Neuroscience
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Acetylcholine (ACh) acts through nicotinic and muscarinic ACh receptors in the ventral midbrain and striatal areas to influence dopamine (DA) transmission. This cholinergic control of DA transmission is important for processes such as attention and motivated behavior, and is manipulated by nicotine in tobacco products. Identifying and characterizing the key ACh receptors involved in cholinergic control of DA transmission could lead to small molecule therapeutics for treating disorders involving attention, addiction, Parkinson's disease, and schizophrenia. α6-Containing nicotinic acetylcholine receptors (nAChRs) are highly and specifically expressed in midbrain DA neurons, making them an attractive drug target. ⋯ To complement these behavioral studies, we studied the ability of in vivo α6(∗) nAChR activation to support plasticity changes in midbrain DA neurons that are relevant to behavioral sensitization and addiction. By coupling local infusion of drugs and brain slice patch-clamp electrophysiology, we show that activating α6(∗) nAChRs in midbrain DA areas is sufficient to enhance glutamatergic transmission in ventral tegmental area (VTA) DA neurons. Together, these results from in vivo studies strongly suggest that α6(∗) nAChRs expressed by VTA DA neurons are positioned to strongly influence both DA-mediated behaviors and the induction of synaptic plasticity by nicotine.
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Comparative Study
Functional differences in face processing between the amygdala and ventrolateral prefrontal cortex in monkeys.
The ability to categorize social information is essential to survive in a primate's social group. In the monkey brain, there are neural systems to categorize social information. Among these, the relationship between the amygdala and the ventrolateral prefrontal cortex (vlPFC) has recently gained focus with regard to emotion regulation. ⋯ Information analyses revealed that the amount of information conveyed by the amygdala neurons about the type of emotion transiently increased immediately after stimulus presentation. In contrast, the information conveyed by the vlPFC neurons showed sustained elevation during stimulus presentation. Therefore, our results suggest that the amygdala processes strong emotion roughly but rapidly, whereas the vlPFC spends a great deal of time processing ambiguous facial information in communication, and make an accurate decision from multiple possibilities based on memory.
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Spinal 5-HT3 receptor (5-HT3R) has been implicated in chronic pain development. The extent to which 5-HT3R contributes to spinal sensitization and diabetic neuropathic pain (DNP) remains elusive and the mechanisms subserving the effects of 5-HT3R activation on spinal pain processing during chronic pain are still unclear. In this study, we evaluated the contribution of spinal 5-HT3R to pain facilitation and spinal sensitization during DNP, exploiting the role of GABAAR-mediated neurotransmission and glial activation in the effects elicited by intrathecal administration of a 5-HT3R antagonist. ⋯ The spinal activation of GABAAR by i.t. administration of muscimol abolished Y25130-driven antinociception. The expression of IBA-1, GFAP and 5-HT3R was unaltered by treatment. These findings point to a GABA-mediated pronociceptive role of spinal 5-HT3R during DNP.
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Sensory events in the space around us trigger specific motor patterns directed toward or away from the spatial location of the sensory source. Spatially-defined sensorimotor associations are well-known in the visual domain but less so for the auditory modality. In particular no spatially-directed audio-motor association has been described for the upper limb. ⋯ We show the presence in the upper limb motor system of auditory spatial tuning. Sound information accesses the motor system at very short latency, potentially compatible with both a subcortical and a cortical origin of the response. The use of TMS-evoked accelerations allowed us to disclose a strict directional tuning in audio-motor associations.
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Prolonged neuronal depression after spreading depression (SD) is followed by a late cellular and synaptic hyperexcitability. Intra- and extracellular recordings of bioelectrical activities were performed in the rodent hippocampus to investigate the role of γ-aminobutyric acid (GABA)-mediated inhibition in the late hyperexcitable state of SD. The effect of KCl-induced negative DC potential shifts was investigated on extracellularly recorded paired-pulse depression (PPD) and bicuculline-induced afterdischarges as well as intracellularly recorded inhibitory post synaptic potentials (IPSPs) in the hippocampal CA1 area. ⋯ Application of low concentrations of bicuculline before the induction of SD enhanced the inhibitory effect of SD on IPSPs. Data indicate the contribution of GABA-mediated inhibition to SD-induced delayed hyperexcitability. Modulation of GABA function in the late hyperexcitability phase of SD may play a role in therapeutic management of SD-related neurological disorders.