The effect of calcitonin gene-related peptide (CGRP), substance P (SP) and electrical stimulation of the tooth on the intradental nerve activtiy (INA) was investigated in anesthetized cats. The INA was recorded from single pulp nerve units dissected from the inferior alveolar nerve under stereomicroscope. The INA elicited by 3 minute application of 4M NaCl in deep dentinal cavity was compared before and after stimulation at 10 minute intervals. The magnitude of INA was calculated as the total number of nerve impulses produced in given period, and the changes of INA are expressed as % of control INA. The results obtained were as follows. 1. 16 single pulp nerve units were classified as 14 $A{\delta}$-fibers (3.4~19.4m/sec) and 2-fibers (1.5~1.7m/sec) according to the conduction velocity. 2. 4M NaCl evoked an irregular bursts of spikes which continued until washing out. Isotonic saline did not affect INA to subsequent applications of the hypertonic NaCl solution (P>0.05). 3. Local application of CGRP ($200{\mu}g$/ml) in deep dentinal cavity reduced the INA induced by 4M NaCl in $A{\delta}$-fiber units (P<0.01) and some units of those responded to CGRP during application. 4. Local application of SP ($100{\mu}g$/ml) in deep dentinal cavity reduced the INA induced by 4M NaCl in AS-fiber units (p<0.05), but increased the INA in C-fiber unit coincided with large reduction of the INA of $A{\delta}$-fiber units. 5. Monopolar electrical stimulation applied to the crown at intensities high enough to excite C-fibers (12V, 5ms, 10Hz, 10~30min) decreased the INA in $A{\delta}$-fiber units (P<0.01) and systemic pretreatment with phenoxybenzamine (3mg/kg, i.v.) enhanced this inhibitory effect (P<0.01). On the contrary, electrical stimulation increased the INA in C-fiber unit.
Neurofascin, one of the members of L1CAM, has been known to have some important roles during the development of nerve fibers. In order to investigate the role of neurofascin associated with the myelination of peripheral nerves, the localization of neurofascin in myelinated rat sciatic nerve fibers was studied with the immuno-fluorescence and immune-electron microscopy and the results are as follows; 1. According to the myelination is going on, neurofascin localization was dramatically changed in the sciatic nerve fibers. 2. In the myelinated fibers, neurofascin was weakly localized along the axolemma at the node of Ranvier. 3. Neurofascin was also apparantly localized at the non-compact area of Schwann cell membrane such as paranodal loop, Schmidt-Lantermann incisure, inner & outer mesaxons in the myelinated fibers. From the above results, neurofascin is likely to have a role to sustain the ideal gap of apposing membranes of Schwann cell, so it may enable to materials transport in the myelin sheath.
Immunohistochemistry combined with electron microscopy was employed to investigate the distribution of substance P -immunoreactive(SP-IR) nerve fibers in the tracheal submucosal gland of cats. SP-IR nerve fibers were found to form network around the glands. Numerous varicosities were also detected within the basement membrane of the acini and secretory tubules. All the intraglandular varicosities showed close spatial contact with serous cells, mucous cells and myoepithelial cells. Our findings suggest that SP-induced mucus secretion from tracheal submucosal glands in cats may be caused not only by glandular contractile response of myoepithelial cells but also by direct stimulation to both serous and mucous cells.
Background: Phenol and alcohol have been used to ablate nerves to treat pain but are not specific for nerves and can damage surrounding soft tissue. Lidocaine at concentrations > 8% injected intrathecal in the animal model has been shown to be neurotoxic. Tests the hypothesis that 10% lidocaine is neurolytic after a peri-neural blockade in an ex vivo experiment on the canine sciatic nerve. Methods: Under ultrasound, one canine sciatic nerve was injected peri-neurally with 10 cc saline and another with 10 cc of 10% lidocaine. After 20 minutes, the sciatic nerve was dissected with gross inspection. A 3 cm segment was excised and preserved in 10% buffered formalin fixative solution. Both samples underwent progressive dehydration and infusion of paraffin after which they were placed on paraffin blocks. The sections were cut at $4{\mu}m$ and stained with hemoxylin and eosin. Microscopic review was performed by a pathologist from Henry Ford Hospital who was blinded to which experimental group each sample was in. Results: The lidocaine injected nerve demonstrated loss of gross architecture on visual inspection while the saline injected nerve did not. No gross changes were seen in the surrounding soft tissue seen in either group. The lidocaine injected sample showed basophilic degeneration with marked cytoplasmic vacuolation in the nerve fibers with separation of individual fibers and endoneurial edema. The saline injected sample showed normal neural tissue. Conclusions: Ten percent lidocaine causes rapid neurolytic changes with ultrasound guided peri-neural injection. The study was limited by only a single nerve being tested with acute exposure.
