Szelényi / Székely Contributions to Thermal Physiology

Satellite Symposium of the 28th International Congress of Physiological Sciences, Pécs, Hungary, 1980
1. Auflage 2013
ISBN: 978-1-4831-9021-1
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 578 Seiten

Advances in Physiological Sciences, Volume 32: Contributions to Thermal Physiology is a collection of papers that details the advances in the understanding of the thermal aspects of physiology. The first part of the title presents articles about central nervous control of body temperature, while the second part covers papers about fever. Next, the selection deals with brain cooling, along with thermoregulation and sleep. The fifth part covers phylogenic aspects of temperature regulation, while the sixth part tackles acclimation. Next, the selection talks about age-related difference in temperature regulation and the peripheral effector mechanisms. The text also covers the brown adipose tissue and the relevance of exercise in regulating body temperature. The book will be of great interest to students, researchers, and practitioners of medicine and biology.

Autoren/Hrsg.

Szelényi, Z.

Székely, M.

Leseproben

FUNCTIONAL ANATOMY OF THE HYPOTHALAMUS FROM THE POINT OF VIEW OF TEMPERATURE REGULATION
CLARK M. BLATTEIS,     Department of Physiology and Biophysics, University of Tennessee Center for the Health Sciences, Memphis, Tennessee 38163, USA Publisher Summary
This chapter discusses the functional anatomy of the hypothalamus from the point of view of temperature regulation. The ability of the hypothalamus to trigger the total pattern of autonomic thermoregulatory responses has been repeatedly shown. The locus of greatest control appears to reside in the PO/AH. Animals with PO/AH lesions or topical anesthesia cannot maintain their body temperatures in cold or warm environments; locally cooling or heating this area causes appropriate autonomic thermoregulatory responses. Both warm- and cool-sensitive neurons have been identified; however, the cool-sensitive neurons may be interneurons receiving inhibitory inputs from nearby warm-sensitive neurons. PO/AH thermosensitive units receive afferent inputs from cutaneous thermoreceptors and from thermosensitive neurons in the spinal cord and the midbrain. The temperature controller function has been ascribed to these temperature-sensitive neurons or, alternatively, to adjacent, temperature-insensitive neurons. Putative neurotransmitters injected directly into the PO/AH induce either increases or decreases of body temperature, depending upon the species and other conditions. Temperature-sensitive units occur in the posterior hypothalamus, but they are few. Thermal stimulation or local injection of neurotransmitters may or may not evoke autonomic thermoeffector responses. Endotherms utilize both autonomic and behavioral means of effector response to maintain body temperature. Both response modes are activated by peripheral and/or central temperature inputs; moreover, the operating characteristics of their controller(s) are similar. However, it is not yet clear whether these two systems are controlled by the same or different neural structures and circuits. A functional and, possibly, a spatial separation of the CNS controllers of the two response modes has been hypothesized. Individual components of autonomic and behavioral thermoregulation also may be controlled separately. This paper reviews the current knowledge in this area from the perspective of functional anatomy. Autonomic Temperature Regulation
Hypothalamic control mechanisms.
Preoptic/anterior hypothalamus (PO/AH). The ability of the hypothalamus to trigger the total pattern of autonomic thermoregulatory responses has been repeatedly shown. The locus of greatest control appears to reside in the PO/AH. Animals with PO/AH lesions or topical anesthesia cannot maintain their body temperatures in cold or warm environments; locally cooling or heating this area causes appropriate autonomic thermoregulatory responses (reviewed by Satinoff, 1974). Both warm- (Nakayama et al., 1963) and cool- (Hardy et al., 1964) sensitive neurons have been identified; however, the cool-sensitive neurons may be interneurons receiving inhibitory inputs from nearby warm-sensitive neurons (Boulant and Hardy, 1974). PO/AH thermosensitive units receive afferent inputs from cutaneous thermoreceptors (Hellon, 1970; Wit and Wang, 1968), and from thermosensitive neurons in the spinal cord (Guieu and Hardy, 1970) and the midbrain (Eisenman, 1974). Temperature controller function has been ascribed to these temperature-sensitive neurons (Boulant and Gonzalez, 1977); or, alternatively, to adjacent, temperature-insensitive neurons (reviewed by Hammel, 1968). Putative neurotransmitters injected directly into the PO/AH induce either increases or decreases of body temperature, depending upon the species and other conditions (reviewed by Bligh, 1979). It is uncertain, however, whether these transmitters act on the thermosensitive or other neurons (Jell, 1974). Zeisberger and Brück (1971) have