence of olfactory and gustatory stimulation. Body weight was defended, caloric density and dilution was compensated for, as were preloads of different density. The role of the vagus in control of gastric emptying and its relation to ingestion was established. Alan’s laboratory was multifaceted and busy. One difficulty experienced by rats with lateral hypothalamic lesions was salivary insufficiency and this led to analyses, with Kissileff, into the contribution of saliva as a lubricant for feeding and with Hainsworth and Stricker on the use of saliva in a thermoregulatory capacity. This last series of studies is a major and meticulous analysis of behaviorphysiology synergism in the rat’s defense of core temperature against heat stress that has not received the attention that it deserves. I arrived in Alan’s lab in 1969, at a very felicitous moment because Alan’s attention was turning again to stimulating the brain directly with substances that the brain naturally receives. He had earlier devised a simple and inexpensive
EPSTEIN MEMORIAM
315
cannula that could be implanted into the brain and kept patent for the animal’s lifetime. He and I provided evidence for thirst osmoreceptors in the preoptic area. The really influential studies, however, came from his collaboration with James Fitzsimons and Barbara Simons (Rolls) who demonstrated that picogram injections of angiotension decapeptide (AII) into the brain would cause copious drinking. This was advanced by Johnson and Epstein’s demonstration that A11 had to gain access to the ventricular space-that the A11 receptors were not on the brain-side of the ventricles but on the ventricular side. Shortly thereafter, Simpson and Epstein demonstrated that A11 injections into the subfornical organ (SFO) that resides in the ventricular space caused drinking. Preventing ventricular flow into the SFO eliminated drinking to intraventicular A11 injection. The developmental studies with which many of the members of this Society are familiar have had a long history. Alan’s first report in 1970’onthe vital role of saliva in suckling demonstrated that saliva formed a sealant on the nipple to provide the suction necessary for the infant to hold the nipple and exert negative pressure for milk withdrawal to occur. Alan’s developmental interests remained active. In 1976, Wirth and Epstein, for the first time, demonstrated the newborn’s ability to behaviorally adjust to dehydration by drinking from a continuous flow. This study set the stage for Hall’s analyses of independent ingestion. There was a lively interest in suckling determinants as well. Houpt and Epstein provided evidence for gastric control over intake and a more detailed analysis by Lorenz Ellis and Epstein in 1982 made a stronger case for upper GI fill as a determinant of intake, but not nipple attachment (Alan and I disagreed on that one-but more on that later). Epstein was interested in the time course of development of hydrational controls as reflected in his studies on angiotension induced drinking (Misantone, Ellis & Epstein; Leshem & Epstein) on alpha- and beta-adrenergic anorexia, and on dehydration induced anorexia (Leshem & Epstein, 1988). As part of his professional lifetime dedication to mechanisms of salt appetite, which I will discuss directly, Alan also studied its ontogeny. Karen Moe demonstrated a protracted tolerance to and preference for very concentrated NaCl solutions until 10 days of age. This striking finding when better understood will provide insights into sodium balance, gustation, and their integration in homeostatis and motivation. And there was the remarkable demonstration by Sakai, Frankmann, Fine, & Epstein on the potentiating effect of prior salt depletion and repletion in later salt ingestion in need-free rats. This was an enormous phenomenon and Alan saw its potential. But his first love was salt appetite. It was the intellectual subject of his imprinting. When an undergraduate with Eliot Stellar at Hopkins, Alan and Eliot published an important article in The Journal of Comparative and Physiological Psychology on “The Control of Salt Preference in the Adrenalectomized Rat.” His interest in this issue gained new momentum with the discovery that angiotension provoked a salt appetite independent of and in addition to one for water. These findings unleashed a sustained attack on the hormonal determinants of sodium appetite, with an important progress report from his laboratory and the international efforts supported by the McCarther Foundation just recently appearing in Volume 10 of the Handbook of Behavioral Neurobiology, edited by Ed Stricker. Thus, we have all suffered the loss of a preeminent behavioral neuroscientistneuroendocrinologist. His work was always characterized by its meticulousness and thoroughness. He attacked the big issues and his findings have been so solid
316
BLASS
and important and stated with such clarity that others have been able to build upon them. His enthusiasm for science and his generosity as a colleague were infectious and often galvanized scientific enterprises that lay dormant. My own recollections, I think, are representative of those of us who had the good fortune of working in Alan’s laboratory and being a friend. It may sound corny, but he sought the truth. Alan was a person of the highest principles and he acted on them professionally and personally. He was incredibly strong willed and determined which, in combination with his basic intelligence, made him a great audience when he agreed with you and a worthy and stimulating adversary when he disagreed with you, which was often. We were equally stubborn in our hold on the truth. Our arguments were always impassioned and exhausted us both. They always ended with a