PERK signalling pathway mediates single prolonged stress-induced dysfunction of medial prefrontal cortex neurons

APOPTOSIS ◽  
2017 ◽  
Vol 22 (6) ◽  
pp. 753-768 ◽  
Author(s):  
Lili Wen ◽  
Bing Xiao ◽  
Yuxiu Shi ◽  
Fang Han
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Signalling Pathway ◽  
Single Prolonged Stress ◽  
Prolonged Stress

scholarly journals Single prolonged stress decreases glutamate, glutamine, and creatine concentrations in the rat medial prefrontal cortex

2010 ◽  
Vol 480 (1) ◽  
pp. 16-20 ◽  
Author(s):  
Dayan Knox ◽  
Shane A. Perrine ◽  
Sophie A. George ◽  
Matthew P. Galloway ◽  
Israel Liberzon
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Single Prolonged Stress ◽  
Prolonged Stress

scholarly journals Single Prolonged Stress Reduces Intrinsic Excitability and Excitatory Synaptic Drive Onto Pyramidal Neurons in the Infralimbic Prefrontal Cortex of Adult Male Rats

2021 ◽  
Vol 15 ◽  
Author(s):  
Nawshaba Nawreen ◽  
Mark L. Baccei ◽  
James P. Herman
Keyword(s):  
Prefrontal Cortex ◽  
Traumatic Stress ◽  
Pyramidal Neurons ◽  
Male Rats ◽  
Intrinsic Excitability ◽  
Repetitive Firing ◽  
Membrane Excitability ◽  
Single Prolonged Stress ◽  
Prolonged Stress ◽  
Synaptic Drive

Post-traumatic stress disorder (PTSD) is a chronic, debilitating mental illness marked by abnormal fear responses and deficits in extinction of fear memories. The pathophysiology of PTSD is linked to decreased activation of the ventromedial prefrontal cortex (vmPFC). This study aims to investigate underlying functional changes in synaptic drive and intrinsic excitability of pyramidal neurons in the rodent homolog of the vmPFC, the infralimbic cortex (IL), following exposure to single prolonged stress (SPS), a paradigm that mimics core symptoms of PTSD in rats. Rats were exposed to SPS and allowed 1 week of recovery, following which brain slices containing the PFC were prepared for whole-cell patch clamp recordings from layer V pyramidal neurons in the IL. Our results indicate that SPS reduces spontaneous excitatory synaptic drive to pyramidal neurons. In addition, SPS decreases the intrinsic membrane excitability of IL PFC pyramidal cells, as indicated by an increase in rheobase, decrease in input resistance, hyperpolarization of resting membrane potential, and a reduction in repetitive firing rate. Our results suggest that SPS causes a lasting reduction in PFC activity, supporting a body of evidence linking traumatic stress with prefrontal hypoactivity.

scholarly journals Daily Optogenetic Stimulation of the Left Infralimbic Cortex Reverses Extinction Impairments in Male Rats Exposed to Single Prolonged Stress

2021 ◽  
Vol 15 ◽  
Author(s):  
Lucas Canto-de-Souza ◽  
Peyton G. Demetrovich ◽  
Samantha Plas ◽  
Rimenez R. Souza ◽  
Joseph Epperson ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Incubation Period ◽  
Conditioned Fear ◽  
Male Rats ◽  
Traumatic Experiences ◽  
Post Traumatic Stress ◽  
Single Prolonged Stress ◽  
Optogenetic Stimulation ◽  
Prolonged Stress ◽  
Stimulation Of

Post-traumatic stress disorder (PTSD) is associated with decreased activity in the prefrontal cortex. PTSD-like pathophysiology and behaviors have been observed in rodents exposed to a single prolonged stress (SPS) procedure. When animals are left alone for 7 days after SPS treatment, they show increased anxiety-like behavior and impaired extinction of conditioned fear, and reduced activity in the prefrontal cortex. Here, we tested the hypothesis that daily optogenetic stimulation of the infralimbic region (IL) of the medial prefrontal cortex (mPFC) during the 7 days after SPS would reverse SPS effects on anxiety and fear extinction. Male Sprague-Dawley rats underwent SPS and then received daily optogenetic stimulation (20 Hz, 2 s trains, every 10 s for 15 min/day) of glutamatergic neurons of the left or right IL for seven days. After this incubation period, rats were tested in the elevated plus-maze (EPM). Twenty-four hours after the EPM test, rats underwent auditory fear conditioning (AFC), extinction training and a retention test. SPS increased anxiety-like behavior in the EPM task and produced a profound impairment in extinction of AFC. Optogenetic stimulation of the left IL, but not right, during the 7-day incubation period reversed the extinction impairment. Optogenetic stimulation did not reverse the increased anxiety-like behavior, suggesting that the extinction effects are not due to a treatment-induced reduction in anxiety. Results indicate that increased activity of the left IL after traumatic experiences can prevent development of extinction impairments. These findings suggest that non-invasive brain stimulation may be a useful tool for preventing maladaptive responses to trauma.

scholarly journals Single Prolonged Stress Reduces Intrinsic Excitability and Excitatory Synaptic Drive onto Pyramidal Neurons in the Infralimbic Prefrontal Cortex of Adult Rats

2021 ◽  
Author(s):  
Nawshaba Nawreen ◽  
Mark L Baccei ◽  
James P Herman
Keyword(s):  
Prefrontal Cortex ◽  
Traumatic Stress ◽  
Pyramidal Neurons ◽  
Brain Slices ◽  
Intrinsic Excitability ◽  
Repetitive Firing ◽  
Membrane Excitability ◽  
Single Prolonged Stress ◽  
Prolonged Stress ◽  
Synaptic Drive

ABSTRACTPost-traumatic stress disorder (PTSD) is a chronic, debilitating mental illness marked by abnormal fear responses and deficits in extinction of fear memories. The pathophysiology of PTSD is linked to decreased activation of the ventromedial prefrontal cortex (vmPFC). This study aims to investigate underlying functional changes in synaptic drive and intrinsic excitability of pyramidal neurons in the rodent homolog of the vmPFC, the infralimbic cortex (IL), following exposure to single prolonged stress (SPS), a paradigm that mimics core symptoms of PTSD in rats. Rats were exposed to SPS and allowed one week of recovery following which brain slices containing the PFC were prepared for whole-cell patch clamp recordings from layer V pyramidal neurons in the IL. Our results indicate that SPS reduces spontaneous excitatory synaptic drive to pyramidal neurons. In addition, SPS decreases the intrinsic membrane excitability of IL PFC pyramidal cells, as indicated by an increase in rheobase, decrease in input resistance, hyperpolarization of resting membrane potential, and a reduction in repetitive firing rate. Our results suggest that SPS causes a lasting reduction in PFC activity, supporting a body of evidence linking traumatic stress with prefrontal hypoactivity.Graphical AbstractSPS causes a decrease in excitatory synaptic drive and intrinsic excitability of IL pyramidal neurons.

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