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Baro‐activated neurons in the caudal ventrolateral medulla (CVLM) are differentially affected by stimulation of the ventrolateral periaqueductal gray (vlPAG)
Author(s) -
Mobley Susan C,
Schreihofer Ann M
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a467-a
Subject(s) - stimulation , medulla , glutamatergic , periaqueductal gray , excitatory postsynaptic potential , glutamate receptor , neuroscience , medulla oblongata , chemistry , endocrinology , biology , central nervous system , biochemistry , midbrain , inhibitory postsynaptic potential , receptor
The vlPAG evokes autonomic responses related to pain and motivated behaviors. Activation of the vlPAG decreases sympathetic nerve activity (SNA) and arterial pressure (AP) in anesthetized rats, but the central pathways are not completely understood. The vlPAG projects to the CVLM, but the nature and function of this projection are unknown. Stimulation of the CVLM decreases SNA and AP by excitation of baro‐activated GABAergic CVLM neurons. We examined the hypotheses that the projection from the vlPAG to the CVLM is excitatory and that stimulation of the vlPAG excites baro‐activated CVLM neurons. Injection of the retrograde tracer, Fluoro‐gold, into the CVLM (6 rats) yielded a robust ipsilateral projection from the vlPAG. The retrogradely labeled neurons spanned −6.5 to −8.0 mm caudal to bregma and most neurons expressed vesicular glutamate transporter 2 mRNA (75 %, 51–100%), suggesting they were glutamatergic. In chloralose‐anesthetized, ventilated rats stimulation of the vlPAG (20 nmol DLH/100 nl) decreased SNA 25+/−2% and AP 15+/−1 mmHg and produced heterogeneous responses in ipsilateral baro‐activated CVLM neurons (n=27). A subset were clearly activated (82+/−13%, n=7), and others were unaffected (n=7), or inhibited (−74+/−12%, n=13; perhaps by the decreased AP). These results suggest that the vlPAG may be an excitatory input to a subset of baro‐activated CVLM neurons and that these CVLM neurons may contribute to the observed vlPAG‐mediated decreases in SNA and AP. Funding NIH HL075174 to AMS.