Brain research
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Adolescent development is associated with major changes in emotional and cognitive functions, as well as a rise in stress-related psychological disorders such as anxiety and depression. It is also a time of significant maturation of the brain, marked by structural alterations in many limbic and cortical regions. Though many elegant human neuroimaging studies have described the adolescent-related changes in these regions, relatively little is known about these changes in non-human animals. ⋯ As many unanswered questions remain in this area of investigation, potential future lines of research are also discussed. A deeper appreciation of how stress affects adolescent brain development will be needed if we are to gain a better understanding of the mechanisms that mediate the increase in stress-related psychological dysfunctions often observed during this stage of development. This article is part of a Special Issue entitled SI: Adolescent plasticity.
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In dorsal root ganglia (DRG), satellite glial cells (SGCs) tightly ensheathe the somata of primary sensory neurons to form functional sensory units. SGCs are identified by their flattened and irregular morphology and expression of a variety of specific marker proteins. In this report, we present evidence that the 3-hydroxy-3-methylglutaryl coenzyme A synthase isoenzymes 1 and 2 (HMGCS1 and HMGCS2) are abundantly expressed in SGCs. ⋯ Western blot showed that HMGCS1 protein level in axotomized L5 DRGs is reduced after SNL to 66±8% at 3 days (p<0.01, n=4 animals in each group) and 58±13% at 28 days (p<0.001, n=9 animals in each group) of its level in control samples, whereas HMGCS2 protein was comparable between injured and control DRGs. These results identify HMGCSs as the alternative markers for SGCs in DRGs. Downregulated HMGCS1 expression in DRGs after spinal nerve injury may reflect a potential role of abnormal sterol metabolism of SGCs in the nerve injured-induced neuropathic pain.
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Comparative Study
Anesthesia specific differences in a cardio-pulmonary resuscitation rat model; halothane versus sevoflurane.
Our asphyxia cardiac arrest (ACA) rat model is well established. The original model was designed in the 1990th using halothane and nitrous oxide for pre-insult anesthesia. Because of its hepato-toxicity and its potential to induce severe liver failures, halothane is no longer used in clinical anesthesia for several years. In order to minimize the health risk for our laboratory staff as well as to keep the experimental settings of our model on a clinically oriented basis we decided to replace halothane by sevoflurane. In this study we intended to determine if the change of the narcotic gas regiment causes changes in the neurological damage and how far our model had to be adjusted. ⋯ Using sevoflurane instead of halothane for anesthesia requires some physiological and experimental changes. However the model keeps its validity. Sevoflurane caused less pronounced neurodegeneration in the CA1 region of the hippocampus. This had to be considered in further resuscitation-studies containing sevoflurane as anesthetic. Institutional protocol number for animal studies: 42502-2-2-947 Uni MD.
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The indoleamine hormone melatonin protects dopamine neurons in the rat nigrostriatal pathway following 6-hydroxydopamine lesioning, and an increase in striatal melatonin levels has been detected in this model of Parkinson's disease. Melatonin induces the expression of tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, in the ventral midbrain, where G protein-coupled melatonin receptors are present. Based on the interaction between the melatonergic and dopaminergic systems, we hypothesized that 6-hydroxydopamine-induced degeneration of dopamine neurons would affect the expression of melatonin receptors in the nigrostriatal pathway. ⋯ There were no significant differences in melatonin MT1 receptor protein expression in the striatum or substantia nigra, between intrastriatally lesioned animals and sham controls. In contrast, lesions in the medial forebrain bundle caused a significant increase in MT1 receptor mRNA expression (p<0.03) on the lesioned side of the ventral midbrain, as compared with the contralateral side. Given the presence of MT1 receptors on neurons in the ventral midbrain, these results suggest that a compensatory increase in MT1 transcription occurs to maintain expression of this receptor and neuroprotective melatonergic signaling in the injured brain.
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Voltage-gated Na+ channels in primary afferent neurons can be divided into tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) Na+ channels. Although previous studies have shown the acid modulation of TTX-R Na+ channels, the effect of acidic pH on tetrodotoxin-sensitive (TTX-S) Na+ channels is still unknown. Here we report the effect of acidic pH on TTX-S Na+ channels expressed in large-sized trigeminal ganglion (TG) neurons using a whole-cell patch clamp technique. ⋯ Acidic pH (pH 6.0) shifted both the activation and steady-state fast inactivation relationships of TTX-S Na+ channels toward depolarized potentials. However, acidic pH (pH 6.0) had no effect on use-dependent inhibition in response to high-frequency stimuli, development of inactivation, and accelerated the recovery from inactivation of TTX-S Na+ channels, suggesting that TTX-S Na+ channels in large-sized TG neurons are less sensitive to acidic pH. Given that voltage-gated Na+ channels play a pivotal role in the generation and conduction of action potentials in neural tissues, the insensitivity of TTX-S Na+ channels expressed in large-sized TG neurons to acidic pH would ensure transmission of innocuous tactile sensation from orofacial regions at acidic pH conditions.