localized an area immediately posterior to the thermosensitive neurons in the PO/AH which is norepinephrine-sensitive and activates heat production. They postulated that these cells generate the reference signal for the temperature regulation system. Posterior hypothalamus (PH). Temperature-sensitive units occur in the PH, but they are few (Edinger and Eisenman, 1970; Wünnenberg and Hardy, 1972). Thermal stimulation or local injection of neurotransmitters may or may not evoke autonomic thermoeffector responses (Adair, 1974; Lipton, 1973); local anesthesia does not affect autonomic thermoregulation (Humphreys et al., 1976). Hence, the PH may not be a controller for this system. On the other hand, this structure is a major site of convergence of temperature inputs (Nutik, 1973), and may be the origin of the central effector signal (Hardy, 1973). Puschmann and Jessen (1978) found in the PH of goats thermosensitive neurons which elicited thermoeffector responses inverse to those expected. They suggested that these units were nonspecific, and may be integrative structures which transduce incoming thermal signals into thermoeffector responses. Similar non-corrective autonomic responses to hypothalamic thermal stimulation have been found in penguins, and also ascribed to nonspecific temperature effects on hypothalamic integrative functions (Simon et al., 1976). The PH also may be providing an ionic reference input to the PO/AH temperature controller (Myers and Veale, 1970). It is generally agreed that the PH contains neurons which mediate shivering (reviewed by Hemingway, 1963). Extrahypothalamic control mechanisms.
Midbrain. The PO/AH, however, may not solely command the full pattern of defenses against thermal stress, because a variable capability for autonomic thermoregulation survives its destruction. Thus, when the midbrain reticular formation (MRF) is completely separated from the hypothalamus, thermoregulation in the cold is lost, but autonomic responses to heat persist (Andersson et al., 1965; Keller, 1963; Bard et al., 1970); however, these are raised to a higher threshold. But, if any tissue remains between the MRF and the hypothalamus, various components of the autonomic responses to heat or cold are evocable (Keller, 1938; Bard et al., 1970). Both warm- (Cabanac and Hardy, 1969) and cool- (Nakayama and Hardy, 1969) sensitive neurons have been identified in the MRF. Thermal stimulation evokes appropriate thermoeffector responses in some species (Cronin and Baker, 1977), but not in others (Adair and Stitt, 1971). Thus, the MRF may have some capacity for independent autonomic thermoregulation, but not in all species. Since the activating stimulus must be increased when its hypothalamic connections are severed, it may be that it usually is tonically inhibited by the PO/AH. Alternatively, since the MRF, and the serotonergic raphe cells it contains, may lie in the pathway through which thermal afferents ascend to the PO/AH (Dickenson, 1977; Eisenman, 1974), and in view of the possible involvement of serotonin in temperature regulation, separation of this area from its connections above could result in reduced responsiveness. Pons and medulla.
A relative independence of thermoregulatory function also exists in pontine and low mesencephalic cats. Thus, when the transection is complete, lack of autonomic defenses against cold and persistence of heat loss responses appearing only at very high body temperatures are noted (Keller, 1963; Bard et al., 1970). However, when the transection spares either lateral or medial pathways, shivering is not impaired in the cold (Keller, 1938); and when the medial pons is ablated but the lateral pons spared, shivering appears even at room temperature (Connor and Crawford, 1969). These latter results have been interpreted as indicating that the shivering pathways (which pass laterally in the pons [Hemingway, 1963]) are facilitated by the medial pons. However, this area also may contain cells from which shivering could originate (Amini-Sereshki, 1977). The reticular formation of the medulla oblongata (MO) also may contain a controller capable of driving autonomic thermoregulatory responses independently of the PO/AH. Thus, thermal stimulation of the MO (Chai and Lin, 1972) produces appropriate autonomic responses, albeit the relation between these and medullary temperature (TMO) is not as precise as that between such responses and TPO/AH. Moreover, the effects of MO thermal stimulation persist and even are enhanced after PO/AH destruction (Lipton, 1973). Medullary lesions cause deficits in temperature regulation against both heat and cold (Lipton et al., 1974). It has been suggested that the MO may provide local temperature information to the PO/AH (Cabanac, 1970); or, it may be a separate, secondary thermoregulatory control with direct, extrahypothalamic links to thermoeffectors, but important only during extreme body temperature changes (Chai and Lin, 1973; Lipton, 1973). It normally may be tonically inhibited by the PO/AH directly via lateral pathways (Lipton et al., 1974); or it...