Role of the lateral hypothalamus in submandibular salivary secretion during feeding in rats.

To evaluate the role of the lateral hypothalamic area (LH) in the masticatory-salivary reflex, we investigated submandibular salivary secretion and the electromyographic (EMG) activity of the jaw-closer masseter muscle in sham-operated rats and rats with unilateral LH lesions. One week prior to surgery and recording, the rats were given daily experience of eating pellets; powder; or hard, medium or soft mash, all of which were composed of laboratory chow. Salivary secretion was induced during eating and grooming behavior. During eating, the powdered food induced the highest salivary flow rate, and the soft (wet) mash induced the lowest salivary flow rate. Conversely, the amount of food consumed (dry weight) was greatest when soft mash was provided and lowest when the powder or pellets (a dry diet) were provided. The EMG activity of the masseter muscle during eating was greatest during consumption of the pellets and weakest during consumption of the powder. LH lesions that were ipsilateral to the examined submandibular gland reduced salivary secretion to about 20-30% of the control value, whereas contralateral LH lesions reduced it to about 40-50% of the control value. Neither masseter muscle EMG activity nor food consumption was markedly affected by the presence of an LH lesion. These results suggest that the texture of food, especially its water content, affects the flow rate of saliva and that the LH is heavily involved in the masticatory-salivary reflex.

Neurochemical and behavioral analyses of the lateral hypothalamic syndrome: a look back.

Philip Teitelbaum is one of the great physiological psychologists of his generation. His early research clarified key issues regarding the effects of electrolytic lesions of the ventromedial or ventrolateral hypothalamus on food intake in rats, a subject of paramount interest during the 1950s and 1960s. Perhaps best known were his extensive studies of the lateral hypothalamic syndrome in rats, which focused on the complex and changing array of symptoms after experimental brain damage. It soon became clear from later work that his research interests were not in the brain's control of food intake but in the effects of lesions to fragment behavior and thereby allow investigators to view its components. He was the foremost proponent of the use of exquisite behavioral analysis to reveal details in movement that allowed insights into brain function, and that approach - old fashioned physiological psychology made modern and at its finest - has infiltrated the entire field of experimental psychology, including studies of ingestive behavior, even while the new field of behavioral neuroscience emerged. He extended his analytic approach to neurological issues such as autism in humans, a promising arena that fully occupied his attention during the later phases of his career. But his influence on his scientific colleagues went well beyond his careful and powerful thinking; his articles and books have been models of clarity and concision. I write in behalf of a grateful field to salute his many great contributions.

The natriuretic effect of oxytocin blocks medial tuberomammillary polydipsia and polyuria in male rats.

Lesions of the tuberomammillary complex, a neuroanatomical system closely related to the hypothalamic supraoptic and paraventricular nuclei, induce strong polydipsia in male rats. It was recently demonstrated that this increase in water intake is immediate, persistent, follows circadian rhythms and appears to be related to sodium regulation. The present study found that urine osmolality was significantly lower in tuberomammillary-lesioned animals vs. their respective controls at 8:00 h after surgery. Therefore, the aim of the present study was to examine the natriuretic effect of intraperitoneal oxytocin (OT) administration on medial ventral tuberomammillary nucleus (E3) polydipsia and polyuria of lesioned and control male rats. At 24:00 h post-lesion, OT blocked the hyperdipsic and polyuric responses of E3-lesioned animals but not those of non-lesioned controls, which did however significantly increase their water intake. Moreover, urinary osmolality and sodium excretion increased in E3 -lesioned animals that received OT but not in lesioned controls receiving physiological saline (992 +/- 187.19 vs. 215.83 +/- 23.39 mOsm/kg; 1.68 +/- 0.13 vs. 0.47 +/- 0.1 mEq/L). At 48:00 h post-lesion, OT administration also induced a higher intake of water and of simultaneously offered hypertonic NaCl (1.5%) in E3-lesioned animals. These results are interpreted in terms of the hypothalamic systems involved in sodium and water homeostasis.

