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The Anatomy and Physiology of Normal Thermoregulation
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
EP is degradated by the liver and kidney and excreted by the kidneys.30 It can be assumed from these data that EP gains entry into the circulation from its site of production, produces its primary effect in the CNS, and is rapidly metabolized and excreted by the kidney, thus only a small portion of the original EP reaches the CNS. The amount of EP in the circulation which is necessary to produce fever is still unknown. It was clearly shown that the preoptic anterior hypothalamus is extremely sensitive to microinjections of EP in several species, causing a rapid increase in rectal temperature associated with vasoconstriction and decreasing peripheral blood flow. The observations suggesting extreme susceptibility of the pre-optic area to EP are supported by reports that identical injections in other sites of the CNS such as lateral and posterior hypothalamus, midbrain, pons, cerebellum, or cerebral cortex failed to cause fever.31-34 Further proof comes from intraneuronal recording from the anterior hypothalamus, showing increased neuronal firing rate in response to proximate injections of EP.35 The posterior hypothalamus which plays a major role in maintaining homothermy does not respond to injections of EP.
The Internal Milieu Brain and Body
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
The critical temperature set point is in the hypothalamus, which balances heat loss and production. Local warming or cooling of thermosensitive neurons in the hypothalamus and spinal regions triggers panting, autonomic responses, and shivering. Thermosensitive neurons in the preoptic nucleus of the anterior hypothalamus respond to warming by initiating sweating and vasodilation. Trauma results in interference with heat-dissipating mechanisms and thus creates hyperthermia. Thermal information is conveyed to the posterior hypothalamus’s effectors for heat generation and dissipation. The hypothalamus generates the circadian rhythm of temperature regulation: a one-to-two-point degree difference in temperature between the 6 AM low point and the 6 PM high point. Damage to the posterior hypothalamus and mesencephalon usually causes hypothermia or poikilothermia (body temperature varies with the ambient temperature). In addition, thermoreceptors of the skin, viscera, and spinal cord provide input to the preoptic anterior hypothalamus to maintain temperature balance (Jacobson & Abrams, 1999).
Histamine as Neurotransmitter
Published in Divya Vohora, The Third Histamine Receptor, 2008
Oliver Selbach, Helmut L. Haas
Histamine is stored in neuronal somata and axon varicosities [23–25], where it is carried into vesicles by exchange of two protons through the vesicular monoamine transporter (VMAT)-2 (Figure 3.1) and released on arrival of action potentials [26]. The level of histamine in brain tissue is to some extent lower than that of other biogenic amines, but its turnover is considerably faster (in the order of minutes) and varies with functional state [27,28]. Brain histamine levels exhibit profound circadian rhythms in accordance with the firing of histamine neurons during waking [29]. Histamine levels in the preoptic/anterior hypothalamus follow the sleep stages: wakefulness > non-rapid eye movement (REM) sleep > REM sleep [30]. A direct correlation between histamine levels in the hypothalamus and behavioral state was determined by electroencephalography [31]. Synthesis and the release of histamine are controlled by H3-autoreceptor-mediated feedback [15,32,33]. The release of histamine is also modulated by transmitters affecting histamine neuron firing and release from varicosities bearing inhibitory M1-muscarinic, α2-adrenergic, and peptidergic receptors [31,34–36].
