PERFORM Publications

17β-Estradiol reduces inhibitory synaptic currents in entorhinal cortex neurons through G protein-coupled estrogen receptor-1 activation of extracellular signal-regulated kinase

Author(s): Batallán Burrowes AA; Moisan É; Garrone A; Buynack LM; Chapman CA;

Estrogens are believed to modulate cognitive functions in part through the modulation of synaptic transmission in the cortex and hippocampus. Administration of 17ß-estradiol (E2) can rapidly enhance excitatory synaptic transmission in the hippocampus and facilitate excitatory synaptic transmission in rat lateral entorhinal cortex via activation of the G p ...

Article GUID: 39150316

Inhibiting amyloid beta (1-42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex

Author(s): Olajide OJ; La Rue C; Bergdahl A; Chapman CA;

Increasing evidence suggests that mitochondrial dysfunction and aberrant release of mitochondrial reactive oxygen species (ROS) play crucial roles in early synaptic perturbations and neuropathology that drive memory deficits in Alzheimer's disease (AD). We recently showed that solubilized human amyloid beta peptide 1-42 (hAß1-42) causes rapid alterati ...

Article GUID: 36275011

G protein-coupled estrogen receptor-1 enhances excitatory synaptic responses in the entorhinal cortex

Author(s): Batallán Burrowes AA; Sundarakrishnan A; Bouhour C; Chapman CA;

Activation of estrogen receptors is thought to modulate cognitive function in the hippocampus, prefrontal cortex, and striatum by affecting both excitatory and inhibitory synaptic transmission. The entorhinal cortex is a major source of cortical sensory and associational input to the hippocampus, but it is unclear whether either estrogens or progestogens ...

Article GUID: 34399010

Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex

Author(s): Olajide OJ; Chapman CA;

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 Aß1-42 on glutamatergic synapses, acute brain slices from wildtype rats were expo ...

Article GUID: 34144329

Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease.

Author(s): Olajide OJ, Suvanto ME, Chapman CA

The entorhinal cortex (EC) is a vital component of the medial temporal lobe, and its contributions to cognitive processes and memory formation are supported through its extensive interconnections with the hippocampal formation. During the pathogenesis of Alzheimer's disease (AD), many of the earliest degenerative changes are seen within the EC. Neurod ...

Article GUID: 33495355

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

Author(s): Sparks DW, Chapman CA

J Neurophysiol. 2016 08 01;116(2):658-70 Authors: Sparks DW, Chapman CA

Article GUID: 27146979

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