Infralimbic cortex pyramidal neuron GIRK signaling contributes to regulation of cognitive flexibility but not affect-related behavior in male mice

2021 ◽  
Vol 242 ◽  
pp. 113597
Author(s):  
Eden M. Anderson ◽  
Skyler Demis ◽  
Benjamin Wrucke ◽  
Annabel Engelhardt ◽  
Matthew C. Hearing
Keyword(s):  
Cognitive Flexibility ◽  
Pyramidal Neuron ◽  
Male Mice ◽  
Infralimbic Cortex

scholarly journals Development-Dependent Plasticity in Vasoactive Intestinal Polypeptide Neurons in the Infralimbic Cortex

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Stuart A Collins ◽  
Ipe Ninan
Keyword(s):  
Sex Differences ◽  
Anxiety Disorders ◽  
Vasoactive Intestinal Polypeptide ◽  
Cortical Plasticity ◽  
Male Mice ◽  
Infralimbic Cortex ◽  
Membrane Excitability ◽  
Gabaergic Transmission ◽  
Intestinal Polypeptide

Abstract The onset of several neuropsychiatric disorders including anxiety disorders coincides with adolescence. Consistently, threat extinction, which plays a key role in the regulation of anxiety-related behaviors, is diminished during adolescence. Furthermore, this attenuated threat extinction during adolescence is associated with an altered synaptic plasticity in the infralimbic medial prefrontal cortex (IL-mPFC), a brain region critical for threat extinction. However, the mechanism underlying the altered plasticity in the IL-mPFC during adolescence is unclear. Given the purported role of vasoactive intestinal polypeptide expressing interneurons (VIPINs) in disinhibition and hence their potential to affect cortical plasticity, we examined whether VIPINs exhibit an adolescence-specific plasticity in the IL-mPFC. We observed an increase in GABAergic transmission and a decrease in excitability in VIPINs during adolescence. Male mice show a significantly higher VIPIN-pyramidal neuron GABAergic transmission compared with female mice. The observed increase in GABAergic transmission and a decrease in membrane excitability in VIPINs during adolescence could play a role in the altered plasticity in the adolescent IL-mPFC. Furthermore, the suppression of VIPIN-mediated GABAergic transmission in females might be relevant to sex differences in anxiety disorders.

scholarly journals Cognitive flexibility deficits in male mice exposed to neonatal hyperoxia followed by concentrated ambient ultrafine particles

2018 ◽  
Vol 70 ◽  
pp. 51-59 ◽  
Author(s):  
Keith Morris-Schaffer ◽  
Marissa Sobolewski ◽  
Kevin Welle ◽  
Katherine Conrad ◽  
Min Yee ◽  
...  
Keyword(s):  
Cognitive Flexibility ◽  
Ultrafine Particles ◽  
Male Mice ◽  
Neonatal Hyperoxia

Dorsal Hippocampus to Infralimbic Cortex Circuit is Essential for the Recall of Extinction Memory

2020 ◽  
Author(s):  
Cheng Qin ◽  
Xin-Lan Bian ◽  
Hai-Yin Wu ◽  
Jia-Yun Xian ◽  
Cheng-Yun Cai ◽  
...  
Keyword(s):  
Memory Impairment ◽  
Stress Disorder ◽  
Dorsal Hippocampus ◽  
Neural Mechanisms ◽  
Male Mice ◽  
Infralimbic Cortex ◽  
Extracellular Signal Regulated Kinase ◽  
Conditional Deletion ◽  
Extracellular Signal ◽  
Extinction Memory

