Intra- and extracellular recordings were performed to investigate the influence of local disinhibition of neocortical circuits on corticostriatal synaptic transmission. In rat brain slices with preserved corticostriatal connections, electrical stimulation of the neocortex elicited composed postsynaptic responses in neostriatal neurons consisting of glutamatergic excitatory postsynaptic potentials (EPSPs) and weakly expressed GABAA receptor-mediated inhibitory postsynaptic potentials (IPSPs). Following local application of the GABAA receptor antagonist bicuculline to the neocortex, neocortical neurons responded to intracortical stimulation with transient paroxysmal depolarizations. Simultaneously, the amplitude of neocortically evoked EPSPs recorded from neostriatal neurons was found to be enhanced without changes in duration. Similarly, the amplitude of IPSPs increased following disinhibition of neocortical circuits. In addition and in contrast to EPSPs, the duration of the IPSPs was found to be markedly prolonged. The results demonstrate that local disinhibition of neocortical neuronal circuits potentiates both excitatory and inhibitory synaptic transmission in striatal neurons. However, compared to AMPA receptor-mediated excitation, GABAA receptor-mediated inhibition becomes more efficient due to a marked prolongation of IPSPs. The pronounced augmentation of inhibition can be attributed to a strong activation of inhibitory interneurons within the striatum.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1006/exnr.1999.7039 | DOI Listing |
The process by which neocortical neurons and circuits amplify their response to an unexpected change in stimulus, often referred to as deviance detection (DD), has long been thought to be the product of specialized cell types and/or routing between mesoscopic brain areas. Here, we explore a different theory, whereby DD emerges from local network-level interactions within a neocortical column. We propose that deviance-driven neural dynamics can emerge through interactions between ensembles of neurons that have a fundamental inhibitory motif: competitive inhibition between reciprocally connected ensembles under modulation from feed-forward selective (dis)inhibition.
View Article and Find Full Text PDFActa Neuropathol
November 2024
Sanders-Brown Center On Aging, University of Kentucky, U. Kentucky, Rm 575 Lee Todd Bldg 789 S. Limestone Ave, Lexington, KY, 40536, USA.
Pure limbic-predominant age-related TDP-43 encephalopathy neuropathologic changes (pure LATE-NC) is a term used to describe brains with LATE-NC but lacking intermediate or severe levels of Alzheimer's disease neuropathologic changes (ADNC). Focusing on pure LATE-NC, we analyzed data from the National Alzheimer's Coordinating Center (NACC) Neuropathology Data Set, comprising clinical and pathological information aggregated from 32 NIH-funded Alzheimer's Disease Research Centers (ADRCs). After excluding subjects dying with unusual conditions, n = 1,926 autopsied subjects were included in the analyses.
View Article and Find Full Text PDFJ Neurosci
January 2025
Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, Geneva 1211, Switzerland
eNeuro
July 2024
Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112
Persistent activity in excitatory pyramidal cells (PYRs) is a putative mechanism for maintaining memory traces during working memory. We have recently demonstrated persistent interruption of firing in fast-spiking parvalbumin-expressing interneurons (PV-INs), a phenomenon that could serve as a substrate for persistent activity in PYRs through disinhibition lasting hundreds of milliseconds. Here, we find that hippocampal CA1 PV-INs exhibit type 2 excitability, like striatal and neocortical PV-INs.
View Article and Find Full Text PDFbioRxiv
March 2024
Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center, New Orleans, LA 70112.
Persistent activity in principal cells is a putative mechanism for maintaining memory traces during working memory. We recently demonstrated persistent interruption of firing in fast-spiking parvalbumin-expressing interneurons (PV-INs), a phenomenon which could serve as a substrate for persistent activity in principal cells through disinhibition lasting hundreds of milliseconds. Here, we find that hippocampal CA1 PV-INs exhibit type 2 excitability, like striatal and neocortical PV-INs.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!