Precollicular decerebration reduces the pressor responses evoked by stimulation of rostral pons but not medulla in cats.

In 30 cats under chloralose (40 mg/kg) and urethane (400 mg/kg) anesthesia, the ponto-medullary region involved in cardiovascular integration were stimulated by rectangular pulses (0.5 ms, 80 or 5 Hz, 100 to 200 microA) and/or by microinjection of sodium glutamate (Glu, 0.25-0.5 M, 70-200 nl). Changes of systemic arterial blood pressure (SAP) and renal sympathetic nerve activity (RNA) following stimulation were compared before and after precollicular decerebration. Precollicular decerebration itself resulted in an immediate but brief (5 to 15 min) hypotension with a decrease in SAP ranging from 40 to 100 mmHg. Stimulation of the lateral tegmental field (FTL) produced depressor responses. After precollicular decerebration, the stimulation induced depressor responses were either abolished or converted to mild pressor responses. Stimulation of the dorsal gigantocellular tegmental field-periventricular grey (dFTG-PVG) produced pressor responses. These responses were abolished after precollicular decerebration without exception. On the other hand, precollicular decerebration did not reduce pressor responses produced by stimulation of the ventrolateral medulla (VLM) and the dorsal medulla (DM). In 7 additional cats killed with an overdose of pentobarbital, the brain stem were processed for dopamine beta-hydroxylase (DBH). The pressor areas of the VLM and DM were DBH positive, indicating the presence of norepinephrine, while the dFTG-PVG and FTL were not. These findings suggest that the depressor mechanism of the FTL and the pressor mechanism of the dFTG, but not of the VLM or DM depend on actions of the brain structures rostral to superior colliculi.