Abstract Posttraumatic stress disorder subjects usually show impaired recall of extinction memory, leading to extinguished fear relapses. However, little is known about the neural mechanisms underlying the impaired recall of extinction memory. We show here that the activity of dorsal hippocampus (dHPC) to infralimbic (IL) cortex circuit is essential for the recall of fear extinction memory in male mice. There were functional neural projections from the dHPC to IL. Using optogenetic manipulations, we observed that silencing the activity of dHPC-IL circuit inhibited recall of extinction memory while stimulating the activity of dHPC-IL circuit facilitated recall of extinction memory. “Impairment of extinction consolidation caused by” conditional deletion of extracellular signal-regulated kinase 2 (ERK2) in the IL prevented the dHPC-IL circuit-mediated recall of extinction memory. Moreover, silencing the dHPC-IL circuit abolished the effect of intra-IL microinjection of ERK enhancer on the recall of extinction memory. Together, we identify a dHPC to IL circuit that mediates the recall of extinction memory, and our data suggest that the dysfunction of dHPC-IL circuit and/or impaired extinction consolidation may contribute to extinguished fear relapses.

scholarly journals Suppression of pyramidal neuron G protein-gated inwardly rectifying K+ channel signaling impairs prelimbic cortical function and underlies stress-induced deficits in cognitive flexibility

2020 ◽  
Author(s):  
Eden M Anderson ◽  
Steven Loke ◽  
Benjamin Wrucke ◽  
Annabel Engelhardt ◽  
Evan Hess ◽  
...  
Keyword(s):  
Cognitive Function ◽  
G Protein ◽  
Cognitive Flexibility ◽  
Pyramidal Neuron ◽  
Pyramidal Neurons ◽  
K Channel ◽  
Cortical Function ◽  
Systemic Injection ◽  
The Impact ◽  
Inwardly Rectifying

AbstractBackgroundImbalance in prefrontal cortical (PFC) pyramidal neuron excitation:inhibition is thought to underlie symptomologies shared across stress-related disorders and neuropsychiatric disease, including dysregulation of emotion and cognitive function. G protein-gated inwardly rectifying K+ (GIRK/Kir3) channels mediate excitability of medial PFC pyramidal neurons, however the functional role of these channels in mPFC-dependent regulation of affect, cognition, and cortical dynamics is unknown.MethodsIn mice harboring a ‘floxed’ version of the kcnj3 (Girk1) gene, we used a viral-cre approach to disrupt GIRK1-containing channel expression in pyramidal neurons within the prelimbic (PL) or infralimbic (IL) cortices. Additional studies used a novel model of chronic unpredictable stress (CUS) to determine the impact on PL GIRK-dependent signaling and cognitive function.ResultsIn males, loss of pyramidal GIRK-dependent signaling in the PL, but not IL, differentially impacted measures of affect and motivation, and impaired working memory and cognitive flexibility. CUS produced similar deficits in affect and cognition that paralleled a reduction in PL pyramidal GIRK-dependent signaling akin to viral approaches. Viral- and stress-induced behavioral deficits were rescued by systemic injection of a novel, GIRK1-selective agonist, ML-297. Unexpectedly, neither ablation of PL GIRK-dependent signaling or exposure to the CUS regimen impacted affect or cognition in female mice.ConclusionsGIRK-dependent signaling in male mice, but not females, is critical for maintaining optimal PL function and behavioral control. Disruption of this inhibition may underlie stress-related dysfunction of the PL and represent a therapeutic target for treating stress-induced deficits in affect regulation and impaired cognition that reduce quality of life.

Cognitive gadgets and genetic accommodation

2019 ◽  
Vol 42 ◽  
Author(s):  
Eva Jablonka ◽  
Simona Ginsburg ◽  
Daniel Dor
Keyword(s):  
Cognitive Flexibility ◽  
Metacognitive Strategies ◽  
Genetic Evolution ◽  
Genetic Accommodation

Abstract Heyes argues that human metacognitive strategies (cognitive gadgets) evolved through cultural rather than genetic evolution. Although we agree that increased plasticity is the hallmark of human metacognition, we suggest cognitive malleability required the genetic accommodation of gadget-specific processes that enhanced the overall cognitive flexibility of humans.

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