scholarly journals Facilitation by drug states does not depend on acquired excitatory strength

2007 ◽  
Vol 176 (2) ◽  
pp. 292-301 ◽  
Author(s):  
M PALMATIER ◽  
R BEVINS
Keyword(s):  
Excitatory Strength

scholarly journals Corticosterone mediates the synaptic and behavioral effects of chronic stress at rat hippocampal temporoammonic synapses

2015 ◽  
Vol 114 (3) ◽  
pp. 1713-1724 ◽  
Author(s):  
Mark D. Kvarta ◽  
Keighly E. Bradbrook ◽  
Hannah M. Dantrassy ◽  
Aileen M. Bailey ◽  
Scott M. Thompson
Keyword(s):  
Spatial Memory ◽  
Chronic Stress ◽  
Glutamate Receptor ◽  
Memory Consolidation ◽  
Emotional Processing ◽  
Emotional Behavior ◽  
Synthesis Inhibitor ◽  
Excitatory Strength ◽  
Brain Structure And Function ◽  
And Function

Chronic stress is thought to impart risk for depression via alterations in brain structure and function, but contributions of specific mediators in generating these changes remain unclear. We test the hypothesis that stress-induced increases in corticosterone (CORT), the primary rodent glucocorticoid, are the key mediator of stress-induced depressive-like behavioral changes and synaptic dysfunction in the rat hippocampus. In rats, we correlated changes in cognitive and affective behavioral tasks (spatial memory consolidation, anhedonia, and neohypophagia) with impaired excitatory strength at temporoammonic-CA1 (TA-CA1) synapses, an archetypical stress-sensitive excitatory synapse. We tested whether elevated CORT was sufficient and necessary to generate a depressive-like behavioral phenotype and decreased excitatory signaling observed at TA-CA1 after chronic unpredictable stress (CUS). Chronic CORT administration induced an anhedonia-like behavioral state and neohypophagic behavior. Like CUS, chronic, but not acute, CORT generated an impaired synaptic phenotype characterized by reduced α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-preferring glutamate receptor-mediated excitation at TA-CA1 synapses, decreased AMPA-type glutamate receptor subunit 1 protein expression, and altered serotonin-1B receptor-mediated potentiation. Repeatedly blunting stress-induced increases of CORT during CUS with the CORT synthesis inhibitor metyrapone (MET) prevented these stress-induced neurobehavioral changes. MET also prevented the CUS-induced impairment of spatial memory consolidation. We conclude that corticosterone is sufficient and necessary to mediate glutamatergic dysfunction underlying stress-induced synaptic and behavioral phenotypes. Our results indicate that chronic excessive glucocorticoids cause specific synaptic deficits in the hippocampus, a major center for cognitive and emotional processing, that accompany stress-induced behavioral dysfunction. Maintaining excitatory strength at stress-sensitive synapses at key loci throughout corticomesolimbic reward circuitry appears critical for maintaining normal cognitive and emotional behavior.

scholarly journals Presynaptic L-Type Ca2+ Channels Increase Glutamate Release Probability and Excitatory Strength in the Hippocampus during Chronic Neuroinflammation

2020 ◽  
Vol 40 (36) ◽  
pp. 6825-6841
Author(s):  
Giorgia Giansante ◽  
Antonella Marte ◽  
Alessandra Romei ◽  
Cosimo Prestigio ◽  
Franco Onofri ◽  
...  
Keyword(s):  
Glutamate Release ◽  
Excitatory Strength ◽  
Release Probability ◽  
Chronic Neuroinflammation ◽  
Ca2 Channels

scholarly journals Impaired GABAB-mediated presynaptic inhibition increases excitatory strength and alters short-term plasticity in synapsin knockout mice

Oncotarget ◽  
2017 ◽  
Vol 8 (52) ◽  
pp. 90061-90076 ◽  
Author(s):  
Pierluigi Valente ◽  
Pasqualina Farisello ◽  
Flavia Valtorta ◽  
Pietro Baldelli ◽  
Fabio Benfenati
Keyword(s):  
Knockout Mice ◽  
Presynaptic Inhibition ◽  
Short Term ◽  
Excitatory Strength ◽  
Short Term Plasticity
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