Brain research
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To further understand how tactile information is carried in somatosensory cortex (S1) and the thalamus (VPL), and how neuronal plasticity after neuroprosthetic stimulation affects sensory encoding, we chronically implanted microelectrode arrays across hand areas in both S1 and VPL, where neuronal activities were simultaneously recorded during tactile stimulation on the finger pad of awake monkeys. Tactile information encoded in the firing rate of individual units (rate coding) or in the synchrony of unit pairs (synchrony coding) was quantitatively assessed within the information theoretic-framework. We found that tactile information encoded in VPL was higher than that encoded in S1 for both rate coding and synchrony coding; rate coding carried greater information than synchrony coding for the same recording area. ⋯ The percent change of mutual-information after stimulation was increased with closed-loop stimulation, but decreased with random stimulation. The underlying mechanisms during closed-loop stimulation might be spike-timing-dependent plasticity, while frequency-dependent synaptic plasticity might play a role in random stimulation. Our results suggest that VPL could be a promising target region for somatosensory stimulation with closed-loop brain-machine-interface applications.
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The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important central areas for the control of sodium appetite. In the present study, we investigated the importance of the facilitatory mechanisms of the CeA on NaCl and water intake produced by the deactivation of LPBN inhibitory mechanisms. Male Holtzman rats (n=7-14) with stainless steel cannulas implanted bilaterally in the CeA and LPBN were used. ⋯ Euhydrated rats treated with muscimol (0.5 nmol/0.2 μl) into the LPBN also ingested 0.3M NaCl (19.1 ± 6.4 ml/4h) and water (8.8 ± 3.2 ml/4h). Muscimol (0.5 nmol/0.2 μl) into the CeA also abolished 0.3M NaCl (0.1 ± 0.04 ml/4h) and water intake (0.1 ± 0.02 ml/4h) in euhydrated treated with muscimol into the LPBN. The present results show that neuronal deactivation of the CeA abolishes NaCl intake produced by the blockade of LPBN inhibitory mechanisms, suggesting an interaction between facilitatory mechanisms of the CeA and inhibitory mechanisms of the LPBN in the control of NaCl intake.