Literature DB >> 10198373

RVLM and raphe differentially regulate sympathetic outflows to splanchnic and brown adipose tissue.

S F Morrison1.   

Abstract

To determine whether neurons in the rostral raphe pallidus (RPa) specifically control the sympathetic nerve activity to brown adipose tissue (BAT SNA), thereby regulating adipocyte metabolism and BAT thermogenesis, the responses in BAT SNA to disinhibition of RPa neurons and to disinhibition of neurons in the vasomotor region of the rostral ventrolateral medulla (RVLM) were compared with those in splanchnic (Spl) SNA, which primarily regulates visceral vasoconstriction. In urethan-chloralose-anesthetized ventilated rats, both acute hypothermia and microinjection of bicuculline into RPa produced significantly larger increases in BAT SNA (542 and 1,949% of control) than in Spl SNA (19 and 24% of control). The enhanced burst discharge in BAT SNA was not coherent with that in Spl SNA or with the arterial pressure (AP) at any frequency except the central respiratory frequency. Microinjections of bicuculline into RVLM evoked increases in Spl SNA (86% of control) and AP (32 mmHg), but reduced BAT SNA to low, normothermic levels. Microinjections of muscimol into RVLM reduced Spl SNA (-82% of control) and AP (-59 mmHg), but did not prevent the increase in BAT SNA after disinhibition of RPa neurons. These results indicate that the neural networks generating BAT SNA in response to disinhibition of RPa neurons are independent of those generating basal Spl SNA and support a model in which sympathetic outflow to tissues involved in thermoregulation and metabolism is regulated by central pathways, including neurons in RPa, that are distinct from those involved in the sympathetic control of the cardiovascular system.

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Year:  1999        PMID: 10198373     DOI: 10.1152/ajpregu.1999.276.4.R962

Source DB:  PubMed          Journal:  Am J Physiol        ISSN: 0002-9513


  55 in total

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Authors:  Wei-Hua Cao; Christopher J Madden; Shaun F Morrison
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9.  Characteristics of thermoregulatory and febrile responses in mice deficient in prostaglandin EP1 and EP3 receptors.

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