Neuroscience
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Emerging evidence suggests that acupuncture treatment has anti-oxidative effects that affect cognitive impairment in vascular dementia (VD) rats. In the present study, we aimed to investigate whether thioredoxin-1 (Trx-1)/thioredoxin reductase-1 (TrxR-1) was involved in the beneficial effects of acupuncture. After 2-weeks of acupuncture treatment, Morris water maze (MWM), dihydroethidium (DHE) staining, Nissl staining and TdT-mediated dUTP nick end labeling (TUNEL) staining were used to assess the effects of acupuncture on cognitive function and hippocampal neuronal injury in two-vessel occlusion (2VO) model. ⋯ Acupuncture also up-regulated the expressions of Trx-1 and TrxR-1, increased the activity of TrxR-1, accompanied with inhibiting the activation of the ASK1-JNK/p38 pathway. However, the effects of acupuncture on improving cognitive function, inhibiting oxidative stress and neuron apoptotic damage were blocked by Trx-1siRNA. In conclusion, these findings indicated that acupuncture treatment improved VD though anti-oxidative and anti-apoptotic mechanisms which involved the up-regulations of Trx-1/TrxR-1 and inhibitions of ASK1-JNK/p38 pathway.
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Profound alterations in both the synaptic and intrinsic membrane properties of neurons that increase the neuronal network excitability are found in epileptic tissue. However, there are still uncertainties regarding the kind of changes in the intrinsic membrane properties occurring during epileptogenesis. Epileptogenesis is typically triggered by the initial brain-damaging insult, and status epilepticus (SE) is one of such insults. ⋯ We found that one day after SE: (1) the intrinsic membrane properties of EC neurons are significantly altered, while the properties of PFC neurons are mostly unchanged; (2) the input resistance and membrane time constant of regular-spiking neurons are reduced due to enhanced leak current; (3) the active membrane properties of neurons are mostly unaffected; and (4) changes in the passive membrane properties diminish the intrinsic neuronal excitability. Therefore, our results suggest that the acute changes in the intrinsic membrane properties of entorhinal neurons following pilocarpine-induced SE do not contribute to network hyperexcitability. In contrast, at the early stage of epileptogenesis, protective homeostatic plasticity of intrinsic membrane properties is observed in the EC; it reduces the neuronal excitability in response to increased network excitability.
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The muscarinic receptor agonist carbachol (CCh) can induce activity in the theta range (4-15 Hz) in the entorhinal cortex (EC), but the underlying network mechanisms remain unclear. Here, we investigated the interplay between interneurons and principal cells in the EC during CCh-induced theta-like field oscillations in an in vitro brain slice preparation using tetrodes. Field oscillations at 10.1 Hz (IQR = 9.5-10.9 Hz) occurred during bath application of CCh (100 μM; n = 32 experiments) and were associated with single-unit (n = 189) firing. ⋯ Blocking ionotropic glutamatergic transmission abolished CCh-induced field oscillations (n = 6), suggesting that ionotropic glutamatergic receptor signaling is necessary for their generation. Our results show that neuronal network interactions leading to CCh-induced theta-like field oscillations rest on the close interplay between interneurons and principal cells and that interneurons modulate principal cell activity during such oscillatory activity. Moreover, they underscore the role of ionotropic glutamatergic transmission in this type of oscillations.
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The hypothalamic energy sensor adenosine 5'-monophosphate-activated protein kinase (AMPK), an important regulator of counter-regulatory responses to hypoglycemia, responds to pharmacological manipulation of hindbrain AMPK activity. Dorsomedial hindbrain A2 noradrenergic neurons express hypoglycemia-sensitive metabolo-sensory biomarkers, including AMPK. Here, adult male rats were pretreated by intra-caudal fourth ventricular administration of the selective neurotoxin 6-hydroxydopamine (6-OHDA) to determine if catecholamine signaling from the aforesaid site governs hypothalamic AMPK activation during insulin-induced hypoglycemia (IIH). ⋯ Results demonstrate site-specific bi-directional adjustments in hypothalamic AMPK reactivity to hypoglycemia. Intensification of ARH/VMH pAMPK by 6-OHDA implies dorsomedial hindbrain improvement of energy balance in those sites during IIH. Neurotoxin-mediated augmentation versus suppression of basal catabolic (ARH POMC/VMH steroidogenic factor-1) or IIH-associated anabolic (ARH NPY) neuropeptide profiles, respectively, may involve local AMPK-dependent against independent mechanisms.
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Blast exposure can cause various auditory disorders including tinnitus, hyperacusis, and other central auditory processing disorders. While this is suggestive of pathologies in the central auditory system, the impact of blast exposure on central auditory processing remains poorly understood. ⋯ Furthermore, the frequency map in the primary auditory cortex was distorted. These changes may contribute to central auditory processing disorders.