Medullary unit responses to changes in local and hypothalamic temperatures in the cat

Lee, H.K.; Chai, C. Y.; Chung, P.M.; Chen, C.C.

doi:10.1016/0361-9230(77)90071-5

Cited by 5 publications

(1 citation statement)

References 25 publications

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“…If this is the case, then decerebrate (midbrain-transected) rats would be unable to generate the full spectrum of SND responses to acute heating. Second, because the brain stem contains thermosensitive neurons (11,15,20,24,25) and is known to play an important role in sympathetic nerve regulation (1), arterial baroreflex function (32,33), and cardiorespiratory coupling (12), it may be that brain stem and spinal neural circuits, in the absence of forebrain systems, are capable of mediating changes in SND frequency components in response to hyperthermia. If this is the case, then heating-induced SND responses would be similar in decerebrate (midbrain-…”

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confidence: 99%

Effects of midbrain and spinal cord transections on sympathetic nerve responses to heating

Kenney

Pickar

Weiss

et al. 2000

American Journal of Physiology-Regulatory, Integrative and Comp

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In the present study, we investigated the contributions of forebrain, brain stem, and spinal neural circuits to heating-induced sympathetic nerve discharge (SND) responses in chloralose-anesthetized rats. Frequency characteristics of renal and splenic SND bursts and the level of activity in these nerves were determined in midbrain-transected (superior colliculus), spinal cord-transected [first cervical vertebra (C1)], and sham-transected (midbrain and spinal cord) rats during progressive increases in colonic temperature (T(c)) from 38 to 41.6-41.7 degrees C. The following observations were made. 1) Significant increases in renal and splenic SND were observed during hyperthermia in midbrain-transected, sham midbrain-transected, C1-transected, and sham C1-transected rats. 2) Heating changed the discharge pattern of renal and splenic SND bursts and was associated with prominent coupling between renal-splenic discharge bursts in midbrain-transected, sham midbrain-transected, and sham C1-transected rats. 3) The pattern of renal and splenic SND bursts remained unchanged from posttransection recovery levels during heating in C1-transected rats. We conclude that an intact forebrain is not required for the full expression of SND responses to increased T(c) and that spinal neural systems, in the absence of supraspinal circuits, are unable to markedly alter the frequency characteristics of SND in response to acute heat stress.

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