smile or a laugh. Alan created an atmosphere in the lab that 1, and others, have tried to emulate. When you were with him, you received his undivided attention. He worked incredibly hard to bring out the best in each of us-he recognized each of our strengths and weaknesses and drew from the first to shore up the latter. He was generous in his praise and clear and direct when we displeased-you always knew where you stood-and you always stood, you were never put down. He filled the lab-he had a sense of himself and of us as his extended family. He was always in the lab observing techniques, developing paradigms, encouraging, and adjusting. It seemed that we were always eating and always talking about science or books or the Phillies or politics. Alan used to congratulate me on my own lab and students. He was so happy that David Olton and I were able to recreate at Hopkins the excitement that he knew with Stellar. It was a great source of joy for me that he took this pride-I once told him in this, as in many other things, he was the model-and he was. His reach extended beyond the lab and touched us deeply. He and I travelled together to Washington to participate in the first Pentagon March. You learn a lot about people under those circumstances. I learned about his deep hurt and outrage at a Government that betrayed his ideals in this terrible war. It all came to a head when we worked our way up to the Pentagon wall protected by soldiers with rifles and fixed bayonets. Just as we got there-and the crowd was peaceful-we heard the orders to fire tear gas. Alan and I ran clear of the conflagration and when we stopped, and I finished venting my anger at the scene, Alan simply said we as citizens have been violated by the Government and we did not speak again till we got to the bus. My last recollection was the day of his memorial service in Philadelphia of Alan’s family and friends gathering to pay an immediate tribute four days after his death. At least 500 people came-many spoke-they relived little and big incidents of his life as a father and grandfather, as an undergraduate, a teacher and colleague, but mainly as a friend: a complex man who filled a wonderful space. I felt then and I still do-it is hard to imagine life being the same withnl*+G-
References Blass, E. M., & Epstein, A. N. (1971). A lateral preoptic osrnosensitive zone for thirst in the rat. Journal of Comparative and Physiological Psychology, 76, 378-394. Epstein, A. N. (1991). Prospectus: Thirst and salt appetite. In E. M. Stricker (Ed.), Neurobioiogy of food andfluid intake (I@, (pp. 489-512). New York: Plenum.
EPSTEIN MEMORIAM
3 17
Epstein, A. N., Fitzsimons, J. T., & Simons, B. J. (1970). Drinking induced by injection of angiotensin into the brain of the rat. Journal of Physiology (London), 210, 457-475. Epstein, A. N., & Stellar, E. (1955). The control of salt preference in the adenalectomized rat. Journal of Comparative and Physiological Psychology, 48, 167-172. Epstein, A. N., & Teitelbaum, P. (1962). Regulation of food intake in the absence of taste, smell and other oropharyngeal sensations. Journal of Comparative and Physiological Psychology, 55, 753-795. Hainsworth, F. R., & Epstein, A. N. (1966). Severe impairment of heat-induced saliva-spreading in rats recovered from lateral hypothalamic lesions. Science, 153, 1255-1257. Hainsworth, F. R., Stricker, E. M., & Epstein, A. N. (1968). The water metabolism of the rat in the heat: Dehydration and drinking. American Journal of Physiology, 214, 983-989. Houpt, K. A., & Epstein, A. N. (1973). The ontogeny of the controls of food intake in the rat: GI fill and glucoprivation. American Journal of Physiology, 225, 58-66. Johnson, A. K., & Epstein, A. N. (1975). The cerebral ventricles as the avenue for the dipsogenic action of intracranial angiotensin. Brain Research, 86, 399-418. Kissileff, H. R., & Epstein, A. N. (1969). Exaggerated prandial drinking in the recovered lateral rat without saliva. Journal of Comparatiue and Physiological Psychology, 67, 301-308. Leshem, M., Boggan, B., & Epstein, A. N. (1988). The ontogeny of drinking evoked by activation of brain angiotensin in the rat pup. Developmental Psychobiology, 21(1), 63-75. Leshem, M., & Epstein, A. N. (1989). Ontogeny of renin-induced salt appetite in the rat pup. Developmental Psychobiology, 22(5), 437-445. Lora-Vilchis, M. C., Chambert, G., Rodriquez-Zendejas, A. M., Soto-Mora, L. M., Russek, M., & Epstein, A. N. (1988). Ontogeny of alpha and beta adrenergic anorexia in rats. American Journal of Physiology, 255, R908-R913. Misantone, L. J., Ellis, S. E., & Epstein, A. N. (1980). Development of angiotensin-induced drinking in the rat. Brain Research, 186, 195-202. Moe, K. E. (1986). The ontogeny of salt preference in rats. Developmental Psychobiology, 19, 185-196. Sakai, R. R., Frankmann, S. P., Fine, W. B., & Epstein, A. N . (1989). Prior episodes of sodium depletion increase the need-free sodium intake of the rat. Behauioral Neuroscience, 103(1), 186- 192. Simpson, J. B., Epstein, A. N., & Camardo, J. S. (1978). Localization of dipsogenic receptors for angiotensin in the subfornical organ. Journal of Comparative and Physiological Psychology, 92, 768-795. Snowdon, C. T., & Epstein, A. N. (1970). Oral and intragastric feeding in vagotomized rats. Journal of Comparative and Physiological Psychology, 71, 59-67. Teitelbaum, P., & Epstein, A. N. (1962). The lateral hypothalamic syndrome: Recovery of feeding and drinking following lesions in the lateral hypothalamus. Psychological Review, 69, 74-90. Wirth, J. R., & Epstein, A. N. (1976). The ontogeny of thirst in the infant rat. American Journal of Physiology, 230, 188-198.
ELLIOTT M. BLASS Psychology and Nutritional Sciences Cornell University Ithaca, N Y