Lesions of the lateral hypothalamus impair pilocarpine-induced salivation in rats.

In the present study we investigated the effects of electrolytic lesions of the lateral hypothalamus (LH) in the salivation induced by intracerebroventricular (i.c.v.) or intraperitoneal (i.p.) injection of the cholinergic agonist pilocarpine. Rats with sham or LH lesions and stainless steel cannulas implanted into the lateral ventricle (LV) were used. In rats anesthetized with urethane (1.25mg/kg of body weight) saliva was collected using pre-weighed cotton balls inserted in the animal mouth during a period of 7 min following i.c.v. or i.p. injection of pilocarpine. Injection of pilocarpine (1mg/kg of body weight) i.p. in sham-operated rats (6h, 2, 7, and 15 days after the surgery) induced salivation (497+/-24, 452+/-26, 476+/-30, and 560+/-75 mg/7 min, respectively). The effects of i.p. pilocarpine was reduced 6h, 2 and 7 days after LH lesions (162+/-37, 190+/-32, and 229+/-27 mg/7 min, respectively), not 15 days after LH lesions (416+/-89 mg/7 min). Injection of pilocarpine (120 micro g/micro l) i.c.v., in sham-operated rats (6h, 2, 7, and 15 days after the surgery) also produced salivation (473+/-20, 382+/-16, 396+/-14, and 427+/-47 mg/7 min, respectively). The salivation induced by i.c.v. pilocarpine was also reduced 6h, 2 and 7 days after LH lesions (243+/-19, 278+/-24, and 295+/-27 mg/7 min, respectively), not 15 days after LH lesions (385+/-48 mg/7 min). The present results show the participation of the LH in the salivation induced by central or peripheral injection of pilocarpine in rats, reinforcing the involvement of central mechanisms on pilocarpine-induced salivation.

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 present study examined whether damage to intrinsic lateral hypothalamic (LH) neurons induced by microinfusions of N-methyl-D-aspartate (NMDA) would produce effects similar to those seen after electrolytic LH lesions. In Experiment 1, rats receiving electrolytic (1.2 mA anodal current, 10 s) LH lesions displayed motor impairments, whereas those receiving NMDA (20 microg/microl) infusions did not. Both electrolytic lesions and NMDA infusions were associated with eating deficits, hyperthermia, and gastric erosion formation 24 hr after surgery. In Experiment 2, either 20 microg/microl or 10 microg/microl NMDA destroyed LH cells and produced dose-dependent gastric mucosal erosions as well as similar increases in body temperature. These results indicate that an alteration in the acute activity of intrinsic LH neurons plays a role in the production of gastric mucosal injury and hyperthermia and lend support to other studies implicating a role of LH neurons in eating behavior.

Daily pattern of EEG activity in rats with lateral hypothalamic lesions.

The experiment was aimed to further elucidate the phenomenon of sleep suppression observed earlier after electrolytic lesions of the lateral hypothalamus (LH). In male Wister rats the amounts of waking (W), slow wave sleep (SWS) and paradoxical sleep (PS) were counted in 1 h samples of EEG taken from the light and dark parts of the circadian cycle, as well as in the whole 12 h diurnal records before lesioning and after electrolytic or sham lesions of LH. Significant increase of W with a simultaneous reduction of SWS and PS was found in 1h and 12h diurnal records; no effect of the lesion on nocturnal EEG was observed. The results suggest that lesion-induced sleep suppression concerns the light part of the day when rats are naturally less active, and that 1h samples of diurnal EEG may be sufficient to diagnose LH insomnia. No correlation was found between the magnitude of waking-sleep disturbances and the intensity of ingestive impairments (aphagia, adipsia, body weight loss) evoked by LH lesions which suggests that LH insomnia may be a result of disruption of a mechanism directly involved in the regulation of waking-sleep cycle rather than a secondary effect of other lesion-induced impairments.