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PubMed1984

Evidence that the neurotrophic actions of alpha-MSH may derive from its ability to mimick the actions of a peptide formed in degenerating nerve stumps.

The ability of alpha-MSH to facilitate the recovery of sensorimotor nerve function following crush lesion is restricted to a critical period following such a lesion. This period coincided with the initiation of sprouting and the disappearance of the 150 kD neurofilament protein from the degenerating distal stump of the nerve. Degenerating nerve contains a factor that is active in a bioassay system for MSH. This factor could not be detected in control nerves. The hypothesis is forwarded that a neurotrophic factor known to be present in degenerating nerve stumps is an alpha-MSH-like peptide formed by the breakdown of the 150 kD neurofilament protein.

Animals↗
PubMed2002

Function and regulation of endothelin-1 and its receptors in salt sensitive hypertension induced by sensory nerve degeneration.

To determine the role of endothelin-1 (ET-1) and its receptors in salt-sensitive hypertension induced by sensory nerve degeneration, selective ET(A) antagonist (ABT-627) and ET(B) antagonist (A-192621) were used. Newborn Wistar rats were given vehicle or 50 mg/kg capsaicin subcutaneously on the first and second days of life. After the weaning period, male rats were divided into eight groups, and subjected to the following treatments for 2 weeks: control + normal salt diet (Con+NS, 0.5%), control + high salt diet (Con+HS, 4%), control + high salt diet + ABT-627 (Con+HS+ABT-627), control + high salt diet + A-192621 (Con+HS+A-192621), capsaicin + normal salt diet (Cap+NS), capsaicin + high salt diet (Cap+HS), capsaicin + high salt diet + ABT-627 (Cap+HS+ABT-627), capsaicin + high salt diet + A-192621 (Cap+HS+A-192621). Both ABT-627 (5 mg/kg/d) and A-192621 (30 mg/kg/d) were given by oral gavage twice a day. Mean arterial pressure (MAP, mm Hg) was higher in Con+HS+A-192621 (141 +/-11) than in Con+NS (94 +/- 10), Con+HS (95 +/- 5), and Con+HS+ABT-627 (97 +/- 6) (P<0.05). MAP was also higher in Cap+HS (152 +/- 6) and Cap+HS+A-192621 (180 +/- 7) than in Cap+NS (99 +/- 3) and Cap+HS+ABT-627 (104 +/- 5) (P<0.05), and it was higher in Cap+HS+A-192621 than in Cap+HS (P<0.05). Enzyme immunometric assay showed that ET-1 plasma concentration (pg/mL) was higher in Con+HS+A-192621 (7.59 +/- 0.78) than in Con+NS (2.68 +/- 0.56), Con+HS (2.50 +/- 0.92), and Con+HS+ABT-627 (3.54 +/- 0.79) (P<0.05). ET-1 plasma concentration was also higher in Cap+HS (8.95 +/-.16), Cap+HS+ABT-627 (9.82 +/- 1.22) and Cap+HS+A-192621 (10.97 +/- 0.57) than in Cap+NS (3.06 +/- 0.73) (P<0.05). We conclude that blockade of the ET(A) receptor prevents the development of salt sensitive hypertension induced by sensory nerve degeneration, indicating that activation of the ET(A) receptor by increased plasma ET-1 level contributes to elevation of blood pressure in this model. In contrast, blockade of the ET(B) receptor leads to an increase in blood pressure in both normal and sensory nerve degenerated rats fed a high salt diet. These results suggest that ET(B) plays an antihypertensive role in response to high salt intake under both normal and sensory nerve degenerated conditions.

Animals↗
PubMed1995

Elongation of wallerian degenerating nerve with a tissue expander: a functional, morphometrical, and immunohistochemical study.