An immunocytochemical investigation has been carried out to localize serotoninimmunoreactive (5-HTi) neurons in suboesophageal ganglion of fifth instar lawn of cabbage worm Pieris rupae. The 285-HTi cell bodies were identified in the rind of suboesophaseal ganglion. The four 5-HTi cell bodies of them are 18rge in size (about 35 Um), while the remaining cell bodies are medium-sized (about 15 Uml. The 5-HTi nerve processes are abundantly located in central large neuropil, circumoesophageal connectives which join the suboesophaseal ganglion to the tritocerebrum of the brain, and connectives between the suboesophageal and the first thoracic ganglia. These results indicate that the 5-HTi nerve fibers, which constitute the central large neuropil, have structural connections with the above two connectives. Especially in central large neuropil, many 5-HTi nenre fibers form a large circular bundle, in which a 5-HTi nerve fiber bundle is crossing.
Bone resorptiion was predominate in compression site, bone formation in tension site of periodontal ligament during tooth movement. The biologic response at compressiion site was different from tension site. Thus the CGHP immuno-positive nerve fiber will respond differently to mechanical force according to the area( compression or tension site). The purpose of this study was to investigate this response of CGRP immune-positive nerve fiber in the periodontal ligament according to the duration of applied force and the area (compression or tension site) during experimental tooth movement. The experimental animals were 7 week old male rat (approximately 200 gm). The orthodontic force was applied mesially to the right maxillary molar using the Ni-Ti coil spring during 12hours, 1, 3, 7, and 120days. Immunohistochemical staining using antibody against CGRP was performed after sacrifice. The results were as follows. The CGRP immune-positive nerve bundle showed reduced immunoreactivity and nerve fibers reduced in density after application of orthodontic force for 12 hours and 1day. The CGRP immune-positive nerve fibers showed many thin branches at the apical periodontal ligament after application of force for 3 days as compared with normal. The tension site in the apical periodontal ligament showed more branches than the compression site. In 7 day group, the CGRP immune-positive nerve fibers increased in terms of the number and had many thin branches in the apical periodontal ligament. The tension site had more branches than the compression site. In 12 day group, the CGRP immune-positive nerve fibers showed similar distribution to normal control at compression site of apical periodontal ligament, but the fibers at the tension site increased in number. The CGRP immuno-positive nerve fibers showed more increased at tension site than compression site after application of orthodontic force. Therefore it seems to have some relation to the bone remodeling besides the local inflammatory process.
The aim of this study was to investigate the effect of herbal organic extracts on the pain response provoked by noxious stimuli on dental nerve and the peripheral nerve conduction. Cats (2-2.5Kg regardless of sex) that were chosen as experimental animals were classified into control group, Asiasari radix application group and Zingiberis rhizoma application group. They were anesthetized with ${\alpha}$-chloralose, then anterior belly of digastric muscle of both sides were exposed and wire electrodes were inserted for recording of Electromyogram (EMG). Cavities were prepared on canines until pulp of the teeth were exposed. And after the drugs solubilized for 2% and 4% concentration (W/V) in vehicle were applied, their effects were compared through the recording of EMG immediately after drug application, 30 minutes, 60 minutes, 120 minutes and 5 days after, respectively. And after both inferior alveolar nerves were exposed, 4% organic extracts of Zingiberis rhizoma and Asiasari radix were applied for 30 minutes then the change of jaw opening reflex provoked by noxious stimuli on pulpal nerves were observed immediately after washing out, at 30, 60 and 90 minutes after drug had been washed out. After saphenous nerve of both sides were exposed, one side of nerve was used for vehicle application and the other side was used for drug application for 30 minutes. Then conduction of action potential of A-${\delta}$ and C-fiders of saphenous nerves, which have changed with time, was recorded. With analysis of these records, the following results were obtained: 1. Organic extract of Zingiberis rhizoma (2% or 4% concentration) greatly suppressed EMG of digastric muscle provoked by noxious stimuli on pulpal nerve at five days after application, the suppressive: effect was greater than that of organic extract of Asiasari radix. 2. Organic extract of Asiasari radix (2% or 4% concentration) suppressed jaw opening reflex provoked by noxious stimuli on pulpal nerve, at 5 days after drug application. 3. Organic extract of Zingiberis rhizoma and Asiasari radix (immediately after 30 minutes application) suppressed neural conduction of A-${\delta}$ and C-fibers, the suppressive effect was greater on A-${\delta}$ fibers than on C-fibers. 4. Jaw opening reflex provoked by noxious stimuli on pulpal nerve in inferior alveolar nerve was greatly suppressed 30 minutes after drug application, this effect was greater by Zingiberis rhizoma than by Asiasari radix.
