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Experiments were done on urethane anesthetized adult rabbits. Long-train electrical stimulation was delivered to the Bötzinger complex (Böt.C) to observe the changes in the peak amplitude of integrated phrenic nerve activity. Then, a long-train electrical stimulation was delivered to the locus coeruleus (LC) or monosodium glutamate was microinjected into the LC . Within a certain period of time, another long-train electrical stimulation was delivered to the Böt.C to observe the responses of phrenic nerve activity. We investigated whether the LC could modulate the inspiratory inhibition induced by electrical stimulation of the Böt.C. The results are as follows: (1) Within a certain period of time after a long-train electrical stimulation applied at the LC, the inspiratory inhibition produced by electrical stimulation at the Böt.C was significantly attenuated. Comparing with the control stimulation that was only delivered at Böt.C without pre-stimulation of the LC, the inspiratory inhibition was decreased by (28.78+/-19.49)%. (2) Similarly, after chemical stimulation of the LC with microinjection of monosodium glutamate, the inspiratory inhibition produced by electrical stimulation of Böt.C was also significantly attenuated [decreased by (19.18+/-8.06)%]. The results obtained suggest that the LC plays a role in the modulation of the inspiratory inhibition of Böt.C stimulation.

The effects of microinjection of sodium glutamate and glycine into ventrolateral nucleus of tractus solitarius (VLNTS) on the discharges of phrenic nerve were observed on 40 anaesthetized, vagotomized, paralyzed and artificially ventilated rabbits. The results were as follows: Phrenic nerve discharges were increased, inspiratory duration prolonged, expiratory duration shortened and respiratory frequency not changed by microinjection of sodium glutamate into VLNTS. While by microinjection of glycine, phrenic nerve discharges were decreased, even abolished, inspiratory duration shortened, expiratory duration irregularly prolonged and respiratory frequency decreased. The above results show that VLNTS exert important effects on the genesis of respiratory rhythm.

On pentobarbital anesthetized rabbits, a three-wavelet compound potential to cervical vagal afferent stimulation was recorded in ipsilateral nucleus tractus solitarius (NTS). The latency of the three wavelets (P1, P2 and P3) was 6.8 +/- 0.6 ms (P1), 25.8 +/- 4.2 ms (P2) and 89.1 +/- 2.7 ms (P3) respectively, which might represent postsynaptic activity of different kinds of vagal afferent fibers. Microinjection of glutamate into ipsilateral locus coeruleus (LC) decreased the amplitude of P2 and P3 significantly. Electrical stimulation of LC could activate 111 units in ipsilateral NTS with a mean latency of 6.3 +/- 1.4 ms. Of the 169 units in the NTS to vagal afferent stimulation, 90 units also responded to LC stimulation. 39 (43.3%) of the ninety, units shows similar response to both stimuli, while the rest show different response. Of the 25 units which showed excitatory response to both LC and vagal stimulation, but when LC stimulation was followed by vagus stimulation, the latter's response was either markedly suppressed (14 units) or completely inhibited (11 units). These results showed that activation of LC exerts an inhibitory effect on the responses of the NTS to vagal afferent stimulation.

The effect of sodium glutamate (Glu) on plasma sialic acid (SA) level was studied by means of microinjection into the nucleus arcuatus (ARC) and ultraviolet spectrophotometry. The results indicate: (1) The plasma SA level was significantly decreased after microinjection of Glu into the ARC (P < 0.01). With increasing Glu concentration, the onset of the decrease occurred earlier. (2) When Glu was microinjected into ARC after intraventricular injection of apomorphine, the plasma SA level was significantly decreased (P < 0.01) and the time required to cause the decrease was shortened. (3) When Glu was microinjected into ARC after intraventricular injection of spiperone, no change was found in the plasma SA level (P > 0.05). The above results suggest that the mechanism underlying the decrease of plasma SA level is probably related to modulated dopamine (DA) release of hypothalamic dopaminergic neurons by DA-D2 receptor.

Experiments were performed on 66 anaesthetized, vagotomized, paralyzed and artificially ventilated rabbits. The effects of microinjection sodium glutamate and glycine into ventrolateral nucleus of tractus solitarius (VLNTS) on hypothalamic arcuatus nucleus evoked potentials were observed. The main results obtained were as follows: (1) Phrenic nerve discharges were increased and the amplitude of P2 and N2 waves of arcuatus nucleus evoked potentials were decreased by microinjection of sodium glutamate into VLNTS. Phrenic nerve discharges were decreased and the amplitude of P2 and N2 waves of arcuatus nucleus evoked potentials were increased by microinjection of glycine into VLNTS. (2) After intravenous injection of naloxone, the phrenic nerve discharges could still be excited by microinjection of sodium glutamate as before, but the effects on the amplitude of P2 and N2 waves of arcuatus nucleus evoked potentials, unlike that of sodium glutamate, were reversed. The results suggest that the excitatory action of respiratory neurons in the VILTS may affect on the sensory function of arcuatus nucleus. The mechanism involved was discussed.

In the present investigation, it was found that the number of beta-endorphin (beta-END)-immunoreactive neurons of hypothalamic arcuate nucleus (ARC) in MSG-treated rats decreased by 60.7%. No significant differences in the baseline pain threshold and the baseline corticosterone (CS) level were observed between the MSG-treated group and the control group. After electrical foot shock for 30 min, the analgesia effect was decreased significantly (P < 0.001) in MSG-treated rats, while the CS levels of both MSG-treated rats and control rats were increased remarked (P < 0.01). The results suggest that the beta-END neurons of ARC were involved in analgesia, but not in CS reaction during stress.