The purpose of this experimental study was to investigate the usefulness and mechanism of the expansion of wallerian degenerating nerve. The study consisted of two experiments: Experiment I, functional and morphometrical analysis, and Experiment II, immunohistochemical analysis. In Experiment I, the rat nerve crush model was used to assess the effects of mechanical expansion of wallerian degenerating nerves on axonal regeneration. In Experiment II, the rat sciatic nerve cut model was used to investigate the effects of nerve expansion on Schwann cell events in wallerian degenerating nerves. In both experiments, nerve expansion was carried out between days 5 and 9 after nerve injury, using a rubber tissue expander placed beneath the sciatic nerve. In Experiment I, rats were divided into the following three groups according to the volume of saline injected: control group (nerves were crushed, without saline injection); 8-ml injection group; and 11-ml injection group. Functional recovery was assessed using the sciatic functional index until 54 days after nerve injury. Rats in all three groups showed good functional recovery, and the morphometrical analysis revealed no significant differences among the three groups. In Experiment II, anti-S-100 protein polyclonal antibody and anti-proliferating cell nuclear antigen monoclonal antibody were used to identify proliferating Schwann cells. Rats were divided into two groups: control group (nerves were cut, without expansion) and nerve expansion group. In the control group, proliferating Schwann cells were observed only between days 3 and 7. By contrast, these cells continued to be seen in the expanded nerves until day 16. These results suggest that the expansion of wallerian degenerating nerve does not have a deleterious effect on the axon-promoting property of Schwann cell tubes and that the expansion is dependent not only on the viscoelasticity of the nerves but also on enhanced proliferation of Schwann cells.

Animals↗
PubMed2001

Methylprednisolone ameliorates cochlear nerve degeneration following mechanical injury.

We investigated whether methylprednisolone sodium succinate can ameliorate cochlear nerve degeneration following compression injury on the cerebellopontine angle portion of the cochlear nerve, using a quantitative animal experimental model that we have developed recently. In this model, cochlear nerve degeneration after compression could be quantitatively evaluated, while cochlear ischemia induced by the compression carefully maintained below the critical limit that causes irreversible damage to the cochlea. Eleven rats were treated with methylprednisolone during the pre- and post-compression period. Two weeks after compression, the numbers of SGC were compared between the rats that received the compression without and with methylprednisolone treatment. Methylprednisolone treatment improved the survival of SGC following cochlear nerve injury statistically highly significantly in the basal turn where the traumatic stress had been less than in the other cochlear turns in our experimental setting. Although it was not statistically significant, greater survival was also observed in the other cochlear turns. The results of this experimental study indicated that at least a portion of injured cochlear nerve had been potentially treatable, and that methylprednisolone might prevent such cochlear neurons from entering into the vicious process of irreversible damaging process.

Animals↗
PubMed1977

Quantitative assay of Schieff and PAS reactivity during nerve degeneration in rats.

Quantative histochemical analysis of nerve degeneration in rats from zero to 192 hours was studied utilizing both Schiff reagent and PAS reaction. In addition, amylase digestion prior to PAS staining and aniline blockade of Schiff reactivity were employed. The staining intensity of all the reaction was measured histophotometrically and the mean optical density (OD) was determined for the following time intervals: 0, 24, 48, 96, and 192 hours.

Amylases↗
PubMedDate not supplied

Optic nerve degeneration and potential neuroprotection: implications for glaucoma.

In order to study the course of optic nerve degeneration and devise possible ways to achieve neuroprotection, a well-controlled, animal model of partial crush injury of the optic nerve was used. Following the controlled partial crush injury of the rat optic nerve, quantitative morphological and electrophysiological measurements were made of primary and secondary neuronal losses. The neuroprotective effects of NMDA-receptor antagonists and alpha 2-adrenoreceptor agonists were also studied. The results suggested that the ongoing progression of the optic nerve degeneration in glaucoma might be a consequence of the toxic extracellular environment produced by neurons that degenerate as a result of the primary cause of the disease (such as increased IOP).

Action Potentials↗
PubMed1975

An electrophysiological examination of the changes in skeletal muscle fibres in response to degenerating nerve tissue.

