Effects of osmotic pressure, glucose, and temperature on neurons in preoptic tissue slices

Silva, N. L.; Boulant, Jack A.

doi:10.1152/ajpregu.1984.247.2.r335

Cited by 66 publications

(53 citation statements)

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“…In another study, the effects of low (1 mM) glucose and hyperosmotic (4.5 mM NaCI or 9 mM mannitol) media were observed on firing rates and thermosensitivities of PO neurons in vitro. These perfusions affected onethird of the temperature-insensitive neurons and nearly half of the thermosensitive neurons, generally exciting warm-sensitive neurons and inhibiting cold-sensitive neurons [61].…”

Section: Effects Of Chemicals On Thermosensitive Neuronsmentioning

confidence: 98%

Thermosensitive neurons in the brain.

Nakayama

1985

Jpn.J.Physiol

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Experimental methods commonly used in brain research, such as transection, ablation, focal lesion, and stimulation of the higher nervous structures have disclosed not only hypothalamic control of body temperature but also temperature sensitivity of the hypothalamus per se. Several classical studies clearly demonstrated that local warming or cooling of the hypothalamus produced appropriate thermoregulatory responses. The existence of thermosensitive neurons in the preoptic and anterior hypothalamic area (POAH) was first reported in the early 1960s [44,45], paving the way for neurophysiological studies on thermoregulation.A neuron that increases its steady discharge frequency at higher or lower local temperature is called a warm-sensitive or cold-sensitive neuron, respectively. The former type is encountered more frequently during microelectrode exploration. POAH thermosensitive neurons have been found not only in mammals, but also in birds, reptiles, and fish. More recent studies have revealed a wide distribution of thermosensitive neurons in the nervous system, including the midbrain, medulla oblongata, and spinal cord.Almost all cell activities in living organisms are, of course, more or less temperature dependent. At least two tests are required to distinguish whether a particular thermosensitive neuron is involved in temperature regulation. One is whether thermal stimulation of the region containing the particular neuron evokes appropriate thermoregulatory responses. From this point of view, the midbrain is the only exception among the areas mentioned above. Another point to be examined is whether a particular neuron is specifically sensitive to local temperature. Various criteria have been proposed to classify neurons into thermosensitive and non-thermosensitive types. Neurons having thermosensitivity of at least 0.8 imp/sec °C are considered warm-sensitive and those with at least -0.6 are considered cold-sensitive [5]. Furthermore, in a brain with complex neural networks, deciding whether a neuron is a true thermoreceptor or a thermosensitive interneuron is difficult even if the neuron shows a relatively high Q1° value. These difficulties led investigators undertake in vitro studies on neuronal thermosensitivity that clearly demonstrated the presence of true thermally sensitive neurons

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Section: Effects Of Chemicals On Thermosensitive Neuronsmentioning

confidence: 98%

Thermosensitive neurons in the brain.

Nakayama

1985

Jpn.J.Physiol

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“…Subsets of thermosensitive neurons in MPO and MnPO responded to changes in osmolality as well as temperature (69,81). However, these studies were not performed under conditions of synaptic blockade, and thus, did not establish whether the MnPO and/or MPO neurons were inherently osmo-or temperature sensitive.…”

Section: Sites For Integration Of Temperature and Fluid Homeostasismentioning

confidence: 99%

Integration of thermal and osmotic regulation of water homeostasis: the role of TRPV channels

