Neuroscience
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Comparative Study
Methamphetamine-induced deficits of brain monoaminergic neuronal markers: distal axotomy or neuronal plasticity.
We examined the effects of methamphetamine (METH) on monoaminergic (i.e. dopamine and serotonin) axonal markers and glial cell activation in the rat brain. Our findings indicate that the loss of dopamine transporters (DAT), serotonin transporters (5-HTT), vesicular monoamine transporter type-2 (VMAT-2) and glial cell activation induced by METH in the striatum and in the central gray are consistent with a degenerative process. Our novel finding of METH effects on monoaminergic neurons in the central gray may have important implications on METH-induced hyperthermia. ⋯ In summary, our findings suggest two neurotoxic endpoints in the brain of METH-exposed animals. Brain regions exhibiting DAT and 5-HTT deficits that co-localize with decreased VMAT-2 levels and glial cell activation may represent monoaminergic terminal degeneration. However, the DAT and 5-HTT deficits in brain regions lacking a deficit in VMAT-2 and glial cell activation may reflect drug-induced modulation of these plasma membrane proteins.
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Comparative Study
Complete sparing of spatial learning following posterior and posterior plus anterior cingulate cortex lesions at 10 days of age in the rat.
Neonatal posterior cingulate cortex lesions spare the spatial deficits that characterize adult lesions. The present experiments examined the possibility that the anterior cingulate cortex mediates the spared spatial behavior. Rats were given bilateral lesions of the posterior cingulate cortex or anterior plus posterior cingulate cortex on postnatal days 4 (P4), 10 (P10), or in adulthood (P120). ⋯ Adult animals were impaired on place learning relative to controls whereas place learning was spared in all the neonatal groups and sparing was complete in the group receiving day 10 lesions. The results are discussed in relation to neural mechanisms, including fiber rerouting, synaptic changes and generation of new neurons, that may mediate spared spatial following neonatal posterior cingulate cortex lesions. Also discussed is evidence indicating that the neonatal brain, especially the day 10, has a special ability to compensate for injury.
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Comparative Study
Spatiotemporal distribution of gp130 cytokines and their receptors after status epilepticus: comparison with neuronal degeneration and microglial activation.
Although numerous studies have demonstrated the neurotrophic capacity of gp130 cytokines, it remains unclear whether endogenously expressed cytokines actually function in a direct neuromodulatory manner. Therefore, using the lithium-pilocarpine status epilepticus model, we performed a detailed in situ hybridization time-course study of five gp130 cytokines (interleukin [IL]-6, leukemia inhibitory factor [LIF], IL-11, oncostatin-m [OSM], and ciliary neurotrophic factor), gp130, and the receptors of the cytokines we found to be induced (IL-6 receptor [IL-6R], LIF receptor [LIF-R], and IL-11 receptor [IL-11R]). Additionally, to further understand the regulation of these cytokines, we compared their expression with the pattern of neuronal degeneration and microglial activation. ⋯ Microglial activation was maximal 24-48 h post-seizure. We speculate that gp130 cytokines play a paracrine, neuromodulatory role in the hippocampus since both before and after seizure, principal cells appear to be the major cell type expressing the receptors for these cytokines. Furthermore, we suggest that activity-dependent mechanisms may be involved in the regulation of cytokines expressed early, and that relatively late occurring cytokine expression may be elicited by injury-related stimuli.
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The innervation of gill muscles of lampreys was investigated in a semi-intact preparation in which the respiratory rhythm was maintained for more than 2 days. Lesion experiments showed that the muscles of gill 1 are innervated by nerves VII (facial) and IX (glossopharyngeal), and those of gill 2 by nerve IX and the first branchial branch of nerve X (vagal). The other gills are supplied by the other branchial branches of nerve X. ⋯ The conduction velocity of VII and caudal X motor axons was found to be the same. Differences in the length of motoneuron axons appear to account for the rostro-caudal delay in gill contraction. The data presented here provide a much needed anatomical and physiological basis for further studies on the neural network controlling respiration in lampreys.
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Comparative Study
Basolateral amygdala lesions impair both cue- and cocaine-induced reinstatement in animals trained on a discriminative stimulus task.
Drug-associated environmental cues can maintain drug use and contribute to relapse even after long periods of abstinence. We investigated the ability of sensory stimuli that signaled periods of reward availability to sustain cocaine self-administration and trigger the reinstatement of reward-seeking behavior. We demonstrate that lesions of the basolateral amygdala (BLA), a structure strongly implicated in attributing salience to environmental stimuli, significantly reduced the power of predictive cues to elicit reward-seeking behavior. ⋯ In sham-lesioned animals, cocaine and the DS, but not the CS or the S-, triggered reinstatement. BLA lesions abolished DS-induced reinstatement and significantly attenuated cocaine-induced reinstatement. These results demonstrate 1) that when tested under the same conditions, a discriminative cue which signals reward availability is a more robust trigger of reward-seeking than a Pavlovian CS which signals reward delivery and 2) that the BLA contributes to reinstatement in response to these discriminative cues.