Endplate free areas of the emebrane of soleus and extensor digitorum longus muscles of the rat, covered fpor 3 days by a piece of nerve from the brachial region, become locally sensitive to ACh applied iontophoretically. Mean ACh sensitivity is increased at this site in the extensor muscle from 0 in areas not covered by the nerve to 6.27 mV/nanocoulombs (nC) +/- 1.28 (S.E.), in the area under the nerve and in soleus from 0.12 mV/nC +/- 0.05 (S.E.) to 24.2 mV/nC +/- 4.6 (S.E.). Increase in sensitivity is accompained by a decrease of resting membrane potential. Mean values are (unaffected areas) 75.0 mV +/- 0.55 (S.E.) to (affected area) 65.0 mV +/- 0.56 (S.E.) in soleus and (unaffected areas) 76.3 mV +/- 0.61 (S.E.) to (affected area) 67.0 mV +/- 0.55 (S.E.) in extensor digitorum longus. These changes are local in individual fibres. Changes in ACh sensitivity and resting membrane potential in the area covered by the nerve are temporary, and after 6 days no sign of increase in sensitivity and drop in membrane potential were observed. The piece of nerve loses its potential to induce AHh sensitivity when it is heated to 98 degrees C for 5 min or soaked for 2 h in distilled water.

Acetylcholine↗
PubMed2002

Temporal pattern of cochlear nerve degeneration following compression injury: a quantitative experimental observation.

OBJECT: It has been empirically recognized that the cochlear nerve is highly vulnerable to traumatic stress resulting from surgical procedures; therefore, careful manipulation of the cochlear nerve is mandatory in preventing trauma-induced hearing loss during cerebellopontine angle (CPA) surgery. There is, however, no precise knowledge about the temporal pattern of cochlear nerve degeneration following trauma. This study was performed to determine the temporal pattern of injury that occurs after cochlear nerve trauma, knowledge of which is indispensable not only to neurosurgeons but also to all those who manage lesions involving the cochlear nerve. METHODS: Right suboccipital craniectomies were performed in groups of rats with the aid of a surgical microscope, and the seventh and eighth cranial nerve trunks were identified at the internal auditory meatus. The cochlear nerve was quantifiably compressed while compound action potentials of the cochlear nerve were monitored and recorded. Following injury, one group of rats was killed for histological examination at the end of each week for 4 weeks. Data from this study disclosed that the degeneration of the compressed cochlear nerve progressed in a relatively rapid manner and was complete within 1 week after the insult. The main pathophysiological mechanisms responsible for cochlear neuronal death in this experimental setting appeared to be necrosis, and an apoptotic mechanism seemed to play a subsidiary role. CONCLUSIONS: Accurate knowledge about the temporal profile of trauma-induced cochlear nerve degeneration is closely linked with the problem of the therapeutic time window. The results of the present study indicated that any measures to ameliorate cochlear nerve degeneration following trauma should be started as early as possible (within 1 week) after an injury.

Animals↗
PubMed1979

Fine structure of sensory nerves in the rat cornea: an experimental nerve degeneration study.

Fine structure of nerve fibres and terminals in the rat cornea was studied after fixation with glutaraldehyde and osmium tetroxide or with potassium permanganate. Superior cervical and/or ciliary ganglionectomy as well as ophthalmic neurotomy were performed in order to verify the origin of the corneal nerves. In the control corneas axon profiles with granular vesicles were observed in the stroma. Other axons containing agranular vesicles were found both in the stroma and in the epithelium. Superior cervical ganglionectomy abolished only the axons containing granular vesicles but did not affect the corneal blink reflex. Ciliary ganglionectomy induced more conspicuous changes in both stromal and intraepithelial axon profiles. The corneal reflex was, however, normal. Some of the axons containing agranular vesicles also showed degenerative changes. However, intact axon profiles with agranular vesicles were seen even after extirpation of both the ciliary ganglion and the superior cervical ganglion (combined autonomic ganglionectomy). On the other hand, all axon profiles with agranular vesicles disappeared after coagulation of the ophthalmic and maxillary nerves (sensory denervation). This operation destroyed most of the axons in all parts of the cornea and abolished the blink reflex. It is concluded that the axon profiles in the corneal epithelium, containing agranular vesicles, are sensory axons of the trigeminal nerve. A possible role of the vesicles in sensory nerves is discussed.

Animals↗