Brain research bulletin
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Brain research bulletin · Mar 2014
Comparative StudyA neuroproteomic and systems biology analysis of rat brain post intracerebral hemorrhagic stroke.
Intracerebral hemorrhage (ICH) is a devastating form of stroke leading to a high rate of death and disability worldwide. Although it has been hypothesized that much of the IHC insult occurs in the subacute period mediated via a series of complex pathophysiological cascades, the molecular mechanisms involved in ICH have not been systematically characterized. Among the best approaches to understand the underlying mechanisms of injury and recovery, protein dynamics assessment via proteomics/systems biology platforms represent one of the cardinal techniques optimized for mechanisms investigation and biomarker identification. ⋯ On the level of global pathway analysis, hemorrhagic stroke proteins were shown to be involved in autophagy, ischemia, necrosis, apoptosis, calpain activation, and cytokine secretion. Moreover, ischemic stroke proteins were related to cell death, ischemia, inflammation, oxidative stress, caspase activation and apoptotic injury. In conclusion, the proteomic responses identified in this study provide key information about target proteins involved in specific pathological pathways.
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Brain research bulletin · Feb 2014
Periodic maternal deprivation may modulate offspring anxiety-like behavior through mechanisms involving neuroplasticity in the amygdala.
Maternal care has been shown to affect the development of behavioral and endocrine systems. In rats, periodic maternal deprivation (PMD) serves as an early life stressor that directly influences maternal care by promoting more pup-directed behaviors in stressed dams. To further assess the qualities of PMD that may ameliorate long-term anxiety effects in trait anxiety animals, we coded behaviors across lactation (postnatal day (PND) 5, 16, 21) in dams phenotyped as high (HAn) and low-anxiety (LAn). ⋯ Further, as adults, HAn male offspring exhibited less anxiety traits than their maternal line with greater %OA time and %OA entries relative to LAn. HAn offspring showed markedly more BDNF immunoreacted cells in the amygdala than LAn. The combination of these findings suggests that the mild stressor, PMD alters anxiety-like behavior in offspring likely by influencing HAn dams' L/G activity and altering stress related proteins in the amygdala.
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Brain research bulletin · Jan 2014
Bicyclol upregulates transcription factor Nrf2, HO-1 expression and protects rat brains against focal ischemia.
Oxidative damage plays a detrimental role in the pathophysiology of cerebral ischemia and may represent a therapeutic target. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) controls the coordinated expression of the important antioxidant and detoxification genes through a promotor sequence termed the antioxidant response element. Bicyclol has been proved to elicit a variety of biological effects through its antioxidant and anti-inflammatory properties. But the underlying mechanisms are poorly understood. In this study, the role of bicyclol in cerebral ischemia and its potential mechanism were investigated. ⋯ Bicyclol protected the rat brain from ischemic damage caused by MCAO, and this effect may be through the upregulation of the transcription factor Nrf2 expression.
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Brain research bulletin · Jan 2014
The expression of vesicular glutamate transporter 3 and vesicular monoamine transporter 2 induced by brain-derived neurotrophic factor in dorsal root ganglion neurons in vitro.
The vesicular glutamate transporter 3 (VGLUT3) and the vesicular monoamine transporter 2 (VMAT2) are expressed in dorsal root ganglion (DRG) neurons and play an important role in packing the neurotransmitter into synaptic vesicles. Brain-derived neurotrophic factor (BDNF) is one of the most profound known regulators of survival in the developing peripheral nervous system (PNS). Whether BDNF regulates the expression of VGLUT3 and VMAT2 in DRG neurons is still unclear. ⋯ The upregulation of VGLUT3 induced by BDNF might be that BDNF improved neuronal outgrowth status by promoting GAP-43 expression to stimulate neurite elongation. The contribution of distinct VGLUT3 and VMAT2 transporter expression induced by BDNF might be one of the mechanisms that BDNF regulates neuropathic pain. These data imply that BDNF signaling system might be a potential target on modifying distinct transporter-mediated biological effects of primary sensory neurons.
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Brain research bulletin · Jan 2014
Somatostatin enhances tooth-pulp-evoked cervical dorsal horn neuronal activity in the rat via inhibition of GABAergic interneurons.
A recent in vitro electrophysiological analysis combined with anatomical approach suggests that a potential disinhibitory mechanism involving somatostatin (SST), which is released by interneurons in the superficial dorsal horn, contributes to nociceptive transmission (Yasaka et al., 2010); however, whether this mechanism occurs in vivo remains to be determined. The aim of the present study was to investigate whether iontophoretic application of SST facilitates the excitability of nociceptive upper cervical spinal dorsal horn (C1) neurons through GABAergic disinhibiton, using extracellular electrophysiological recording with multibarrel electrodes and immunohistochemical techniques. Immunoreactivity of SST2A receptors was found in layer II of the C1 dorsal horn in the rat and most of these neurons co-expressed the GABA synthesizing enzyme glutamate decarboxylase 67. ⋯ There was no significant difference in the relative number of spikes between SST and bicuculline applications. These results suggest that a local release of SST facilitates the excitability of trigeminal nocicepitve C1 neuronal activity via inhibition of GABAergic neurons. Therefore, SST2A receptors expressed in layer II GABAergic inhibitory interneurons play an important role in trigeminal nociceptive transmission and are a potential therapeutic target in the treatment of trigeminal pain, including hyperalgesia.