期刊
NEUROSCIENCE
卷 102, 期 4, 页码 905-910出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0306-4522(00)00513-3
关键词
defensive freezing; quiescence; immobility; cardiovascular regulation; pain modulation; excitatory amino acid
Activation of the ventrolateral periaqueductal gray produces immobility and antinociception. It has been argued that these behaviors are part of either a defensive fear response to threat or a recuperative quiescence response to deep tissue injury. Data collected in anesthetized animals showing that activation of the ventrolateral peraqueductal gray has a hypotensive effect supports the quiescence hypothesis. Our objective was to determine whether activation of the ventrolateral periaqueductal gray in awake, freely moving rats results in a decrease in blood pressure as it does in anesthetized animals. Changes in blood pressure produced by microinjection of the neuroexcitant D,L-homocysteic acid were measured using radio telemetry while rats were awake and while anesthetized with pentobarbital. Consistent with earlier reports. microinjection of D,L-homocysteic acid into the ventrolateral periaqueductal gray caused a decrease in blood pressure in anesthetized rats. In contrast, microinjection at the same ventrolateral periaqueductal gray sites while rats were awake had no effect on blood pressure. even though the animals became immobile and hear? rare decreased. Thus, the immobility evoked from ventrolateral periaqueductal gray is not associated with a fall in mean arterial pressure. Two conclusions can be drawn from these data. (1) Caution must be used in generalizing from data collected in anesthetized animals. (2) The ventrolateral periaqueductal gray is as likely to contribute to defensive fear as to recuperative quiescence. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.
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