Contributions to Thermal Physiology. Satellite Symposium of the 28th International Congress of Physiological Sciences, Pécs, Hungary, 1980

458 Pages·1981·65.765 MB·English

by  Z. Szelényi and M. Székely (Eds.)

ADVANCES IN PHYSIOLOGICAL SCIENCES
Proceedings of the 28th International Congress of Physiological Sciences
Budapest 1980
Volumes
1 — Regulatory Functions of the CNS. Principles of Motion and Organization
2 — Regulatory Functions of the CNS. Subsystems
3 — Physiology of Non-excitable Cells
4 — Physiology of Excitable Membranes
5 — Molecular and Cellular Aspects of Muscle Function
6 — Genetics, Structure and Function of Blood Cells
7 — Cardiovascular Physiology. Microcirculation and Capillary Exchange
8 — Cardiovascular Physiology. Heart, Peripheral Circulation and Methodology
9 — Cardiovascular Physiology. Neural Control Mechanisms
10 — Respiration
11 — Kidney and Body Fluids
12 — Nutrition, Digestion, Metabolism
13 — Endocrinology, Neuroendocrinology, Neuropeptides — I
14 — Endocrinology, Neuroendocrinology, Neuropeptides — II
15 — Reproduction and Development
16 — Sensory Functions
17 — Brain and Behaviour
18 — Environmental Physiology
19 — Gravitational Physiology
20 — Advances in Animal and Comparative Physiology
21 — History of Physiology
Satellite symposia oj the 28th International Congress oj Physiological Sciences
22 — Neurotransmitters in Invertebrates
23 — Neurobiology of Invertebrates
24 — Mechanism of Muscle Adaptation to Functional Requirements
25 — Oxygen Transport to Tissue
26 — Homeostasis in Injury and Shock
27 — Factors Influencing Adrenergic Mechanisms in the Heart
28 — Saliva and Salivation
29 — Gastrointestinal Defence Mechanisms
30 — Neural Communications and Control
31 — Sensory Physiology of Aquatic Lower Vertebrates
32 — Contributions to Thermal Physiology
33 — Recent Advances of Avian Endocrinology
34 — Mathematical and Computational Methods in Physiology
35 — Hormones, Lipoproteins and Atherosclerosis
36 — Cellular Analogues of Conditioning and Neural Plasticity
(Each volume is available separately.)
ADVANCES IN
PHYSIOLOGICAL SCIENCES
Satellite Symposium of the 28th International Congress of Physiological Sciences
Pecs, Hungary 1980
Volume 32
Contributions to Thermal Physiology
Editors
Z. Szelenyi
M. Szekely
Pecs, Hungary
(■§)
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British Library Cataloguing in Publication Data
International Congress of Physiological Sciences.
Satellite Symposium (28th : 1980 : Pecs)
Advances in Physiological sciences.
Vol. 32: Contributions to thermal physiology
1. Physiology — Congresses
I. Title: II. Szelenyi, Z.
II. Szekely, M.
591.1 QP1 80-41854
Pergamon Press ISBN 0 08 026407 7 (Series)
ISBN 0 08 027354 8 (Volume)
Akademiai Kiado ISBN 963 05 2691 3 (Series)
ISBN 963 05 2525 9 (Volume)
In order to make this volume available as economically and as
rapidly as possible the authors' typescripts have been reproduced in
their original forms. This method unfortunately has its typographi
cal limitations but it is hoped that they in no way distract the reader.
Printed in Hungary
FOREWORD
As satellite to International Congresses of Physiology, symposia were organiz­
ed in New Haven 1968, Dublin 1971, Jerusalem 1974, and Lille 1977. On each
occasion, the material of these symposia was put together in a single volume or a
special issue of a scientific journal. Following this tradition, the present volume has
been published by the Organizers of the Fifth International Symposium on Temper­
ature Physiologie Pecs 1980, a satellite of the IUPS International Congress of
Physiology. It contains short communications and lectures. The subject of short
communications was left open; lectures were solicited from contributors, and titles
suggested to them. However, texts have not been revised. The authors of the
lectures are experts, with major contributions in their fields, and so one can expect
the lectures to be authoritative reviews of these fields.
As "in my Father's house there are many mansions", temperature physiology
is a vast house, built on bioenergetics and roofed by temperature regulation.
