Neuroscience
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Successful response inhibition relies on the suppression of motor cortex activity. The striatum has previously been linked to motor cortex suppression during the act of inhibition (reactive), but activation was also seen during anticipation of stop signals (proactive). More specifically, striatal activation increased with a higher stop probability. ⋯ We found that striatal activity during reactive inhibition was higher when subjects expected stop signals. These results help explain conflicting findings of previous studies on the association between striatal activation and inhibition, since we demonstrate a crucial role of the subjects' expectation of a stop signal and thus their ability to prepare for a stop in advance. In conclusion, the current results show for the first time that striatal contributions to reactive response inhibition are, in part, related to subjective anticipation.
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Following tissue injury, phosphorylation of p38 MAPK in the primary afferent neurons drives sensitization of peripheral nerve. Dexmedetomidine extends the duration of reginal analgesia by local anesthetics. The effect of regional analgesia on the peripheral nerve sensitization is not known. ⋯ Levobupivacaine without dexmedetomidine could not inhibit p38 MAPK phosphorylation in the DRG completely. However, Levobupivacaine and dexmedetomidine completely inhibited p38 MAPK phosphorylation, and reduced macrophage accumulation and TNF-α amount in the plantar tissue. Inhibition of p38 MAPK phosphorylation via TNF-α suggests dexmedetomidine has a peripheral mechanism of anti-inflammatory action when used asan adjunct to local anesthetics, and provides a molecular basis for the prevention of peripheral sensitization following surgery.
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Cortical spreading depolarization (CSD) has an important role in brain diseases such as stroke, subarachnoid hemorrhage, migraine with aura, and epilepsy. Several anti-epileptic drugs (AEDs) are used to treat paroxysmal brain diseases and are thus known to suppress CSD. One of these AEDs is gabapentin (GBP) which has been traditionally used for treatment of some CSD-related neurological diseases. ⋯ These data support an effect of GBP on GABA-mediated inhibition in the late hyperexcitable phase of CSD. Modulations of synaptic properties and post-CSD GABAergic function are likely GBP's mechanisms of action in CSD-related disorders. These mechanisms could be targeted for further drug discovery in CSD-related diseases.
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In the neocortex, interaction and cooperation between different areas are important for information processing, which also applies to different areas within one sensory modality. In the temporal cortex of rodents and cats, both the primary auditory cortex (A1) and the anterior auditory field (AAF) have tonotopicity but with a mirrored frequency gradient. ⋯ We found that activation of A1 axon terminals in AAF did not change AAF responses, but activating A1 neuronal cell bodies could increase the sound-evoked responses in AAF, as well as decrease the intensity threshold and broaden the frequency bandwidth, while suppressing A1 could cause the opposite effects. Our results suggested that A1 could modulate the general excitability of AAF through indirect pathways, which provides a potential relationship between these two parallel auditory ascending pathways.
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Sites and mechanisms by which trigeminal nerve stimulation (TNS) exerts beneficial effects on symptoms of drug-resistant epilepsy and depression are still unknown. Effects of short-term TNS on brain regions involved in the physiopathology of these disorders were investigated in this study. Forty male rats were assigned to three groups: TNS (undergoing electrical stimulation of the left infraorbitary nerve via surgically implanted cuff electrodes); Sham (undergoing surgical procedure but without a stimulation); Naïve rats. ⋯ In the TNS group the number of BrdU-positive cells in the dentate gyrus was significantly greater with respect to both Naïve and Sham groups. Data show that acute TNS effectively counteracted PTZ-induced seizures and boosted hippocampal cell proliferation in rats. TNS increased c-Fos-like immunoreactivity in brainstem and forebrain structures which play a pivotal role in the physiopathology of epilepsy and depression.