Integration of the Proprioceptive and Central Inspiratory Inhibitory Afferent Inputs by Pontine Noradrenergic A5 Neurons in Rats.

Inhibitory afferent inputs to pontine A5 noradrenergic neurons (A5 NN) are not known, except partial baroreceptor input. In spontaneously breathing pentobarbital-anesthetized rats, we registered 35 A5 NN that were activated by hypoxia (100% N, 10 sec) by more than 5 times in comparison with the background. Cooling of retrotrapezoid nucleus (15°C, 6 sec) completely blocked the motor inspiratory output and A5 NN discharge frequency increased (23/23) by more than 7 times in comparison with the background values.

NMDA Receptors of A5 Area in the Regulation of Blood Pressure and Respiratory Activity during Hypoxia in Rats.

In narcotized (40 mg/kg sodium ethaminal intraperitoneally) spontaneously breathing albino rats, experimental short-term hypoxia induced BP drop and increased phrenic nerve firing rate. Unilateral microinjection of a selective NMDA receptor blocker ketamine hydrochloride (50 nl; 4 mM) into A5 area did not affect BP and phrenic nerve fi ring rate. However, against the background of preliminary NMDA receptor blockage, hypoxia more markedly stimulated rhythmic activity of the respiratory center and hypotensive response.

Role of NMDA- and non-NMDA subtypes of glutamate receptors in A5 neuronal structures in the regulation of respiration and circulation during thermal nociceptive stimulation in rats.

In narcotized albino rats, thermal nociceptive stimulation elevated systemic blood pressure and increased the frequency of respiratory rhythm generation. Unilateral microinjection of ketamine hydrochloride, a selective blocker for NMDA receptors, into A5 region did not change the baseline parameters of multineuronal activity in the phrenic nerve and systemic blood pressure. Under conditions of NMDA-receptor blockade, thermal nociceptive stimulation evoked more pronounced respiratory response (in comparison to that observed before ketamine treatment), but induced smaller blood pressure rise.

Control of respiratory and hypotensive response during hypoxic chemoreflex by A5 region neurons in rats.

The responses of A5 region neurons, the phrenic nerve, and systemic blood pressure to short-term hypoxia were examined in rats under conditions of spontaneous respiration. Tonic and respiration-modulated neurons increasing their discharge activity during hypoxia were identified. This hypoxia-induced response was more pronounced in the neurons with baseline discharge rate of 0.

Nitric oxide in the A5 region modulates reaction of the respiratory center and blood pressure to hypoxia in rats.

Hypoxia was followed by more pronounced activation of the respiratory center and pronounced hypotensive response after unilateral injection of nitric oxide synthase blocker L-NAME into the A5 region. Microinjection of exogenous nitric oxide donor sodium nitroprusside into the A5 region abolished the effect of L-NAME on hypoxia-induced changes in activity of the respiratory center and blood pressure. Bilateral transection of the vagal and sinocarotid nerves suppressed the response of the respiratory center to hypoxia.