Experimental results revealed that in neocortex inhibitory fast-spiking (FS) interneurons interact also by electrical synapses (gap-junctions). They receive sensory information from thalamus and transfer it to principal cells by feedforward inhibition. Moreover, their synchronous discharge enhances their inhibitory control of pyramidal neurons. By using a biophysical model of FS interneurons the synchronization properties of a network of two synaptically coupled units are investigated. In the case they interact only by inhibitory synapses, well defined regions exist in the parameters space described by the strength and duration of the synaptic current, where synchronous regimes occur. Then an empirical protocol is proposed to determine approximately the borders of the synchronization manifold (SM). When electrical synapses are included, the region of synchronous discharge of the two interneurons becomes larger. In both cases, the coherent states are characterized by discharge frequencies in the gamma range. Lastly, the effects of heterogeneity, either obtained by using different stimulation currents or unidirectional inhibitory coupling, are studied.
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http://dx.doi.org/10.1016/s0303-2647(02)00062-x | DOI Listing |
Cell Rep
December 2024
Department of Psychiatry and Neuroscience & Physiology, New York University Grossman School of Medicine, New York, NY 10016, USA. Electronic address:
The posterior "tail" region of the striatum receives dense innervation from sensory brain regions and is important for behaviors that require sensorimotor integration. The output neurons of the striatum, D1 and D2 striatal projection neurons (SPNs), which make up the direct and indirect pathways, are thought to play distinct functional roles, although it remains unclear if these neurons show cell-type-specific differences in their response to sensory stimuli. Here, we examine the strength of synaptic inputs onto D1 and D2 SPNs following the stimulation of upstream auditory pathways.
View Article and Find Full Text PDFPreterm birth is a leading risk factor for atypicalities in cognitive and sensory processing, but it is unclear how prematurity impacts circuits that support these functions. To address this, we trained adult mice born a day early (preterm mice) on a visual discrimination task and found that they commit more errors and fail to achieve high levels of performance. Using , we found that the neurons in the primary visual cortex (V1) and the V1-projecting prefrontal anterior cingulate cortex (ACC) are hyper-responsive to the reward, reminiscent of cue processing in adolescence.
View Article and Find Full Text PDFMol Psychiatry
December 2024
Center for Nitric Oxide Metabolite, Wonkwang University, Iksan, Republic of Korea.
Central nervous system parvalbumin-positive interneurons (PV-INs) are crucial and highly vulnerable to various stressors. They also play a significant role in the pathological processes of many neuropsychiatric diseases, especially those associated with cognitive impairment, such as Alzheimer's disease (AD), vascular dementia (VD), Lewy body dementia, and schizophrenia. Although accumulating evidence suggests that the loss of PV-INs is associated with memory impairment in dementia, the precise molecular mechanisms remain elusive.
View Article and Find Full Text PDFLayer 4 of rabbit V1 contains fast-spiking GABAergic interneurons (suspected inhibitory interneurons, SINs) that receive potent synaptic input from the LGN and generate fast, local feed-forward inhibition. These cells display receptive fields with overlapping ON/OFF subregions, non-linear spatial summation, very broad orientation/directional tuning, and high spontaneous and visually-driven firing rates. Such fast-spike interneurons are also found in layer 5 (L5), which receives a much sparser input from the LGN, but the response properties and thalamocortical connectivity of L5 SINs are relatively unstudied.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
State Key Laboratory of Toxicology and Medical Countermeasures, Beijing Key Laboratory of Neuropsychopharmacology, Beijing Institute of Pharmacology and Toxicology, 27th Taiping Road, 100850, Beijing, China. Electronic address:
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