Brain research
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Comparative Study
Fiber composition of the rat sciatic nerve and its modification during regeneration through a sieve electrode.
Recovery after peripheral nerve transection is seldom complete, the outcome depending both on lesion and repair conditions, and on the type and neurochemical properties of axons. The interposition between the stumps of a perforated, or regenerative electrode (RE) is a promising avenue in the use of chronic nerve bioimplants, but represents an additional challenge to regeneration. We applied stereological methods to ultrathin and immunostained semithin sections to examine quantitatively the axon types that make up the sciatic nerve in control adult rats, and their changes 2 months after an RE implant. ⋯ Differential growth of axons from sensory and motor neurons through a regenerative electrode: a stereological, retrograde tracer, and functional study in the rat. Neuroscience 128, 605-615.], this study shows that regeneration through the RE is much less successful for MAx than UAx, that motor axons regenerate more poorly than sensory axons, and that some subclasses of sympathetic fibers regenerate better than others. The study also proves the value of the combined methodological approach presented here to assess the fiber composition of a nerve under normal, pathological or experimental conditions.
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Prior research has reliably found high blood (hyperserotonemia) - but low brain - serotonin levels in autistic individuals. At early stages of development, high levels of serotonin in the blood may enter the brain of a developing fetus, causing a loss of serotonin terminals through negative feedback and thus disrupting subsequent serotonergic function. The current study extends earlier findings in a developmental hyperserotonemia (DHS) model of autism in Sprague-Dawley rats by treating 8 dams of developing rat pups with a serotonergic agonist, 5-methoxytryptamine (5-MT; 1 mg/kg) during development (from gestational day 12 to post-natal day 20; PND 20). ⋯ However, there were no changes in anxiogenic behavior using the elevated plus maze (p>0.05). Post mortem analyses revealed that DHS animals had a loss of oxytocin (OT)-containing cells in the paraventricular nucleus in the hypothalamus (PVN; p<0.05) as well as an increase in calcitonin-gene related peptide (CGRP; p<0.05, one tailed) processes in the central nucleus of the amygdala (CeA) on PND 198. These results may correspond to hypothalamic and amygdalar changes in the human condition and suggest that the hyperserotonemia model of autism may be a valid model which produces many of the social, behavioral, and peptide changes inherent to autism.
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Nicotine is neuronal stimulating drug in the central nervous system and elicits various effects through nicotinic acetylcholine receptors. As previously reported, nicotine has an antinociceptive effect through activation of endogenous opioid neurons. However, detailed mechanisms of nicotine-induced antinociception are uncertain. ⋯ The mRNA levels of preprodynorphin and preproopiomelanocortin were not increased by nicotine (5 mg/kg, s.c.). In the dorsal horn of the lumbar spinal cord, methionine-enkephalin (Met-ENK)-like IR was remarkably reduced at 0.5 h following nicotine administration and recovered to control levels by 2 h after nicotine (3 mg/kg, s.c.) administration. These results suggest that nicotine has an antinociceptive effect by promoting the release of Met-ENK, but not dynorphins and endorphins, from activated opioidergic neurons in spinal cord.
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Parkinson's disease (PD) is characterized by a bilateral progressive degeneration of nigrostriatal dopaminergic neurons. Among several toxin-induced animal models of PD, a single intrastriatal injection of 6-hydroxydopamine (6-OHDA) has been reported to provoke a retrograde degeneration of nigral dopaminergic neurons and may reflect an early stage of PD. However, the lack of a progressive neuronal loss in those acute models limits the suitability for the assessment of neuroprotective therapeutics. ⋯ Motor performance was unaltered after single and repeated treatments, except of a slight cataleptic behavior and shortened stride-length performance in mice treated over 7 d. The present data show for the first time that daily intrastriatal injections of 6-OHDA over 5 d can enhance the nigrostriatal neurodegeneration in mice. However, the extent of the neuronal loss was moderate and the technical expense limits the utility as a subchronic model.
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We investigated in different experimental rat models the potential facilitatory contribution of the medullary dorsal reticular nucleus (DRt) descending pathway to the expressions of the sensory spinal neuron sensitization such as increased spontaneous and noxious evoked activities, responsivity to heterotopic afferences stimulation and long lasting afterdischarges (ADs). We carried out experiments by recording from ipsilateral lumbar Wide Dynamic Range (WDR) neurons and by simultaneously monitoring the DRt neuron activity in neuropathic pain rats with chronic constriction injury of one sciatic nerve (CCI), in sham-operated and in "intact" rats. In particular, we recorded the spinal neuron spontaneous activities and the activities evoked by noxious stimulations of ipsi- and contralateral sciatic supplied areas before and during DRt activity blockade. ⋯ We found that during DRt activity blockade in CCI rat neurons and in "intact" rat NMDA-treated neurons, the spontaneous activity was significantly reduced, the responses to contralateral sciatic area stimulation were reduced or suppressed, the responses to ipsilateral sciatic area were poorly affected (slightly reduced or unaffected), except for the poststimulus afterdischarges that were mostly suppressed. In sham-operated rats, the neuronal activity was not affected by DRt blockade. The finding that during the DRt nucleus blockade some expressions of spinal neurons sensitization, seemingly associated to sensory disorders in neuropathic pain, fade or extinguish designates a likely facilitatory role of DRt in the maintenance of neuronal sensitization and thus a contribution to neuropathic pain state.