Brain research
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Previous research with transcranial magnetic stimulation (TMS) indicates that coil orientation (TMS current direction) and muscle activation state (rest or active) modify corticospinal and intracortical excitability of upper limb muscles. However, the extent to which these factors influence corticospinal and intracortical excitability of lower limb muscles is unknown. This study aimed to examine how variations in coil orientation and muscle activation affect corticospinal and intracortical excitability of tibialis anterior (TA), a lower leg muscle. ⋯ TMS coil orientation and muscle activation influence measurements of intracortical excitability recorded in the tibialis anterior, and are therefore important considerations in TMS studies of lower limb muscles.
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Developmental malnourishment impacts the energetic metabolism control throughout life. In rat offspring, a 0% protein diet during the first 10 days of lactation results in leptin resistance and in alterations in: feeding behavior, serum leptin and neuropeptide Y (NPY) levels in the hypothalamic arcuate nucleus (ARC)/paraventricular (PVN) pathway. Here, the distributions of alpha-melanocyte stimulating hormone (α-MSH) and cocaine and amphetamine regulated transcript (CART), anorexigenic molecules, were immunohistochemically assessed in the ARC, PVN and lateral hypothalamus (LH) nuclei. ⋯ In conclusion, aproteic diet altered the ontogenetic distribution of both anorexigenic molecules. In the PVN, the peak was delayed to P30, which coincides with the leptin peak and follows the previously described NPY (orexigenic) peak in this model. The permanent LH CART and α-MSH increase may be associated with the previously observed PFG hypophagia.
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Diminished synaptic inhibition in the superficial spinal dorsal horn contributes to exaggerated pain responses that accompany peripheral inflammation and neuropathy. α2GABAA receptors (α2GABAAR) constitute the most abundant GABAAR subtype at this site and are the targets of recently identified antihyperalgesic compounds. Surprisingly, hoxb8-α2-/- mice that lack α2GABAAR from the spinal cord and peripheral sensory neurons exhibit unaltered sensitivity to acute painful stimuli and develop normal inflammatory and neuropathic hyperalgesia. Here, we provide a comprehensive analysis of GABAergic neurotransmission, of behavioral phenotypes and of possible compensatory mechanisms in hoxb8-α2-/- mice. ⋯ Tonic GABAergic currents, glycinergic IPSCs, and sensory afferent-evoked EPSCs did not show significant changes in hoxb8-α2-/- mice rendering a compensatory up-regulation of other GABAAR subtypes or of glycine receptors unlikely. Although expression of serotonin and of the serotonin producing enzyme tryptophan hydroxylase (TPH2) was significantly increased in the dorsal horn of hoxb8-α2-/- mice, ablation of serotonergic terminals from the lumbar spinal cord failed to unmask a nociceptive phenotype. Our results are consistent with an important contribution of α2GABAAR to spinal nociceptive control but their ablation early in development appears to activate yet-to-be identified compensatory mechanisms that protect hoxb8-α2-/- mice from hyperalgesia.
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Trans bulbar B-mode sonography (TBS) is a recently proposed method but there is little known about its diagnostic accuracy in patients with multiple sclerosis without acute optic neuritis. Therefore we assessed the correlation between OND, ONSD and OND/ONSD ratio with clinical/para clinical parameters. ⋯ TBS showed significantly lower amounts of OND, ONSD and OND/ONSD ratio in MS patients without current attack compared to their healthy controls indicating a subclinical axonal loss over time. It is suggested that TBS could be an applicable tool for early detection of optic nerve damages along with clinical and para-clinical findings.
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Traumatic brain injury (TBI) is one of the leading causes of mortality and disability worldwide. Emerging studies have shown that endoplasmic reticulum (ER) stress plays an important role in the pathophysiology of TBI. Dexmedetomidine (Dex), a highly selective α2-adrenoreceptor agonist, has been shown to attenuate ER stress. ⋯ Dexmedetomidine significantly reduced ER stress and ER stress-related neuronal apoptosis induced by experimental TBI. In addition, dexmedetomidine significantly improved neurological function and alleviated brain oedema. These findings indicate that dexmedetomidine alleviates severe, post-traumatic ER stress and attenuates secondary brain damage.