Because temperature regulation is a "pure function" with no organs of its own -
except brown fat — temperature physiology includes many aspects of all fields,
from subcellular to higher nervous functions. From the contribution of a large
number of researchers, knowledge increases and it becomes more and more difficult
for a temperature physiologist to follow his own field's progress. The more
temperature physiology is lured towards new frontiers, the more varied it becomes
and so vulnerable to this very progress. Comprehensive reviews are therefore
desirable. It is nevertheless impossible to cover the old and the new entirely with
lectures in one symposium. The present programme was selected by the IUPS
Commission on Thermal Physiology. The local organizers, therefore, are not to
blame for any errors or insufficiencies in this programme. Let us hope that future
satellite symposia will cover the fields not treated here. The lectures of tomorrow
already mushroom in the numerous short communications presented at this
symposium.
On behalf of the community of thermal physiologists and the IUPS Commis­
sion, I wish to express our gratitude to those colleagues who made the satellite
symposium possible, and published this book in time for the meeting: Professor Sz.
Donhoffer, Honorary Chairman of the symposium, Professor S. Koväcs, Chairman
of the Local Committee, and M. Szekely, Z. Szelenyi ,M. Farkas, and I. Komäromi,
members.
Michel Cabanac
Chairman
IUPS Commission on Thermal Physiology
V
Satellite of 28. Int. Congress ofPhysiol. Sei., Pecs, 1980
Z. Szelenyi and M. Szekely (eds)
FUNCTIONAL ANATOMY OF THE HYPOTHAL AM US
FROM THE POINT OF VIEW OF TEMPERATURE REGULATION
CLARK M. BLATTEIS
Department of Physiology and Biophysi cs. University of Tennessee Center for the H—lth sciences,
Memphis, Tennessee 38163, USA
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 differ­
ent neural structures and circuits. A functional and, possibly, a spatial
separation of the CNS controllers of the two response modes has been hypo­
thesized. Individual components of autonomic and behavioral thermoregula-
tion 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 au­
tonomic 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 ap­
propriate 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 neu­
rons may be interneurons receiving inhibitory inputs from nearby warm-sen­
sitive neurons (Boulant and Hardy, 1974). PO/AH thermosensitive units re­
ceive 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 neu­
rons (Boulant and Gonzalez, 1977); or, alternatively, to adjacent, temper-
ature-insensitive neurons (reviewed by Hammel, 1968). Putative neuro-
transmitters injected directly into the PO/AH induce either increases or
decreases of body temperature, depending upon the species and other condi­
tions (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-sensi-
tive and activates heat production. They postulated that these cells gen­
erate the reference signal for the temperature regulation system.
Posterior hypothalamus (PH). Temperature-sensitive units occur in
2* 3
4 C M, Blatteis
the PH, but they are few (Edinger and Eisenman, 1970; Wiinnenberg and Har­
dy, 1972). Thermal stimulation or local injection of neurotransmitters
may or may not evoke autonomic thermoeffector responses (Adair, 1974; Lip-
ton, 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 respons­
es inverse to those expected. They suggested that these units were non­
specific, and may be integrative structures which transduce incoming ther­
mal signals into thermoeffector responses. Similar non-corrective auto­
nomic responses to hypothalamic thermal stimulation have been found in
penguins, and also ascribed to nonspecific temperature effects on hypotha­
lamic integrative functions (Simon e_t aJL· , 1976) . The PH also may be pro­
viding 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 sur­
vives 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 hy­
pothalamus, 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 ther­
moef fector 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 func­
tion also exists in pontine and low mesencephalic cats. Thus, when the
transection is complete, lack of autonomic defenses against cold and per­
sistence of heat loss responses appearing only at very high body tempera­
tures are noted (Keller, 1963; Bard et^ al^ , 1970). However, when the
transection spares either lateral or medial pathways, shivering is not im­
paired in the cold (Keller, 1938); and when the medial pons is ablated but
the lateral pons spared, shivering appears even at room temperature (Con­
nor 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-Seresh-
ki, 1977). The reticular formation of the medulla oblongata (MO) also may
contain a controller capable of driving autonomic thermoregulatory re-
Hypothalamus and temperature regulation 5
sponses 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 regula­
tion against both heat and cold (Lipton <e_t al. , 1974). It has been sug­
gested that the MO may provide local temperature information to the PO/AH
(Cabanac, 1970); or, it may be a separate, secondary thermoregulatory con­
trol with direct, extrahypothalamic links to thermoeffectors, but impor­
tant only during extreme body temperature changes (Chai and Lin, 1973;
Lipton, 1973). It normally may be tonically inhibited by the PO/AH. di­
rectly via lateral pathways (Lipton eMt_ al., 1974); or it may be inhibited
by the MRF alone (Chambers et_ al. , 1974), the inhibitory influence of
which in turn may be inhibited by the PO/AH (Satinoff, 1974).
