Experimental neurology
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Experimental neurology · Oct 1997
Chronic spinal nerve ligation induces changes in response characteristics of nociceptive spinal dorsal horn neurons and in their descending regulation originating in the periaqueductal gray in the rat.
We studied whether a chronic neuropathy induced by unilateral spinal nerve ligation changes the response characteristics of spinal dorsal horn wide-dynamic range (WDR) neurons or their periaqueductal gray (PAG)-induced descending modulation. Experiments were performed in rats with behaviorally demonstrated allodynia induced by spinal nerve ligation and in a group of nonneuropathic control rats. The stimulus-response functions of WDR neurons for mechanical and thermal stimuli and the modulation of their peripherally evoked responses by electrical stimulation of the PAG were determined under pentobarbital anesthesia. ⋯ The results indicate that spinal nerve ligation induces increased spontaneous activity and enhanced responses to mechanical stimuli in the spinal dorsal horn WDR neurons, whereas noxious heat-evoked responses are not significantly changed or if anything, attenuated. Moreover, the inhibition of noxious heat stimuli by PAG stimulation is attenuated in the neuropathic side. It is proposed that the observed changes in the response characteristics of the spinal dorsal horn WDR neurons and in their descending modulation may contribute to the neuropathic symptoms in these animals.
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Experimental neurology · Oct 1997
New growth of axons in the cochlear nucleus of adult chinchillas after acoustic trauma.
This study determined the effect of acoustic overstimulation of the adult cochlea on axons in the cochlear nucleus. Chinchillas were exposed to an octave-band noise centered at 4 kHz at 108 dB sound pressure level for 1.75 h. One chinchilla was never exposed to the noise, and several others had one ear protected by an ear plug or prior removal of the malleus and incus. ⋯ Between 2 and 8 months small axonal endings appeared next to neuronal cell bodies. This later increase of thinner axons and endings is consistent with a reactive growth of new axons of relatively small diameter. The emergence of small perisomatic boutons suggests that the new axons formed synaptic endings, which might contribute to an abnormal reorganization of the central auditory system and to the pathological changes that accompany acoustic overstimulation.
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Experimental neurology · Sep 1997
Experimental spinal cord injury: Wallerian degeneration in the dorsal column is followed by revascularization, glial proliferation, and nerve regeneration.
The presence of adequate blood supply is a critical factor in recovery from traumatic injuries. We have examined whether the revascularization of the injured tissues is as crucial a precondition for wound healing in the spinal cord as in other organs. The development of the initial primary lesion (PL) after spinal crush injury in rats is followed by the formation of a unique tunnel-like dorsal column lesion (DCL) that extends rostrocaudally for many millimeters from the primary injury site. ⋯ By 8 weeks it was highly vascularized, contained abundant nerve fibers, and lacked any trace of cavitation. These findings amplify the current view that ischemia plays a critical role in spinal cord trauma by showing that revascularization precedes tissue repair and nerve regeneration in the dorsal columns. We conclude (a) that a well-vascularized lesion permits the ingrowth of glial and other cells which give rise to a supportive matrix for the nerve regeneration and (b) that procedures which induce revascularization or angiogenesis will ameliorate the cascade of progressive tissue necrosis.
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Experimental neurology · Aug 1997
Cyclosporin A attenuates the decrease in tyrosine hydroxylase immunoreactivity in nigrostriatal dopaminergic neurons and in striatal dopamine content in rats with intrastriatal injection of 6-hydroxydopamine.
To explore new therapeutic strategies for Parkinson's disease, we studied the possible protective effect of an immunosuppressant, cyclosporin A (CsA), treatment on changes in dopaminergic function in rats with intrastriatal injections of 6-hydroxydopamine (6-OHDA). Four weeks after injection of 6-OHDA, dopamine (DA) and dihydroxyphenylacetic acid in the striatum were depleted by 70-80%, and repeated high-dose CsA (20 mg/kg) treatment for 1 week significantly protected against these depletions. Tyrosine hydroxylase immunoreactivity (TH-IR) of the cell bodies in the substantia nigra pars compacta (SNc) ipsilateral to the injection were lower than on the contralateral side at 4 weeks but not at 1 week after 6-OHDA injection. ⋯ By 28 days postinjection, the staining had decreased to control levels in the SA group but was still above the control in the 6-OHDA group. CsA treatment did not affect this staining in either group. These results suggest that CsA protects against 6-OHDA-induced injury of nigrostriatal DA neurons by a mechanism not involving microglia.
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Experimental neurology · Jul 1997
Time course of changes in lactate and free fatty acids after experimental brain injury and relationship to morphologic damage.
Regional levels of lactate and free fatty acids (FFA) were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min after injury, tissue concentrations of lactate were elevated in the cortices and hippocampi of both ipsilateral and contralateral hemispheres. Whereas lactate levels had returned to normal by about 20 min after injury in the penumbra and contralateral cortices, their elevation persisted in the ipsilateral injured cortex and hippocampus for 24 h after injury. ⋯ In general, these elevations persisted for as long as 6 to 24 h in the injured cortex and for 2.5 to 24 h after injury in the ipsilateral hippocampus. Histologic studies revealed a similar extent of damage in the cortex between 5 min and 24 h after injury, whereas damage in the CA3 region of the ipsilateral hippocampus increased during that period. These findings suggest a role for lactic acid and FFA, two secondary injury factors, in neuronal cell loss after brain injury.