Cholecytokinin activates baro‐activated neurons in rat caudal ventrolateral medulla

Abstract

Cholecystokinin (CCK) is a gastointestinal hormone that produces intestinal vasodilation, which appears to be mediated by reduced sympathetic nerve activity to the gut. Intravenous injection of CCK inhibits splanchnic nerve activity (SNA) and reduces the firing of a subset of pre-sympathetic neurons in the rostral ventrolateral medulla (RVLM) in chloralose-anesthetized rats. We determined whether the inhibition of RVLM neurons could be produced by the activation of GABAergic neurons in the caudal ventrolateral medulla (CVLM). In chloralose-anesthetized, artificially ventilated, paralyzed rats, we measured the effects of CCK (10 μg/kg, iv) on arterial pressure (AP), SNA, heart rate, and the firing of baro-activated, pulse-modulated CVLM neurons. CCK decreased SNA (49±10 %), heart rate (42±7 bpm), and AP (24±10 mmHg). The firing of 3 of 5 baro-activated CVLM neurons was increased by CCK (4 to 11 spikes/sec), but 2 of 5 did not change or were inhibited during the accompanying decrease in AP. In contrast, 8 of 10 neighboring baro-inhibited neurons were inhibited by CCK (3 to 0.4 spikes/sec). Four of these cells were silenced briefly. These data suggest a subset of baro-activated CVLM neurons are activated by CCK and may produce the inhibition observed in some pre-sympathetic RVLM neurons. Furthermore, these data suggest that baro-activated CVLM neurons may be subdivided into CCK-sensitive and CCK-insensitive neurons. Supported by NIH: RO1 HL075174.