AIMTo explore the cerebral cortex mechanism of visceral nociceptive sensation and its characteristics on the cell level, we investigated the membrane electrical properties of 176 stimulus-relative neurons of greater splanchnic nerve (GSN) in anterior cingulate gyrus (ACG) of 20 adult healthy cats.

METHODSWe used intracellular recording techniques of glass microelectrode and injected polarizing current into the neurons in ACG.

RESULTSAmong 176 neurons, 148 were visceral nociceptive neurons (VNNs) and 28 non-visceral nociceptive neurons (NVNNs). The membrane resistance (Rm), time constant (tau), membrane capacity (Cm), and the I-V curve of both VNNs and NVNNs in ACG were significantly different. The discharge frequency and amplitude of both VNNs and NVNNs produced by injecting depolarized current were different, too.

CONCLUSIONThe results suggest that structure of cell membrane, volume of the soma, and other aspects of morphology between VNNs and NVNNs in ACG may have significant differences. The results also might provide progressively experimental evidence for specific theory of pain sensation.

Animals ; Cats ; Gyrus Cinguli ; cytology ; physiology ; Membrane Potentials ; Nociceptors ; physiology ; Splanchnic Nerves ; physiology ; Visceral Afferents ; physiology

Differences in intravaginal ejaculation latency reflect normal biological variation, but the causes are poorly understood. Here, we investigated whether variation in ejaculation latency in an experimental rat model is related to altered sympathetic nervous system (SNS) activity and expression of N-methyl-D-aspartic acid (NMDA) receptors in the paraventricular nucleus of the hypothalamus (PVN). Male rats were classified as "sluggish," "normal," and "rapid" ejaculators on the basis of ejaculation frequency during copulatory behavioral testing. The lumbar splanchnic nerve activity baselines in these groups were not significantly different at 1460 ± 480 mV, 1660 ± 600 mV, and 1680 ± 490 mV, respectively (P = 0.71). However, SNS sensitivity was remarkably different between the groups (P < 0.01), being 28.9% ± 8.1% in "sluggish," 48.4% ± 7.5% in "normal," and 88.7% ± 7.4% in "rapid" groups. Compared with "normal" ejaculators, the percentage of neurons expressing NMDA receptors in the PVN of "rapid" ejaculators was significantly higher, whereas it was significantly lower in "sluggish" ejaculators (P = 0.01). In addition, there was a positive correlation between the expression of NMDA receptors in the PVN and SNS sensitivity (r = 0.876, P = 0.02). This study shows that intravaginal ejaculatory latency is associated with SNS activity and is mediated by NMDA receptors in the PVN.
Animals ; Copulation ; Ejaculation/physiology* ; Female ; Male ; Neurons/physiology* ; Paraventricular Hypothalamic Nucleus/physiology* ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism* ; Sexual Behavior, Animal/physiology* ; Splanchnic Nerves/physiology* ; Sympathetic Nervous System/physiology*

AIMTo study the effect of atropine, muscarinic cholinergic antagonist, on the central analgesic action of melatonin (MT) and to explore the mechanism of MT analgesia.

METHODSAs an indicator of visceral pain, the unit discharges of the neurons in the posterior group of thalamic nuclei (PO) were caused by stimulating the great splanchnic nerve (GSN) of the cat. The cranial stereotaxic and extracellular glass microelectrode record technique were used. The drugs were given through the intra-cranial-ventricle (icv).

RESULTS0.1% MT (10 micrograms.kg-1, icv) was shown to inhibit the unit discharge of the neurons in PO of the cat, whether the long latency or the short latency, which was evoked by stimulating GSN. The inhibition of 0.1% MT (10 micrograms.kg-1, icv) on the short latency discharge of neurons in PO was antagonized by 0.1% atropine (20 micrograms, icv). However, 0.1% atropine (20 micrograms, icv) did not show antagonistic effect on the inhibition of 0.1% morphine (5 micrograms, icv) at the same latency.

CONCLUSIONMT exhibited central analgesic action with mechanism different from morphine. It was suggested that the cholinergic system may be involved in analgesic process of MT.

Analgesics ; administration & dosage ; pharmacology ; Animals ; Atropine ; pharmacology ; Cats ; Electric Stimulation ; Evoked Potentials ; drug effects ; Female ; Injections, Intraventricular ; Male ; Melatonin ; administration & dosage ; pharmacology ; Morphine ; pharmacology ; Muscarinic Antagonists ; pharmacology ; Neurons ; physiology ; Splanchnic Nerves ; physiology ; Thalamic Nuclei ; drug effects ; physiology