C1 neurons excite locus coeruleus and A5 noradrenergic neurons along with sympathetic outflow in rats.

C1 neurons activate sympathetic tone and stimulate the hypothalamic­pituitary­adrenal axis in circumstances such as pain, hypoxia or hypotension. They also innervate pontine noradrenergic cell groups, including the locus coeruleus (LC) and A5. Activation of C1 neurons reportedly inhibits LC neurons; however, because these neurons are glutamatergic and have excitatory effects elsewhere, we re-examined the effect of C1 activation on pontine noradrenergic neurons (LC and A5) using a more selective method. Using a lentivirus that expresses channelrhodopsin2 (ChR2) under the control of the artificial promoter PRSx8, we restricted ChR2 expression to C1 neurons (67%), retrotrapezoid nucleus neurons (20%) and cholinergic neurons (13%). The LC contained ChR2-positive terminals that formed asymmetric synapses and were immunoreactive for vesicular glutamate transporter type 2. Low-frequency photostimulation of ChR2-expressing neurons activated LC (38 of 65; 58%) and A5 neurons (11 of 16; 69%) and sympathetic nerve discharge. Locus coeruleus and A5 inhibition was not seen unless preceded by excitation. Locus coeruleus activation was eliminated by intracerebroventricular kynurenic acid. Stimulation of ChR2-expressing neurons at 20 Hz produced modest increases in LC and A5 neuronal discharge. In additional rats, the retrotrapezoid nucleus region was destroyed with substance P­saporin prior to lentivirus injection into the rostral ventrolateral medulla, increasing the proportion of C1 ChR2-expressing neurons (83%). Photostimulation in these rats activated the same proportion of LC and A5 neurons as in control rats but produced no effect on sympathetic nerve discharge owing to the destruction of bulbospinal C1 neurons. In conclusion, low-frequency stimulation of C1 neurons activates pontine noradrenergic neurons and sympathetic nerve discharge, possibly via the release of glutamate from monosynaptic C1 inputs.

[The sympathetic baroreflex is enhanced during emotional stress in rats]. / Sensibilisation du baroréflexe sympathique durant le stress émotionnel chez le rat.

The sympathetic component of the baroreceptor reflex might play a major role in limiting hypertensive effects of emotional stress. However, it has been suggested that this type of stress inhibits or even suppresses the baroreflex. The aim of the present study was, therefore, to determine the effects of emotional stress on the sympathetic baroreflex in conscious rats. In 11 Sprague Dawley rats, arterial pressure (AP) and renal sympathetic nerve activity (RSNA) were recorded simultaneously before and during exposure to a mild emotional stressor (jet of air). Under both conditions, baroreflex function curves relating AP and RSNA were constructed by fitting a sigmoid function to RSNA and AP measured during sequential nitroprusside and phenylephrine administrations. Air-jet stress significantly (P<0.01) increased the mean levels of AP (from 112 +/- 2 to 124 +/- 2 mmHg), heart rate (from 381 +/- 10 to 438 +/- 18 beats/min) and RSNA (from 0.80 +/- 0.14 to 1.49 +/- 0.23 microV). Sympathetic baroreflex function curves were shifted to a higher level of AP, and this was accompanied by an increase (P<0.01) in the maximum gain (from 9.0 +/- 1.3 to 16.2 +/- 2.1 normalized units (NU)/mmHg). The latter effect was a consequence of an increase (P<0.01) in the maximal range of variations of RSNA (from 285 +/- 33 to 619 +/- 59 NU). Finally, the operating range of the sympathetic baroreflex, which corresponds to the AP range over which the reflex is able to alter RSNA, was increased (from 34 +/- 2 to 41 +/- 3 mmHg; P<0.01). In conclusion, the baroreflex control of RSNA is sensitized and operates over a larger range during emotional stress in rats, which suggests that renal vascular tone, and possibly AP, are very efficiently controlled by the sympathetic nervous system under this condition.