Keyword search (4,163 papers available)

"entorhinal cortex" Keyword-tagged Publications:

Title Authors PubMed ID
1 17β-Estradiol reduces inhibitory synaptic currents in entorhinal cortex neurons through G protein-coupled estrogen receptor-1 activation of extracellular signal-regulated kinase Batallán Burrowes AA; Moisan É; Garrone A; Buynack LM; Chapman CA; 39150316
PSYCHOLOGY
2 Inhibiting amyloid beta (1-42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex Olajide OJ; La Rue C; Bergdahl A; Chapman CA; 36275011
HKAP
3 G protein-coupled estrogen receptor-1 enhances excitatory synaptic responses in the entorhinal cortex Batallán Burrowes AA; Sundarakrishnan A; Bouhour C; Chapman CA; 34399010
PSYCHOLOGY
4 Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex Olajide OJ; Chapman CA; 34144329
PSYCHOLOGY
5 Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease. Olajide OJ, Suvanto ME, Chapman CA 33495355
PSYCHOLOGY
6 Heterosynaptic modulation of evoked synaptic potentials in layer II of the entorhinal cortex by activation of the parasubiculum. Sparks DW, Chapman CA 27146979
PSYCHOLOGY

 

Title:Heterosynaptic modulation of evoked synaptic potentials in layer II of the entorhinal cortex by activation of the parasubiculum.
Authors:Sparks DWChapman CA
Link:https://www.ncbi.nlm.nih.gov/pubmed/27146979?dopt=Abstract
DOI:10.1152/jn.00095.2016
Publication:Journal of neurophysiology
Keywords:Ihentorhinal cortexheterosynapticparasubiculumplasticity
PMID:27146979 Category:J Neurophysiol Date Added:2019-06-20
Dept Affiliation: PSYCHOLOGY
1 Centre for Studies in Behavioural Neurobiology, Department of Psychology, Concordia University, Montréal, Québec, Canada.
2 Centre for Studies in Behavioural Neurobiology, Department of Psychology, Concordia University, Montréal, Québec, Canada andrew.chapman@concordia.ca.

Description:

Heterosynaptic modulation of evoked synaptic potentials in layer II of the entorhinal cortex by activation of the parasubiculum.

J Neurophysiol. 2016 08 01;116(2):658-70

Authors: Sparks DW, Chapman CA

Abstract

The superficial layers of the entorhinal cortex receive sensory and associational cortical inputs and provide the hippocampus with the majority of its cortical sensory input. The parasubiculum, which receives input from multiple hippocampal subfields, sends its single major output projection to layer II of the entorhinal cortex, suggesting that it may modulate processing of synaptic inputs to the entorhinal cortex. Indeed, stimulation of the parasubiculum can enhance entorhinal responses to synaptic input from the piriform cortex in vivo. Theta EEG activity contributes to spatial and mnemonic processes in this region, and the current study assessed how stimulation of the parasubiculum with either single pulses or short, five-pulse, theta-frequency trains may modulate synaptic responses in layer II entorhinal stellate neurons evoked by stimulation of layer I afferents in vitro. Parasubicular stimulation pulses or trains suppressed responses to layer I stimulation at intervals of 5 ms, and parasubicular stimulation trains facilitated layer I responses at a train-pulse interval of 25 ms. This suggests that firing of parasubicular neurons during theta activity may heterosynaptically enhance incoming sensory inputs to the entorhinal cortex. Bath application of the hyperpolarization-activated cation current (Ih) blocker ZD7288 enhanced the facilitation effect, suggesting that cholinergic inhibition of Ih may contribute. In addition, repetitive pairing of parasubicular trains and layer I stimulation induced a lasting depression of entorhinal responses to layer I stimulation. These findings provide evidence that theta activity in the parasubiculum may promote heterosynaptic modulation effects that may alter sensory processing in the entorhinal cortex.

PMID: 27146979 [PubMed - indexed for MEDLINE]





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