Brain temperature and its role in physiology and pathophysiology: Lessons from 20 years of thermorecording
Published in Temperature, 2019
Classic views on regulation of body temperature consider temperature-sensitive neurons located in the preoptic/anterior hypothalamus as primary central temperature sensors [133–135]. However, cells in many other structures also exhibit a high degree of temperature sensitivity, which is often similar or greater than that in hypothalamic neurons. For example, 22% of medial thalamic neurons have a positive thermal coefficient >0.8 imp/s/°C [136], exceeding the number of temperature-sensitive cells in the anterior (8%) and posterior (11.5%) hypothalamus. In the superchiasmatic nucleus, ~18% of neurons are warm-sensitive [137], while >70% decrease their activity rate with cooling below physiological baseline (37–25°C) [138]. Finally, high temperature sensitivity was found in electrophysiologically identified substantia nigra DA neurons in vitro [139]. Within the physiological range (35–39°C), their discharge rate increases with warming (Q10 = 3.7) and dramatically decreases (Q10 = 8.5) with cooling below this range (34–29°C). This latter finding questions the validity of basal electrophysiological properties and responses of DA neurons studied in vitro at low, non-physiological temperatures. When studied in awake, freely moving conditions, this neuronal population is much more heterogeneous with multiple subgroups that are not apparent in assessments made in brain slices and anesthetized animal preparations [73].
Influence of temperature on cerebellar metabolite levels
Published in International Journal of Hyperthermia, 2018
Although the cerebellum is extremely sensitive to heat-induced changes [6], this study showed that seasonal temperature does not influence cerebellar metabolite levels. Seasonal temperature changes may not affect the brain temperature. Body temperature regulation is a fundamental homeostatic function that involves numerous involuntary effector responses and is governed by the preoptic anterior hypothalamus [9,10]. An increased warm signal input may activate heat loss effectors, while an increased cold signal input may increase heat production [11].
Use of the heat tolerance test to assess recovery from exertional heat stroke
Published in Temperature, 2019
Katherine M. Mitchell, Samuel N. Cheuvront, Michelle A. King, Thomas A. Mayer, Lisa R. Leon, Robert W. Kenefick
Although the exact mechanism for EHS is unknown, several possible mechanisms, or a combination of mechanisms, are hypothesized to be responsible for the uncontrolled increase in body temperature and subsequent organ damage that occurs (Figure 2). Direct thermal injury to the cell is one potential pathway that can lead to the adverse sequelae and multi-organ dysfunction seen in EHS. It is clear that prolonged excessive elevations in body temperature result in direct thermal injury to tissues, as cells begin to degrade and proteins unfold around 42°C [19,20]. However, it has been established that a core temperature of up to 41.9°C can be well tolerated in exercising individuals with little or no adverse sequela [21]. It should also be noted that while the most direct estimate of tissue temperature in human EHS victims is currently body core temperature, this may not be an exact measure of the specific tissue temperature. A second pathway proposes that ischemia reperfusion is concurrently responsible for cell damage and the subsequent inflammatory response. The prevailing theory surmises that prolonged intestinal ischemia due to the redirection of blood flow to the skin and exercising skeletal muscle causes a breakdown of the gut membrane that increases permeability and allows endotoxin and other bacterial products to leak into the circulation to induce a systemic inflammatory response syndrome [22,23]. Coagulopathies represent a complication of the systemic inflammatory response syndrome that can progress to disseminated intravascular coagulation. Tissue damage from the above mechanisms can result in organ dysfunction or failure of the liver, kidneys, intestines, lungs, heart, vascular tissue, and brain [24]. Frequent complications of EHS include acute hepatic and renal dysfunction or failure, disseminated intravascular coagulation, metabolic acidosis, and electrolyte imbalances [24]. Rhabdomyolysis has anecdotally been regarded as a frequent comorbidity of EHS, particularly among Service Members and athletes undergoing vigorous training, and could further compromise renal function. Although, by definition, EHS always presents with central nervous system dysfunction at the time of collapse, structural damage to the brain is rare and reserved to the most severe cases [24]. Among EHS fatalities, structural brain damage was most evident within the cerebellum but less evident or nonexistent in other regions [25,26]. Because the preoptic anterior hypothalamus is responsible for temperature regulation where thermosensory neurons reside, it has been hypothesized that damage to this structure is responsible for loss of thermoregulation resulting in EHS, although this has never been demonstrated [25–28]. As such, it is unlikely that temperature fluctuations witnessed during EHS or in recovery are due to a dysfunctional preoptic anterior hypothalamus [24].