Spinal cord. The existence of thermosensitive structures in the spi­
nal cord has been amply verified (reviewed by Simon, 1974). Both warm-
and cool-responsive neurons have been identified. They are distributed
over the length of the spinal cord (e.g., dogs [Simon et^ aüL· , 1964]), or
concentrated in its lower cervical and upper thoracic segments (e.g., gui­
nea pigs [Wünnenberg and Brück, 1968a]). Their activation by changes in
local temperature stimulates appropriate thermoeffeetor responses. Spinal
heating of animals with transections of the anterolateral tracts anterior
to the area of thermal stimulation does not suppress ambient cold-induced
shivering (Wünnenberg and Brück, 1968b) or heat-induced panting (Kosaka et
al. , 1969), indicating that spinal temperature signals are conducted to
the brainstem and integrated there to evoke thermoregulatory responses.
Wünnenberg and Brück (1970) have traced these ascending channels to the
AH. On the other hand, coordinated thermoeffector reactions also can be
induced in spinalized and midbrain-transected preparations by thermal
stimulation of the spinal cord (Thauer, 1935; Simon et al_., 1966) or the
skin (Kosaka and Simon, 1968), indicating the existence of independent
thermoregulatory control functions at the spinal level as well.
Summarizing, autonomic thermoregulatory functions may be attributed
to brain areas outside of the PO/AH. These mechanisms appear to be sub­
sidiary controls, may have their own (direct?) links to thermoeffectors,
and are capable of operating independently of the PO/AH, although i riey
normally may be influenced by it through ascending and/or descending con­
nections. Thus, the role of the PO/AH in temperature regulation may be
seen as not essential, but nevertheless pre-eminent in the control of ap­
propriate, coordinated, and low-threshold thermoregulatory responses. In
this role, it receives afferent information from thermosensitive regions
throughout the body, and is connected with all the thermoeffectors.
Possible independent receptor-effector loops. However, other evi­
dence suggests that the PO/AH may not be the dominant area of integrative
control. Following earlier observations by Lipton et al^. (1974), Gilbert
and Blatteis (1977) found that the neural connections subserving heat and
cold thermoeffectors, although closely arranged, nevertheless could be
separated by precise microknife cuts. Thus, they localized different
sites in the hypothalamus of rats which separately control different auto­
nomic thermoregulatory functions, viz., cold-induced skin vasoconstriction
in the PO, shivering activity in the PH, and heat-induced skin vasodila-
tion in the AH or the MO. They, moreover, showed that the integrity of
6 C. M. Blatteis
the PO is indispensable in rats for the control of cold-induced cutaneous
vasoconstriction, but not for that of cold thermogenesis and heat-induced
cutaneous vasodilation. They concluded that autonomic thermoregulatory
mechanisms may be organized in separate receptor-effector pathways. Sati-
noff jit_ al. (1976b) have reported that PO/AH lesions in rats produce defi­
cits in autonomic cold defense mechanisms, the components of which recover
in patterns that are independent of each other, but depend on the locus of
the initial damage. A gradual recovery of cold tolerance after extensive
hypothalamic lesions also has been noted by others (Hamilton and Brobeck,
1964; Chowers et al., 1972). Hence, these results suggest that individual
components of the total pattern of thermoregulatory responses may be con­
trolled separately at different sites in the brainstem. The disparate
thermoregulatory effects of seemingly similar lesions observed by differ­
ent workers may have been due to variations in the specific populations of
temperature receptors and/or of pathways from these to thermoeffectors af­
fected by the experimental procedures, variously affecting heat production
or heat loss capacity in each case. (It should be noted in this context
that the ventromedial region of the hypothalamus [just posterior to the
AH] may modulate efferent peripheral sympathetic activity [Ban, 1975].)
Each response in a pattern may have its own operating characteristics.
The fact that thermoregulatory responses often occur together may be re­
lated to the intensity and locus of the activating signals; if adequate,
they may stimulate them all (simultaneously?). Under conditions of moder­
ate thermal stress, all thermoeffeetor responses do not, in fact, begin
together, but rather appear in sequence (Blatteis, 1960). Thus, the re­
cruitment of the various thermoeffector mechanisms into appropriate and
coordinated autonomic thermoregulatory responses may involve the integra­
tion of afferent and efferent signals through functionally independent
neural networks distributed from the PO/AH to the MO (and' spinal cord?).
