Brain research bulletin
-
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.
-
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.
-
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.