4.3 Article

Contribution of infralimbic cortex in the cardiovascular response to acute stress

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00573.2011

关键词

medial prefrontal cortex; dorsomedial hypothalamus; heart rate; blood pressure

资金

  1. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico do Brasil [CNPq 301519/2009-9]
  2. Fundacao de Amparo a Pesquisa do Estado de Minas Gerais (FAPEMIG)
  3. National Insitutes of Health [NS-19883]

向作者/读者索取更多资源

Muller-Ribeiro FCF, Zaretsky DV, Zaretskaia MV, Santos RAS, DiMicco JA, Fontes MAP. Contribution of infralimbic cortex in the cardiovascular response to acute stress. Am J Physiol Regul Integr Comp Physiol 303: R639-R650, 2012. First published July 11, 2012; doi: 10.1152/ajpregu.00573.2011.-The infralimbic region of the medial prefrontal cortex (IL) modulates autonomic and neuroendocrine function via projections to subcortical structures involved in the response to stress. We evaluated the contribution of the IL to the cardiovascular response evoked by acute stress. Under anesthesia (80 mg/kg ketamine-11.5 mg/kg xylazine), rats were implanted with telemetry probes or arterial lines for recording heart rate and blood pressure. Guide cannulas were implanted to target the IL for microinjection of muscimol (100 pmol/100 nl), N-methyl-D-aspartate (NMDA) (6 pmol/100 nl), or vehicle (100 nl). Microinjection of muscimol, an agonist of GABA(A) receptors, into the IL had no effect on stress-evoked cardiovascular and thermogenic changes in any of the paradigms evaluated (cage switch, restraint plus air-jet noise, or air-jet stress). However, microinjection of the excitatory amino acid NMDA into the IL attenuated the pressor and tachycardic response to air-jet stress. Pretreatment with the selective NMDA antagonist DL-2-amino-5-phosphonopentanoic acid (AP-5, 100 pmol/100 nl) blocked the effect of NMDA on the cardiovascular response to air-jet stress. We conclude that 1) the IL region is not tonically involved in cardiovascular or thermogenic control during stress or under baseline conditions, and 2) activation of NMDA receptors in the IL can suppress the cardiovascular response to acute stress exposure.

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