Behavioral Temperature Regulation
PO/AH control mechanisms. The hypothalamus also is involved in the
nervous control of behavioral thermoregulatory mechanisms. Postural adap­
tive reactions have been observed on warming (Hellström and Hammel, 1967)
or cooling (Freeman and Davis, 1959) the hypothalamus. Again, the primary
temperature controller may lie in the PO/AH region. To wit, warming or
cooling the PO/AH elicits appropriate behavioral responses (reviewed by
Cabanac, 1974; Satinoff and Hendersen, 1977). The magnitude of these
changes is, in general, proportional to the displacement of TPOAH above or
below specific thresholds (Laudenslager, 1976). Thus, behavioral thermo­
regulatory responses have operating characteristics similar to those that
influence autonomic responses, and may be activated by the same elements,
i.e., the two systems may be regulated by the same primary controller.
Extra-PO/AH control mechanisms. However, like the autonomic, behav­
ioral thermoregulatory responses also may not be integrated solely in the
PO/AH. Thus, thermal stimulation of the PH elicits corrective behavioral
thermoregulatory responses in monkeys (Adair, 1974), albeit not in rats
(Lipton, 1971). On the other hand, thermal stimulation or local anesthe­
sia of the MRF does not influence behavioral thermoregulation (Adair and
Stitt, 1971; Lipton, 1971; Humphreys et al., 1976). However, heating or
cooling the MO causes appropriate adaptive behaviors which parallel those
induced by thermal stimulation of the PO/AH, but are independent of it be­
cause they still occur and even are enhanced after its 'destruction (Lip­
ton, 1973). Similarly, thermal stimulation of the spinal cord evokes ap­
propriate behavioral responses, generally identical with those induced by
Hypothalamus and temperature regulation 7
external or hypothalamic heating or cooling (Carlisle and Ingram, 1963).
In sum, as in the case of autonomic thermoregulation, there also ex­
ist multiple loci, from the PO/AH to the spinal cord, from which behavior­
al thermoregulatory responses can be elicited. While the neuronal ele­
ments regulating these two systems overlap at some sites, they appear to
be completely separate at others. This would imply that the neural net­
works for each may be distinct.
Independence of autonomic and behavioral networks. That this may be
the case is supported by evidence that the two functions can be further
dissociated. Thus, in rats, PO/AH lesions disrupt the autonomic, but not
the behavioral, responses to exposure to cold (Rüdiger and Seyer, 1965;
Carlisle, 1969; Satinoff and Rutstein, 1970; Van Zoeren and Strieker,
1977) and to warm (Lipton, 1968; Strieker and Hainsworth, 1970; Toth,
1973) environments; the rats do not maintain their body temperatures. By
contrast, lateral hypothalamic (LH) lesions impair behavioral thermoregu­
lation in the cold (Rüdiger and Seyer, 1965; Satinoff and Shan, 1971; Van
Zoeren and Strieker, 1977) and in the heat (Hainsworth and Epstein, 1966),
but do not affect autonomic regulation except transiently; these animals'
body temperatures are well maintained.
The findings that PO/AH lesions impair autonomic thermoregulatory re­
sponses are consistent with expectations (see above). The fact that this
function survives after LH lesions, however, is unexpected, since the
pathways for autonomic regulation against cold pass laterally from the PO/
AH into the median forebrain bundle (MFB) and then to the LH (Sherwood et
al., 1954; McCrum, 1953; Lipton £t al., 1974; Gilbert and Blatteis, 1977),
while those against heat occupy a more diffuse, dorso-lateral position
(Gilbert and Blatteis, 1977; Lipton et_ al., 1974). In view of the appar­
ent, relative discreteness of individual thermoreceptor-autonomic thermo-
effector pathways (Gilbert and Blatteis, 1977), the discrepancy might be
ascribed to the possibility that these gross lesions spared the relevant
pathways in the LH. Indeed, conflicting results have been reported.
Strieker and Hainsworth (1970) found that LH lesions of rats suppressed
(autonomic) saliva secretion, but not (behavioral) saliva spreading
(grooming) in a warm environment, while Laudenslager (1976) saw neither
autonomic nor behavioral effects in squirrel monkeys after thermal stimu­
lation of the LH. Humphreys jat_ al. (1976) found that local LH anestheti­
zation did not significantly affect behavioral thermoregulation, although
the animals became hypothermic in a thermoneutral and hyperthermic in a
warm environment.
