PERFORM Publications

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Title		Authors	PubMed ID
1	Dopamine inhibits excitatory synaptic responses in layer I of the rat parasubiculum	Carter F; Hobishi H; Chapman CA;	40818632 PSYCHOLOGY
2	Progesterone and allopregnanolone facilitate excitatory synaptic transmission in the infralimbic cortex via activation of membrane progesterone receptors	Rahaei N; Buynack LM; Kires L; Movasseghi Y; Chapman CA;	39722289 PSYCHOLOGY
3	Reduced 17β-estradiol following ovariectomy induces mitochondrial dysfunction and degradation of synaptic proteins in the entorhinal cortex	Olajide OJ; Batallán Burrowes AA; da Silva IF; Bergdahl A; Chapman CA;	39617168 HKAP
4	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
5	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
6	Ovariectomy reduces cholinergic modulation of excitatory synaptic transmission in the rat entorhinal cortex	Batallán Burrowes AA; Olajide OJ; Iasenza IA; Shams WM; Carter F; Chapman CA;	35939438 CSBN
7	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
8	Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex	Olajide OJ; Chapman CA;	34144329 PSYCHOLOGY
9	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
10	State-Dependent Entrainment of Prefrontal Cortex Local Field Potential Activity Following Patterned Stimulation of the Cerebellar Vermis.	Tremblay SA, Chapman CA, Courtemanche R	31736718 HKAP
11	Heterosynaptic modulation of evoked synaptic potentials in layer II of the entorhinal cortex by activation of the parasubiculum.	Sparks DW, Chapman CA	27146979 PSYCHOLOGY
12	Gap Junction Modulation of Low-Frequency Oscillations in the Cerebellar Granule Cell Layer.	Robinson JC, Chapman CA, Courtemanche R	28421552 HKAP
13	Exposure to cues associated with palatable food reward results in a dopamine D₂ receptor-dependent suppression of evoked synaptic responses in the entorhinal cortex.	Hutter JA, Chapman CA	24093833 CSBN
14	Dopaminergic enhancement of excitatory synaptic transmission in layer II entorhinal neurons is dependent on D₁-like receptor-mediated signaling.	Glovaci I, Caruana DA, Chapman CA	24220689 PSYCHOLOGY
15	Diurnal influences on electrophysiological oscillations and coupling in the dorsal striatum and cerebellar cortex of the anesthetized rat.	Frederick A, Bourget-Murray J, Chapman CA, Amir S, Courtemanche R	25309348 BIOLOGY
16	Activation of Phosphatidylinositol-Linked Dopamine Receptors Induces a Facilitation of Glutamate-Mediated Synaptic Transmission in the Lateral Entorhinal Cortex.	Glovaci I, Chapman CA	26133167 PSYCHOLOGY
17	Optogenetic Activation of the Infralimbic Cortex Suppresses the Return of Appetitive Pavlovian-Conditioned Responding Following Extinction.	Villaruel FR, Lacroix F, Sanio C, Sparks DW, Chapman CA, Chaudhri N	29045570 PSYCHOLOGY
18	Dopamine suppresses persistent firing in layer III lateral entorhinal cortex neurons.	Batallán-Burrowes AA, Chapman CA	29524644 PSYCHOLOGY
19	The role of the paraventricular nucleus of the thalamus in the augmentation of heroin seeking induced by chronic food restriction.	Chisholm A, Iannuzzi J, Rizzo D, Gonzalez N, Fortin É, Bumbu A, Batallán Burrowes AA, Chapman CA, Shalev U	30623532 CSBN
20	Serotonin 5-HT1A Receptor-Mediated Reduction of Excitatory Synaptic Transmission in Layers II/III of the Parasubiculum.	Carter F, Chapman CA	30902681 PSYCHOLOGY
21	Dopamine induces release of calcium from internal stores in layer II lateral entorhinal cortex fan cells.	Glovaci I, Chapman CA	30999216 PSYCHOLOGY

Title:	Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex
Authors:	Olajide OJ, Chapman CA
Link:	https://pubmed.ncbi.nlm.nih.gov/34144329/
DOI:	10.1016/j.neurobiolaging.2021.05.006
Publication:	Neurobiology of aging
Keywords:	Alzheimer'; s disease; Amyloid beta peptide; Astrocytes; Entorhinal cortex; Excitotoxicity; NMDA glutamate receptors;
PMID:	34144329	Category:	Date Added:	2021-06-19
Dept Affiliation:	PSYCHOLOGY 1 Division of Neurobiology, Department of Anatomy, University of Ilorin, Ilorin, Nigeria; Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montréal, Québec, Canada. 2 Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montréal, Québec, Canada. Electronic address: andrew.chapman@concordia.ca.

Description:

The hippocampus and entorhinal cortex (EC) accumulate amyloid beta peptides (Aß) that promote neuropathology in Alzheimer's disease, but the early effects of Aß on excitatory synaptic transmission in the EC have not been well characterized. To assess the acute effects of Aß_1-42 on glutamatergic synapses, acute brain slices from wildtype rats were exposed to Aß_1-42 or control solution for 3 hours, and tissue was analyzed using protein immunoblotting and quantitative PCR. Presynaptically, Aß_1-42 induced marked reductions in synaptophysin, synapsin-2a mRNA, and mGluR3 mRNA, and increased both VGluT2 protein and Ca²⁺-activated channel KCa2.2 mRNA levels. Postsynaptically, Aß_1-42 reduced PSD95 and GluN2B protein, and also downregulated GluN2B and GluN2A mRNA, without affecting scaffolding elements SAP97 and PICK1. mGluR5 mRNA was strongly increased, while mGluR1 mRNA was unaffected. Blocking either GluN2A- or GluN2B-containing NMDA receptors did not significantly prevent synaptic changes induced by Aß_1-42, but combined blockade did prevent synaptic alterations. These findings demonstrate that Aß_1-42 rapidly disrupts glutamatergic transmission in the EC through mechanisms involving concurrent activation of GluN2A- and GluN2B-containing NMDA receptors.

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