Long-lasting synaptic modifications of excitatory and inhibitory synaptic transmissions induced by theta-burst stimulation (TBS) were examined in the spinal trigeminal subnucleus interpolaris (Vi). We found that conditioning afferents of another subnucleus caudalis (Vc) to the Vi with TBS produced long-term depression (LTD). However, when GABAA and glycine receptors were blocked, the same stimulation paradigm produced long-term potentiation (LTP). The induction of LTP involved neither NMDA receptors nor a presynaptic change. The expression of LTP was obviously suppressed by the activation of group I mGluRs because its magnitude increased in the presence of antagonists for group I mGluRs. Besides the LTP at excitatory synapses, TBS also induced LTP at inhibitory GABAergic synapses, which required the activation of NMDA receptors and NO-cGMP signaling but was not involved in the increase of postsynaptic Ca(2+) concentration. Therefore, this study shows, for the first time, an activity-dependent plasticity at excitatory and inhibitory synapses in the Vi by the same conditioning stimulation.
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http://dx.doi.org/10.1016/j.neulet.2014.05.019 | DOI Listing |
Front Pharmacol
December 2024
Addiction Research Group, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
Introduction: Prenatal nicotine exposure (PNE) from maternal smoking disrupts regulatory processes vital to fetal development. These changes result in long-term behavioral impairments, including mood and anxiety disorders, that manifest later in life. However, the relationship underlying PNE, and the underpinnings of mood and anxiety molecular and transcriptomic phenotypes remains elusive.
View Article and Find Full Text PDFencodes a UDP-galactose transporter essential for glycosylation of proteins and galactosylation of lipids and glycosaminoglycans. Germline genetic variants have been identified in congenital disorders of glycosylation and somatic variants have been linked to intractable epilepsy associated with malformations of cortical development. However, the functional consequences of these pathogenic variants on brain development and network integrity remain elusive.
View Article and Find Full Text PDFPLoS Comput Biol
January 2025
Donders Institute for Brain, Cognition and Behavior, Radboud University, Nijmegen, The Netherlands.
Although the primary function of excitatory-inhibitory (E-I) homeostasis is the maintenance of mean firing rates, the conjugation of multiple homeostatic mechanisms is thought to be pivotal to ensuring edge-of-bifurcation dynamics in cortical circuits. However, computational studies on E-I homeostasis have focused solely on the plasticity of inhibition, neglecting the impact of different modes of E-I homeostasis on cortical dynamics. Therefore, we investigate how the diverse mechanisms of E-I homeostasis employed by cortical networks shape oscillations and edge-of-bifurcation dynamics.
View Article and Find Full Text PDFPsychophysiology
January 2025
Department of Psychiatry and Behavioral Sciences, Boston Children's Hospital, Boston, Massachusetts, USA.
The aperiodic "slope" of the EEG power spectrum (i.e., aperiodic exponent, commonly represented as a slope in log-log space) is hypothesized to index the cortical excitatory-inhibitory balance.
View Article and Find Full Text PDFFront Cell Neurosci
December 2024
Istituto Italiano di Tecnologia, Synaptic Plasticity of Inhibitory Networks, Genova, Italy.
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