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Spontaneous firing of suprachiasmatic nucleus (SCN) neurons and the effect of melatonin (MEL) were examined in hypothalamic slices made from pinealectomized rats or from the rats exposed to constant light. The results are as follows. (1) Under normal light cycle (light dark=12 12), SCN neurons displayed a circadian rhythm in spontaneous discharges. A peak about 8.3 Hz was presented at CT (circadian time) 6 8 and a trough about 3.8 Hz at CT18 20. The circadian rhythm persisted after pinealectomy, but disappeared after constant light exposure. (2) The response of SCN neurons to MEL was mainly inhibitory. Under normal light exposure, the inhibitory proportion was higher during the subjective day with the largest proportion of about 42% at CT8 10, and was lower during the subjective night with the largest proportion of about 26% at CT22 24. Under both constant light exposure and pinealectomy, the circadian rhythm of the response of SCN neurons to MEL disappeared. (3) The inhibitory effect of MEL on spontaneous discharges of SCN neurons was blocked by ML-1 receptor antagonist luzindole, but not by ML-2 receptor antagonist prazosin. The above results suggest that pineal gland, as a regulator of the organization of circadian rhythm, regulates the circadian rhythm of SCN neurons at two responsive time windows (CT8 10 and CT22 24) through high affinity ML-1 receptors in SCN.

Aim: To study the role of interleukin-2 (IL-2) and mediobasal hypothalamus (MBH) in analgesia produced by Coriolus versicolor polysaccharide peptide (PSP)., Methods: The IL-2 antiserum was injected i.c.v. or i.p. and the MBH was destroyed electrolytically., Results: PSP i.g. 1 g.kg-1.d-1 for 6 d increased the pain threshold in tail stimulation-vocalization test in rats. This PSP-produced analgesia was blocked by i.c.v., but not i.p., IL-2 antiserum and disappeared after electrolytic lesion of MBH., Conclusion: The analgesia produced by PSP is mediated by IL-2 which is activated by PSP and interacts with IL-2 receptors in the MBH.

The effect of dorsal raphe nucleus (DR) stimulation on the unit discharge of suprachiasmatic nucleus (SCN) neurons was studied and analyzed pharmacologically in the Wistar rats. Experimental results showed that DR stimulation could significantly inhibit the light-induced discharge of SCN neurons. Pharmacologically, this inhibition could be enhanced by monoamine oxidase inhibitor pargyline, attenuated by 5-hydroxytryptamine (5-HT) synthesis inhibitor parachlorophenylalanine and blocked by 5-HT receptor antagonist cyproheptadine. It was suggested that the inhibitory effect of DR stimulation on the light-sensitive SCN neuron discharge might be mediated by 5-HT.

Aim: The nervous mechanism of the immune potentiating effect of Coriolus versicolor polysaccharides peptides (PSP) was studied in Wistar rats., Methods: The unit discharge of the mediobasal hypothalamus (MBH) neurons was recorded extracellularly and the lymphocyte proliferation was measured., Results: PSP 1 g.kg-1 ig for 5 d increased the T-lymphocytes and promoted T-lymphocyte proliferation in spleen and peripheral blood. This promoting effect of PSP was blocked by MBH lesion. PSP increased the discharge frequency of MBH neurons, but no increase in discharge frequency was observed after treatment of PSP plus immune inhibitor, cyclosporin A., Conclusion: MBH is involved in the immune-potentiating effect of PSP.

The effects of hypothalamic arcuate nucleus (ARC) or anterior lobe of pituitary (AL) stimulation on the nociceptive responses of thalamic parafascicular (Pf) neurons were studied in rats with electrophysiological technique. The results showed that ARC stimulation could inhibit the nociceptive discharges of Pf neurons, namely, the immediate inhibition because of its very short latency and duration. AL stimulation could also inhibit the nociceptive discharges of Pf neurons, but this inhibition was a delayed one because of its longer latency and duration. Hypophysectomy diminished the immediate inhibition due to ARC stimulation, while ARC lesion diminished the delayed inhibition due to AL stimulation. Both kinds of inhibition were blocked by dexamethasone pretreatment. The above results suggest that neuroendocrine relationship between ARC and AL is involved in pain modulation.

Relationship between pituitary gland and hypothalamic arcuate nucleus (ARC) in the modulation of pain threshold was investigated in Wistar rats with method of focal lesion and stimulation of pituitary gland. Experimental results indicated that electrolytic lesion of the pituitary intermediate and anterior lobes resulted in a decrease of pain threshold and disappearance of the analgesia immediately produced by ARC stimulation. Stimulation of the same area of pituitary gland could induce a delayed analgesia, which could be blocked by ARC lesion.

