Sympathoexcitatory CVLM neurons mediate responses to caudal pressor area stimulation

Madhusudan Natarajan , Shaun F. Morrison, American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Published 1 August 2000 Vol. 279 no. R364-R374. The caudal pressor area is capable of causing increases in BP and sympathetic nerve activity when stimulated. The purpose of this article was to determine the mechanism by which the CPA is able to increase SNA and BP. Using microinjection technique they gave bic into the RVLM and saw they got increases in BP and SSNA. Next they wanted to determine whether CPA was mediating its response by removal of inhibitory input to RVLM. Bilateral Bic injections into RVLM was done and resulted in increases in BP and SSNA. Following disinhibition of RVLM they gave Bic into the CPA and that SSNA and BP went up even further. Next they want to determine the role of CVLM in in the CPA sympathoexcitatory pathway, so GABA A receptors were blocked in the CVLM and Bic was injected in the CPA and this resulted in decrease in BP and SNA. When the reverse was done there were increases in BP and SSNA. They investigated whether glutamate was playing a role in driving CVLM activity. Bic was injected bilateral into both CVLM and the CPA followed by a unilateral microinjection of DLH into CPA and saw increases in BP and SSNA. Next they wanted to see if kynurenic acid would block the effects of DLH activation of CPA. So They unilateral blocked glutamate receptors in the CVLM and gave DLH into the contralateral CPA and showed that the response was abolished. These data demonstrate that CPA activates excitatory neurons in the CVLM with glutamate as its neurotransmitter. -MD