Sladek

Johnson

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Sladek CD, Johnson AK. Integration of thermal and osmotic regulation of water homeostasis: the role of TRPV channels. Am J Physiol Regul Integr Comp Physiol 305: R669 -R678, 2013. First published July 24, 2013 doi:10.1152/ajpregu.00270.2013.-Maintenance of body water homeostasis is critical for preventing hyperthermia, because evaporative cooling is the most efficient means of dissipating excess body heat. Water homeostasis is achieved by regulation of water intake and water loss by the kidneys. The former is achieved by sensations of thirst that motivate water acquisition, whereas the latter is regulated by the antidiuretic action of vasopressin. Vasopressin secretion and thirst are stimulated by increases in the osmolality of the extracellular fluid as well as decreases in blood pressure and/or blood volume, signals that are precipitated by water depletion associated with the excess evaporative water loss required to prevent hyperthermia. In addition, they are stimulated by increases in body temperature. The sites and molecular mechanisms involved in integrating thermal and osmotic regulation of thirst and vasopressin secretion are reviewed here with a focus on the role of the thermal and mechanosensitive transient receptor potential-vanilloid (TRPV) family of ion channels. thirst; TRPV; vasopressin; hypothalamus MAINTENANCE of a constant body temperature by homeotherms is critically dependent on body water homeostasis, because evaporative cooling is the most efficient means that homeotherms have for dissipating excess body heat. Even at rest, heat is generated as a by-product of basal cellular metabolism and the ongoing muscle activity of the heart beating, respiration, and gastrointestinal motility. For a typical 70-kg man the resting (basal) rate of metabolic heat production is about 80 kcal/h, but intense exercise can increase heat production to 400 -600 kcal/h. Thus the body must have efficient mechanisms for dissipating heat to prevent hyperthermia. In humans, body heat is dissipated by passive transfer of heat from the skin to the air. The heat generated by muscles and internal organs is transferred to the skin by the blood flowing through epidermal capillaries. Thus heat loss can be increased by increasing skin blood flow and by increasing the movement of air next to the skin by removing clothing and standing near a fan or in a breeze. However, evaporative cooling significantly augments heat loss from the skin, because evaporation of 1 gram of water from the skin dissipates 0.6 kcal. Thus a sweat rate of 1 l/h could theoretically remove 600 kcal/h from the body. Furcovered mammals also rely heavily on evaporative cooling for maintaining body temperature with increased body temperature promoting panting, increased salivation, and saliva spreading in dogs, cats, and rats. However, water loss of the magnitude required in many instances to adequately dissipate excess body heat must be compensated to prevent electrolyte imbalance and preserve blood volume for adequate cardiovascular function. Thus mechanis...

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“…WSN are typically investigated for their role in regulating fever or response to peripheral and local changes in temperature. However, electrophysiological studies and molecular characterization demonstrated that these specialized cells also respond to nutrient signals (2,(6)(7)(8)(9)(10). Nutrient homeostasis is likewise regulated centrally and primarily in the hypothalamus (11).…”

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confidence: 99%

Insulin-like growth factor 1 receptor regulates hypothermia during calorie restriction

Cintrón-Colón

Sanchez‐Alavez

Nguyen

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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When food resources are scarce, endothermic animals can lower core body temperature (T b ). This phenomenon is believed to be part of an adaptive mechanism that may have evolved to conserve energy until more food becomes available. Here, we found in the mouse that the insulin-like growth factor 1 receptor (IGF-1R) controls this response in the central nervous system. Pharmacological or genetic inhibition of IGF-1R enhanced the reduction of temperature and of energy expenditure during calorie restriction. Full blockade of IGF-1R affected female and male mice similarly. In contrast, genetic IGF-1R dosage was effective only in females, where it also induced transient and estrusspecific hypothermia in animals fed ad libitum. These effects were regulated in the brain, as only central, not peripheral, pharmacological activation of IGF-1R prevented hypothermia during calorie restriction. Targeted IGF-1R knockout selectively in forebrain neurons revealed that IGF signaling also modulates calorie restriction-dependent T b regulation in regions rostral of the canonical hypothalamic nuclei involved in controlling body temperature. In aggregate, these data identify central IGF-1R as a mediator of the integration of nutrient and temperature homeostasis. They also show that calorie restriction, IGF-1R signaling, and body temperature, three of the main regulators of metabolism, aging, and longevity, are components of the same pathway.IGF-1R | temperature | calorie restriction | energy homeostasis | aging

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Effects of osmotic pressure, glucose, and temperature on neurons in preoptic tissue slices

Cited by 66 publications

References 0 publications

Thermosensitive neurons in the brain.

Thermosensitive neurons in the brain.

Integration of thermal and osmotic regulation of water homeostasis: the role of TRPV channels

Insulin-like growth factor 1 receptor regulates hypothermia during calorie restriction

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