Aphagia, gastric pathology, hyperthermia, and sensorimotor dysfunctions following lateral hypothalamic lesions: Effects of insulin pretreatments

Further studies on salt appetite following lateral hypothalamic lesions: Effects of preoperative alimentary experiences.

“…Requests for reprints should be sent to Jay Schulkin, Department of Anatomy, University of Pennsylvania, Philadelphia, Pennsylvania 19104. perience of thirst or hunger protected most effectively against the postoperative adipsia or aphagia, respectively, and to a lesser extent against the sensorimotor deficits that follow LH lesions (Grijalva, 1980;Schallert, 1982). Thus the protection seems to be specific to the preoperative treatment.…”

“…In addition, if they are given preoperative thirst-inducing treatments, the adipsia is diminished (Schallert, 1982). The evidence further suggests that the preoperative experience of thirst or hunger protected most effectively against the postoperative adipsia or aphagia, respectively, and to a lesser extent against the sensorimotor deficits that follow LH lesions (Grijalva, 1980; Schallert, 1982). Thus the protection seems to be specific to the preoperative treatment.…”

“…The rats of the insulin-induced-hunger group, 6 days prior to receiving lesions, were injected twice a day with 0.2 ml of 3 U of insulin (protamine zinc). This procedure is known to ameliorate the gastric pathology and aphagia that results from LH lesions (Grijalva, 1980), Part 1C: Limitations of protective effect. Thirty rats were used: 18 lesion and 12 intact controls.…”

Infusion of neurotoxic doses of N-methyl-D-aspartate into the lateral hypothalamus in rats produces stomach erosions, hyperthermia, and a disruption in eating behavior.

“…The lateral hypothalamus (LH) comprises a large and diffuse area in the diencephalon that has been shown to be involved in ingestion, digestion, autonomic regulation, and general metabolic responses, as well as in sensory and motor functions (see Bernardis & Bellinger, 1993; Grijalva, Lindholm, & Roland, 1989; Grijalva & Novin, 1990). For example, experimental lesions of the LH are associated with drinking and feeding deficits and body weight reduction (Anand & Brobeck, 1951; Teitelbaum & Epstein, 1962), homeostatic disturbances involving olfaction (Scott & Leonard, 1971), salivation (Epstein, 1971; Schallert, Leach, & Braun, 1978), gastrointestinal properties (Grijalva, Lindholm, Schallert, & Bicknell, 1976; Lindholm, Shumway, Grijalva, Schallert, & Ruppel, 1975) and temperature regulation (Corbett, Wilterdink, & Keesey, 1985; DeRyck & Teitelbaum, 1978; Harrell, de Castro, & Balagura, 1975; Grijalva, 1980; Grijalva & Lindholm, 1980; Lennie, Hirvonen, McCarthy, & Keesey, 1995; Monda, Amaro, Sullo, & De Luca, 1996; Refinetti & Carlisle, 1987), as well as motor, sensorimotor, and activational deficits (Baillie & Morrison, 1963; Levitt & Teitelbaum, 1975; Marshall & Teitelbaum, 1974; Balagura, Wilcox, & Coscina, 1969).…”