The effects of electrical stimulation to the nucleus termination nervi trigemini (NTV) on the activities of genioglossus were studied in 35 rabbits anesthetized with urethane. Electrical stimulation of NTV could cause facilitatory response of genioglossal muscle markedly. Monosodium glutamate microinjected into NTV also produced significant increase of genioglossal activities. The latency of genioglossal response to electrical stimulation of dorsal or ventral part of NTV were respectively 5.9 +/- 0.7 ms and 3.0 +/- 0.4 ms. When the nucleus hypoglossus was stimulated, the latency was 2.2 +/- 0.2 ms. These results suggested that the excitation of NTV could enhance the genioglossal activities so that the resistance of upper airway might be decreased.

Experiments were performed on 55 urethane anesthetized and flaxedil immobilized rabbits under artificial respiration. Injection of L-Glutamate into the locus coeruleus area led to a marked augmentation of respiration. This effect of L-Glutamate could be significantly attenuated or reversed by a previous injection of prazosin, yohimbine and propranolol into the NTS area. These results indicate that the neurons in the locus coeruleus are involved in the regulation of the respiration as a result of mediation by alpha and beta receptors in the NTS area.

The role of hypothalamic paraventricular nucleus (PVH) in acupuncture analgesia was investigated by local brain stimulation and cauterization. The results showed that electrical or L-glutamate sodium stimulation of PVH could enhance the effect of analgesia of Zusanli acupuncture, both in a dose dependent manner. Electrical cauterization of PVH decreased the effect of acupuncture analgesia, while removal of pituitary had no effect on the enhancing effect by L-glutamate sodium injection.

Hypertension was induced by chronic foot-shock and noise stress in adult male Sprague-Dawley rats. Microinjection of 0.3 microliters (150 mmol) sodium glutamate (Glu) into the nucleus arcuatus (ARC) elicited a significant depressor effect in rats with chronic stress-induced hypertension. The depressor effect induced by excitation of ARC neurons was attenuated significantly by microinjection of 0.3 microliters beta-endorphin antiserum (beta-EPAS) into the dorso-medial periaqueductal gray (PAG) or 0.1 microliters into the area of locus coeruleus (LC) due to blockage of beta-endorphinergic fibres from ARC to PAG or LC.

Experiments were performed on 45 urethane-anesthetized, vagotomized and spontaneously breathing rabbits. By electrical stimulation of or microinjection of L-glutamate into nucleus raphe obscurus (NRO), the following results were observed: (1) A long stimulus train (50-200 microA, 100Hz, 4-6 s) delivered to NRO resulted in a decrease in integrated phrenic amplitude (IPA) or complete cessation of phrenic nerve discharge. The decrease of IPA was dependent upon current intensity and frequency of stimulation. (2) Short train stimulation (100-200 microA, 50-100 Hz, 5-20 pulses) delivered to NRO during the inspiratory phase terminated this phase prematurely, i.e., inspiratory off-switch (IO-S). The IO-S time varied according to the current intensity and the delivery time of stimulation in the inspiratory phase. (3) Microinjection of L-glutamate (1 mol/L, 1 microliter) into NRO caused a transient depression of phrenic nerve activity followed by a shortening of inspiratory time (Ti) and a lengthening of expiratory time (Te).

Experiments were done on urethane anesthetized, tubocurarine immobilized and artificially ventilated rats and the following results were observed: (1) Injection of sodium L-glutamate (Glu) into locus coeruleus (LC) could evoke a pressor response, but heart rate was not significantly affected; while depressor and bradycardia effects were observed when injecting into closely adjacent areas. (2) The LC-pressor response decreased after a brain transection caudal to nucleus paraventricularis was made but remained unchanged if the transection was rostral to the nucleus; The LC-pressor response could also be attenuated by preinjection of phentolamine propranolol or atropine respectively into the rostral ventrolateral medulla (RVL). The above results suggest that LC-pressor response is not only mediated by RVL, but also by nucleus paraventricularis.

In urethane-anesthetized, tubocurarine-immobilized artificially ventilated rats, the following results were observed: (1) Sodium glutamate (Glu) microinjection into the caudal ventrolateral part of the periaqueductal gray matter (PAG) produced a marked rise in blood pressure. (2) This effect was attenuated by phentolamine or propranolol but not by atropine, injected bilaterally into the rostral ventrolateral medulla (RVL), indicating that this pressor response is mediated by RVL and alpha- and beta-receptors. (3) Propranolol-injection into RVL also attenuated the pressor response induced by electrical stimulation of the nucleus parabrachialis ventralis (NPV), while the pressor response initiated by injecting Glu into the same area (NPV) was not affected. Taken together with the previous findings that phentolamine blocks the pressor response produced by NPV-electrostimulation, but not of Glu-injection into NPV, the above results suggest that neurons in the caudal ventrolateral part of PAG may either send axons passing through the nucleus parabrachialis (NPB) and directly acting upon beta-receptors in RVL, or relay in NPB and act indirectly on alpha-receptors in RVL to produce the pressor response.