The depressor caudal ventrolateral medulla: its correlation with the pressor dorsomedial and ventrolateral medulla and the depressor paramedian reticular nucleus.
The functional correlation of the depressor caudal ventrolateral medulla (CVLM) with the two pressor regions, i.e. rostral ventrolateral medulla (RVLM) and dorsomedial medulla (DM), and with another inhibitory region, i.e. the paramedian reticular nucleus (PRN), were studied in cats anesthetized intraperitoneally with chloralose (40 mg/kg) and urethane (400 mg/kg). Systemic arterial pressure (SAP), heart rate (HR) and the sympathetic vertebral nerve activity (VNA) were recorded. The correct location of CVLM, RVLM or DM was determined by their specific responses, i.e. decreases of SAP, HR and VNA, for CVLM increases of these parameters for RVLM and DM, elicited first by electrical stimulation (80 Hz, 0.5 ms, 50-100 microA) then followed by microinjection of glutamate (Glu, 0.25 M, 70 nl). The depressor action of PRN was produced by electrical stimulation only. It was found that the depressor responses caused by the CVLM stimulation were greatly reduced 2 h after lesioning either the RVLM or DM by microinjection of kainic acid (KA, 24 mM, 200 nl) ipsilateral to the side of CVLM stimulation. The CVLM responses were further reduced after the remaining side of RVLM or DM was lesioned. The reduction of the CVLM-depressor responses was more apparent after the RVLM than DM lesioning. Data suggest that the CVLM-depressor responses are mediated through inhibition of the sympathetic-pressor neurons in both RVLM and DM with predominance of the former. Lesioning the PRN by KA and/or combination with DC electrolytic lesion reduced the CVLM-induced depressor responses. In turn, lesioning the CVLM by KA reduced the PRN-induced depressor responses. The reduction in the later manipulation was more apparent in the PRN-depressor responses than the CVLM-depressor responses. Data suggest that part of the PRN depressor action is mediated through activation of the CVLM.
Hsieh
J H
JH
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Wu
J J
JJ
Yen
C T
CT
Chai
C Y
CY
D000818:Animals; D001237:Asphyxia / Q000503:physiopathology; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D001921:Brain / Q000502:physiology; D002415:Cats; D004558:Electric Stimulation; D004594:Electrophysiology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D005260:Female; D018698:Glutamic Acid / Q000008:administration & dosage / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology
D018690:Excitatory Amino Acid Agonists; D018698:Glutamic Acid; D007608:Kainic Acid