• The Korean Journal of Physiology
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• v.24 no.2
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• pp.389-402
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• 1990

The physiological characteristics of the neurons receiving the ventral root afferent inputs were investigated in the cat. A total of 70 cells were identified in the lumbosacral spinal cord. All these cells responded only to the C-strength stimulation of the distal stump of cut ventral root and the estimated conduction velocities of the VRA fibers were not faster than 4 m/sec. The majority of them were silent in resting state. For 49 cells, their peripheral receptive fields were characterized. Among them, 25 cells were exclusively excited by VRA inputs, 8 were inhibited and the remaining cells recevied both excitatory and inhibitory VRA inputs. According to the response pattern to the mechanical stimuli applied to their receptive fields, only a fourth of them were typical high threshold cell, a sixth, wide dynamic range cells, while remainings were a rather complex cells. Most of the cells receiving VRA inputs, received only the A ${\delta}-peripheral$ nerve inputs. Intravenous injection of morphine decreased the response of spinal cells to the VRA activation. The responses were abolished completely by counter irritation to the common peroneal nerve with C-strength-low frequency stimuli. These physiological properties of the spinal neurons receiving the VRA inputs are differ in some aspect from the spinal neurons receiving nociceptive inputs from the periphery, but still were consistent with the contention that VRA system might carry nociceptive informations arising from the spinal cord and/or neraby surrounding tissues.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.133-141
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• 1994

The discharge patterns and peripheral nerve inputs to cardiovascular neurons were investigated in rostral ventrolateral medulla (RVLM) and raphe nucleus of cats. The data from the two were compared to determine their roles in cardiovascular regulation and the endogenous analgesic system. Animals were anesthetized with ${\alpha}-chloralose$ and single cell activities were recorded by carbon-filament microelectrode and their relationships with cardiovascular activity were analyzed. In RVLM area, a total of thirty-three cells were identified as cardiovascular neurons. During one cardiac cycle, the mean discharge rate of the neurons was $1.96{\pm}0.29$ and the peak activity was observed 45 ms after the systolic peak of arterial blood pressure. Thirteen cells could be activated antidromically by stimulation of the the $T_2$ intermediolateral nucleus. Forty-three raphe neurons were identified as cardiovascular neurons whose mean discharge rate during one cardiac cycle was $1.02{\pm}0.12$. None of these cells could be activated antidromically. Study of the interval time histogram of RVLM neurons revealed that the time to the first peak was $128{\pm}20.0\;ms$, being shorter than the period of a cardiac cycle. The same parameter found from the raphe neurons was $481{\pm}67.2\;ms$, which was much longer than the cardiac cycle length. Of seventeen RVLM neurons examined ten received only the peripheral $A{\delta}-afferent$ inputs, whereas six RVLM neurons received both $A{\delta}-$ and C-inputs; the remaining one cell received an inhibitory peripheral C-input. In contrast, nine of eleven raphe neurons were found to receive $A{\delta}-inputs$ only. We conclude that the main output of cardiovascular regulatory influences are mediated through the RVLM neurons. The cardiovascular neurons in the raphe nucleus appear to serve as interneurons transferring cardiovascular afferent information to the raphespinal neurons mediating the endogenous analgesic mechanisms.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.3
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• pp.143-147
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• 2005

Following peripheral nerve injury, excessive nociceptive inputs result in diverse physiological alterations in the spinal cord substantia gelatinosa (SG), lamina II of the dorsal horn. Here, I report the alterations of excitatory or inhibitory transmission in the SG of a rat model for neuropathic pain ('spared nerve injury'). Results from whole-cell recordings of SG neurons show that the number of distinct primary afferent fibers, identified by graded intensity of stimulation, is increased at 2 weeks after spared nerve injury. In addition, short-term depression, recognized by paired-pulse ratio of excitatory postsynaptic currents, is significantly increased, indicating the increase of glutamate release probability at primary afferent terminals. The peripheral nerve injury also increases the amplitude, but not the frequency, of spontaneous inhibitory postsynaptic currents. These data support the hypothesis that peripheral nerve injury modifies spinal pain conduction and modulation systems to develop neuropathic pain.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.5
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• pp.281-288
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• 2004

The present study was undertaken to confirm whether melittin, a major constituent of whole bee venom (WBV), had the ability to produce the same nociceptive responses as those induced by WBV. In the behavioral experiment, changes in mechanical threshold, flinching behaviors and paw thickness (edema) were measured after intraplantar (i.pl.) injection of WBV (0.1 mg & 0.3 mg/paw) and melittin (0.05 mg & 0.15 mg/paw), and intrathecal (i.t.) injection of melittin $(6{\mu}g)$. Also studied were the effects of i.p. (2 mg & 4 mg/kg), i.t. $(0.2{\mu}g\;&\;0.4{\mu}g)$ or i.pl. (0.3 mg) administration of morphine on melittin-induced pain responses. I.pl. injection of melittin at half the dosage of WBV strongly reduced mechanical threshold, and increased flinchings and paw thickness to a similar extent as those induced by WBV. Melittin- and WBV-induced flinchings and changes in mechanical threshold were dose- dependent and had a rapid onset. Paw thickness increased maximally about 1 hr after melittin and WBV treatment. Time-courses of nociceptive responses induced by melittin and WBV were very similar. Melittin-induced decreases in mechanical threshold and flinchings were suppressed by i.p., i.t. or i.pl. injection of morphine. I.t. administration of melittin $(6{\mu}g)$ reduced mechanical threshold of peripheral receptive field and induced flinching behaviors, but did not cause any increase in paw thickness. In the electrophysiological study, i.pl. injection of melittin increased discharge rates of dorsal horn neurons only with C fiber inputs from the peripheral receptive field, which were almost completely blocked by topical application of lidocaine to the sciatic nerve. These findings suggest that pain behaviors induced by WBV are mediated by melittin-induced activation of C afferent fiber, that the melittin-induced pain model is a very useful model for the study of pain, and that melittin-induced nociceptive responses are sensitive to the widely used analgesics, morphine.