Since the PO/AH-lesioned animals continue to perform their operant
tasks, these behaviors could be initiated by structures outside of the PO/
AH. It cannot be ascertained at present which of the potential loci,
i.e., LH, PH, or MO, is responsible for the effects observed. Satinoff
(1974) has suggested that the controllers of such behaviors may be located
in the LH. However, other evidence has indicated that LH lesions may dis­
rupt a common activational component of motivation. (It should be noted
that all the above results are based on thermally motivated instrumental
responding, i.e., operant behavior.) Thus, Stein (1964) has proposed that
the MFB, which courses through both the LH and PH, may be part of a. moti­
vational system which facilitates several operant behaviors. Indeed, be­
sides motivated thermoregulatory behaviors, other non-thermoregulatory op­
erant behaviors also can be disrupted by LH lesions (Teitelbaum and Ep-
8 C. M. Blatteis
stein, 1962). Moreover, since not all these behaviors are affected equal­
ly by LH lesions, i.e., all possible combinations of losses can occur (Sa-
tinoff and Shan, 1971; Van Zoeren and Strieker, 1977), each component of
these motivated behaviors may be independent of the others. This implies
that each may pass through the LH by separate pathways, with thermoregula-
tory behavior being just one of these. Hence, if the effective part of
the conscious perception of thermal states were the motivation for" thermo-
regulatory behavior, then damage to the central controls of motivational
activities could account for the decreased responding exhibited by LH-le-
sioned rats. Alternatively, this reduced behavior may reflect the wider
sensorimotor dysfunctions characteristically produced by LH lesions
(Strieker and Zigmond, 1976; Marshall and Teitelbaum, 1977); or it may re­
flect sensory deficits alone. Thus, the MFB may be part of a pathway re­
laying cutaneous thermal afferents to various parts of the hypothalamus
(Gilbert and Blatteis, 1977). Therefore, animals with LH lesions may not
be sensitive to peripheral cold stimuli and for that reason not press for
heat in the cold until their internal temperature has fallen appreciably.
In summary, hypothalamic as well as extrahypothalamic areas may in­
fluence thermoregulatory behaviors, and not all the integration of this
response mode may occur in the PO/AH. Moreover, although autonomic and
behavioral thermoregulations probably possess common sources of informa­
tion, they may not be integrated by a single controller. Indeed, observa­
tions in pigeons have revealed an antagonistic activation of autonomic and
behavioral thermoregulatory defense responses during hypothalamic thermal
stimulation (Schmidt, 1978). Hence, these two classes of regulation may
be functionally and anatomically separate.
Independent neural loops. The control system for behavioral thermo-
regulation, like that for autonomic thermoregulation, also may be organ­
ized into networks independent of each other. Thus, localized diathermic
warming of various areas of the brainstem of rats has revealed that indi­
vidual components of their behavioral response to heat are located in dif­
ferent, but partially overlapping, areas, viz., prone extension in the PO/
AH region, grooming in the PH and the anterior ventral midbrain, and loco­
motion in the septal area, the ventromedial midbrain, and the dorsal me­
dial MO (Roberts and Mooney, 1974). Lesioning of these areas affects only
the specific responses localized therein (Roberts and Martin, 1977). A
similar functional and anatomical separation between grooming and postural
relaxation exists in the opossum (Roberts et^ aj^. , 1969) .
Fever: Localization of EP Action
It is generally agreed that fever is produced by the action of an en­
dogenous pyrogen (EP) carried in the blood to the PO/AH region. Thus, EP
elicits the most rapidly-developing and most intense febrile response when
injected into the PO/AH (Cooper e^t al., 1967; Rosendorf f and Mooney, 1971;
fittman ^t al., 1975; Jackson, 1967; Blatteis and Smith, 1979). However,
EP also may act at extra-POAH sites to drive the fever-producing mechan­
isms. Ranson et^ al^. (1939) reported that cats with hypothalamic lesions
which impaired autonomic thermoregulation could still develop normal fe­
brile reactions to systemic pyrogens. Similarly, AH and LH lesions do not
alter the febrile response (Guerra and Barbour, 1943; Bard et^ al_. , 1970;
Chambers et al., 1949; Haerting and Masserman, 1942). Relatively normal
fevers also are produced following intravenous or intracerebroventricular
endotoxin or EP after electrolytic destruction of the PO/AH (Andersson et_
al. , 1965; Lipton and Trzcinka, 1976; Cooper <e_t al. , 1976). Moreover, a