The arterial blood pressure response elicited by stimulating the peripheral afferent fibers of different groups and origins was studied in cats. Experimental animals were anesthetized with a-chloralose [60mg/kg] and artificially ventilated with a respirator. The lumbosacral spinal cord was exposed through a laminectomy and L7 ventral root was isolated. The sural, medial gastrocnemius and common peroneal nerves were also exposed in the hindlimb. The arterial blood pressure was monitored continuously while the exposed peripheral nerves and L7 ventral root were being stimulated. Then, spinal lesions were made on the dorsolateral sulcus area, dorsolateral funiculus and other areas at the thoracolumbar junction. The arterial blood pressure responses were compared before and after making spinal lesions. The following results were obtained. 1. The mean arterial blood pressure was elevated from 103*7.3 to 129*8, 1 [mean*S.E.] mmHg [p<0.001] during stimulation of the sural nerve with C-strength [1000T], 20Hz. Stimulation with Ad-strength, 1Hz resulted in the depression of the arterial pressure by 8 mmHg [p<0.01]. 2. Stimulation of the medial gastrocnemius nerve with Ad-strength did not elicit any significant change in arterial blood pressure. Stimulation with C-strength, 20 Hz induced a pressor response from 102*6.2 to 117*6.4 mmHg [p<0.01] while that with C-strength, 1Hz induced a depressor response from 104*6.1 to 93*4.9 mmHg [p<0.001]. 3. A pressor response by 56 [from 107*7 5 to 163*9.4] mmHg [p<0.001] was induced during stimulation of the common peroneal nerve with C-strength, 20Hz stimuli. Stimulation with A4-strength, 1Hz depressed the arterial blood pressure from 111~9.3 to 94*7.8 mmHg [P<0.005]. The activation of the ventral root afferent fibers with C-strength, 20 Hz stimuli induced a pressor response by 22 mmHg [from 115*9.4 to 137*8.6 mmHg] [p<0.001]. 4. The pressor response elicited during stimulation of the sural nerve was abolished by making lesions on the dorsolateral sulcus area bilaterally. With the medial gastrocnemius nerve, the pressor response had not been abolished completely by the dorsolateral sulcus lesions. The pressor response disappeared completely with addition of the bilateral dorsolateral funiculus lesions. 5. The depressor response induced by stimulation of the sciatic nerve with Ad-strength, 1Hz was decreased by making lesions on the dorsolateral funiculus. 6. From the above results it is concluded that the difference in the blood pressure responses to the activation of the muscular afferent and the cutaneous afferent fibers is responsible for the groups of afferent fibers and the spinal ascending pathways.
Among the various physiological factors that affect nerve conduction velocity (NCV), temperature is the most important. Because the influence of temperature is the most important source of error. It is known from animal experiments that conduction is eventually completely blocked at low temperatures, the myelinated A fibers being the first affected and the thin fibers of group C the last. Many studies showed that the NCV decreases linearly with lowering temperature within the physiological range. The distal motor latency increased by $0.2msec/^{\circ}C$ drop in temperature between $25^{\circ}C$and $35^{\circ}C$ in the median, ulnar and peroneal nerves. The temperature affect the neuromuscular transmission; The miniature endplate potential (MEPP) and endplate potential (EPP) are increase with increasing temperature. In myasthenia gravis, the reduction in the decremental response is observed following cooling. The lowering temperature make increase the amplitude of sensory compound action potential; make enlarge the surface area of compound muscle action potential with very little increase in amplitude; make diminish the fibrillation potential and increase the myotonia in needle electromyography (EMG). Because of these findings mentioned above, the skin temperature should be routinely monitored and controlled during nerve conduction tests and needle EMG and should be taken into account when interpreting the findings.
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.
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