Brain research bulletin
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Brain research bulletin · Aug 2009
Cerebellar peduncle injury in patients with ataxia following diffuse axonal injury.
No diffusion tensor imaging (DTI) study has yet investigated ataxia in diffuse axonal injury (DAI). In the current study, we used DTI to investigate cerebellar peduncle lesions of patients who showed severe ataxia following DAI. Six patients with severe ataxia following DAI and six age-and sex-matched control subjects were recruited. ⋯ In each of the 20 cerebellar peduncles, all the lesions displaying the lowest FA values relative to that of normal controls (11 peduncles; 55%) were located in the junction between brain stem and cerebellum and post-junctional area (nine peduncles; 45%). The junction and peri-junctional areas between the brain stem and cerebellum appear to be the most vulnerable area by DAI, with the order of incidence SCP, ICP, and MCP. Evaluation of the cerebellar peduncles using DTI can be helpful in patients with ataxia following DAI.
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Brain research bulletin · Aug 2009
N-Methyl-D-aspartate receptor antagonist d-AP5 prevents pertussis toxin-induced alterations in rat spinal cords by inhibiting increase in concentrations of spinal CSF excitatory amino acids and downregulation of glutamate transporters.
Recently, we found that intrathecal (i.t.) pertussis toxin (PTX) injection produces thermal hyperalgesia and is associated with increasing concentrations of excitatory amino acids (EAAs) in spinal cerebrospinal fluid (CSF) dialysates; a reduction in the antinociceptive effects of morphine and glutamate transporters (GTs) was also observed. The reduction in the morphine-induced analgesic effects is directly related to increased extracellular EAA levels, which are maintained by GTs at physiological levels. In this study, we aimed to examine the role of GT isoforms in thermal hyperalgesia, determine the EAA concentrations in CSF dialysates, and elucidate the role of N-methyl-d-aspartate (NMDA) receptors in PTX-induced reduction in the antinociceptive effects of morphine. ⋯ The microdialysis probe was used to collect CSF dialysates for EAA measurements by high-performance liquid chromatography. Intrathecal morphine failed to produce antinociceptive effects in PTX-treated rats, and d-AP5 coinfusion prevented the PTX-induced reduction in the antinociceptive effect and associated downregulation of the GTs. We conclude that NMDA receptor suppression inhibits EAA excitation and reduces the morphine-induced antinociception in PTX-treated rats.
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Brain research bulletin · Aug 2009
Role of excitatory amino acids in the mediation of tracheobronchial cough induced by citric acid inhalation in the rabbit.
We investigated the role of ionotropic glutamate receptors located within the caudal portions of the nucleus tractus solitarii (cNTS) and the caudal ventral respiratory group (cVRG) in the mediation of coughing evoked by citric acid inhalation in spontaneously breathing rabbits under pentobarbitone anaesthesia. Bilateral microinjections (30-50nl) of 10mM CNQX and 10mM D-AP5 were performed to block non-NMDA and NMDA receptors, respectively. An attempt was also made to investigate the effects of ionotropic glutamate receptor blockade within the cVRG on sneezing induced by mechanical stimulation of the nasal mucosa. ⋯ As to sneezing, blockade of non-NMDA receptors within the cVRG suppressed the expiratory thrusts without affecting the inspiratory preparatory bursts, while blockade of NMDA receptors only strongly attenuated the expiratory thrusts. This study is the first to provide evidence that ionotropic glutamate receptors, and especially non-NMDA receptors, are involved in the mediation of coughing induced by citric acid inhalation and to suggest that citric acid-activated cough-related afferents terminate within the cNTS. Present data also corroborate the notion that the cVRG is involved in the generation of the whole cough motor pattern, but seems to represent merely an expiratory output system for sneezing.
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Brain research bulletin · Aug 2009
The effects of acetaldehyde on nicotine-induced transmitter levels in young and adult brain areas.
The aim of the present study was to examine the effect of acetaldehyde administration on neurotransmitters in the presence of nicotine in brain areas associated with cognition and reward. We assayed these effects via microdialysis in conscious freely moving male Sprague-Dawley rats. It was reported that low doses of acetaldehyde enhance nicotine self-administration in young, but not in adult rats. ⋯ Because acetaldehyde did not induce elevated DA levels in the NAccS of the young, we believe that the higher reward in the young caused by acetaldehyde is not likely due to DA changes in the accumbens. The increase of NE and 5-HT in the brain areas of the young only raises the possibility that they may play an important role in reward in some cases when DA in the accumbens does not. Areas involved in cognitive mechanisms and a number of transmitters seem to play a role in reward stimulation.
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Brain research bulletin · Aug 2009
Post-ischemic hypothermia for 24h in P7 rats rescues hippocampal neuron: association with decreased astrocyte activation and inflammatory cytokine expression.
Hypothermia is an effective method for reducing the neuronal damage induced by hypoxia-ischemia (HI) but the underlying mechanism remains unclear. To investigate the effects of post-HI hypothermia on the developing brain, 7-day-old rats were subjected to left carotid artery ligation followed by 8% oxygen for 2h. They were divided into a hypothermia group (rectal temperature 32-33 degrees C for 24h) and a normothermia group (36-37 degrees C for 24h) immediately after hypoxia-ischemia. ⋯ However, GDNF protein level was significantly increased in the hypothermia group. On the other hand, mRNA and protein levels of the inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) were dramatically decreased in the hypothermia compared with the normothermia group. The present findings highlight an apparent association between inhibition of hippocampal neuron loss by hypothermia and decreased astrocytosis and inflammatory cytokine release after hypoxia-ischemia in the developing brain.