McKitrick DJ, Calaresu FR.
Brain Res. 1996 Dec 2;742(1-2):203-10.
In our lab we tend to think mostly of the activity in the RVLM as increasing sympathetic nerve activity because of signals coming from the baroreceptors through the NTS and the CVLM. This paper examines the interaction between the sympathetic and parasympathetic nerve activity (PSNA) by injecting glutamate into the nucleus ambiguus (NA, excited by the NTS to activate PSNA) and measuring the effect on the activity of neurons in the RVLM of urethane-anesthetized rats. Because activating the NA would cause a direct drop in cardiac output which would also activate the RVLM, they used atropine to block the inhibitory effect of the NA on the heart.
The cells they examined fired at about 7Hz at resting. They were not examined for latency or conduction velocity via antidromic activation because they considered the cardiac rhythmicity and barosensitivity to be indicitive of presympathetic neurons, but they mentioned that the possibility exists that some of them may not have been. Of the neurons they tested, 24 of 36 decreased activity after microinjection of glutamate into the nucleus ambiguus (NA), hinting at an inhibitory connection between the two structures. Injection of the inhibitory amino acid, glycine, into the NA, did not cause an increse in firing frequency, but did enhance the cardiac rhythmicity. They discuss that the data suggests that the NA might have a a direct effect on the RVLM, but they suggest that there might be other pathways in play, such as a direct connection from the NTS to the RVLM, that they did not eliminate in their preparation. So they can't conclude in this paper that that the NA directly connects to the RVLM, but it hints at a possible mechanism for a cool effect. -DJH
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