Rats with adjuvant arthritis were used as an animal model of pathological pain in this experiment and the nociceptive response of neurons in parafascicular nucleus (Pf) were recorded and intracerebroventricular (icv) injection of naloxone and atropine was adopted in order to investigate the effect of electroacupuncture (EA) and to analyze the neurotransmitters involved. The main results were as follows: (1) The nociceptive response of the majority of Pf neurons (29/34) in arthritic rats was significantly inhibited by EA at acupoints of "Zusanli" and "Sanyinjiao"; (2) The inhibitory effect of EA was reversed in 12/13 units by icv injection of naloxone (4 micrograms/10 microliters); (3) The inhibitory effect of EA was also reversed in 11/12 units by icv injection of atropine (5 micrograms/10 microliters) (4) The spontaneous unit discharge of Pf neurons in arthritic rats was increased after icv injection of naloxone or atropine. Experimental results suggest that EA could have an inhibitory effect on the nociceptive response of Pf neurons in arthritic rats, which might be mediated by opioid system and cholinergic system in the brain, and that opioid system and cholinergic system might have a tonic inhibitory effect on the spontaneous unit discharge of Pf neurons in arthritic rats.

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.

To induce arthritis, the adjuvant with heat-killed Mycobacterium tuberculosis was injected into the ankle joint in rats. Local redness, swelling, hotness, pain, and motor dysfunction of the inflamed joint (as well as mental dullness) were observed 48 h after inoculation. At this time, the maximal binding capacity (Bmax) of muscarinic receptors in limbic system was increased, while the dissociation constant (Kd) was unchanged. Injection of morphine (5 mg.kg-1) 3 times within 48 h after the inoculation resulted in a decrease of Bmax and an increase of Kd of M-receptors, together with diminution of pain and disappearance of dullness.

It has been demonstrated in animal model of somatic pain that hypothalamic paraventricular nucleus (PVN) participates in acupuncture analgesia, probably by mediation of vasopressin release. The role of PVN in acupuncture analgesia for experimental visceral pain in rats was further investigated in the present study. Experimental results demonstrated that electroacupuncture could inhibit the writhing response, produced by intraperitoneal injection of antimonium potassium tartrate and this inhibitory effect could be enhanced by electrical stimulation of PVN, but decreased by electrolytical lesion of PVN, intracerebroventricular injection of vasopressin antiserum (14 microliters) or the vasopressin antagonist, d(CH2)5Tyr(Me)-AVP (500 ng/5 microliters). Intraperitoneal administration of the latter drug (10 micrograms/kg), however, was ineffective. The above experimental results suggest that vasopressinergic neurons in PVN also participate in the inhibition of visceral pain by electroacupuncture.

This study was undertaken to evaluate the analgesic effect of paraventricular nucleus (PVN) stimulation with tail stimulation-vocalization test. The mechanism of this analgesia was analysed with nuclear lesion and microinjection technique. The main results were as follows: (1) Electrical stimulation of the PVN could significantly enhance the pain threshold and increase the content of AVP in brainstem measured by radioimmunoassay. (2) Solitary tract nucleus (STN) lesion could eliminate the analgesic effect induced by PVN stimulation. (3) Intranuclear microinjection of AVP-antagonist and AVP-antiserum into the STN could block the analgesic effect of PVN stimulation. (4) Intranuclear microinjection of AVP into the STN could mimick the analgesic effect similar to that of PVN stimulation. These results suggest that electrical stimulation of the PVN could produce an analgesic effect. This effect might be mediated by the activation of VP-ergic neurons in PVN and upon releasing VP from the descending fibers, the activities of neurons in the STN are influenced.

Previous studies have demonstrated that locus coeruleus (LC)-noradrenergic neuronal system plays an important role in pain modulation and electroacupuncture (EA) analgesia. In the present experiment, the effect of LC stimulation and EA on nociceptive response of spinal dorsal horn neurons was investigated. The main results were: 1) LC stimulation and electroacupuncture produced a significant inhibitory effect on nociceptive response of dorsal horn neurons; 2) The inhibitory effect of LC stimulation was not affected by the lesion of nucleus raphe magnus or by the injection of naloxone; 3) These inhibitory effects of LC stimulation and electroacupuncture could be enhanced by alpha 2-agonist clonidine, and decreased slightly by alpha-antagonist phentolamine. These results suggest that the inhibitory effect of LC stimulation and electroacupuncture on the nociceptive response of dorsal horn neurons might be mediated by alpha 2-receptors.