scholarly journals Aggression-reducing effects of F15599, a novel selective 5-HT1A receptor agonist, after microinjection into the ventral orbital prefrontal cortex, but not in infralimbic cortex in male mice

2013 ◽  
Vol 230 (3) ◽  
pp. 375-387 ◽  
Author(s):  
Dirson João Stein ◽  
Klaus A. Miczek ◽  
Aldo Bolten Lucion ◽  
Rosa Maria Martins de Almeida
2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Stuart A Collins ◽  
Ipe Ninan

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.


eNeuro ◽  
2021 ◽  
pp. ENEURO.0045-21.2021
Author(s):  
Philip Vassilev ◽  
Andrea Haree Pantoja-Urban ◽  
Michel Giroux ◽  
Dominique Nouel ◽  
Giovanni Hernandez ◽  
...  

2021 ◽  
pp. 118-152
Author(s):  
Richard E. Passingham

The orbital prefrontal cortex (PF) receives inputs from the olfactory, gustatory, somatosensory, visceral, and visual cortex. It is also interconnected with the amygdala which represents the current value of the resources, given the internal state of the animal. The worth of the different foods is compared in a ‘common currency’ of value. The central sector of the orbital prefrontal cortex uses vision to predict the value of the resources. These changes depend on the extent to which the animal has already become satiated on a particular food, and an interaction between the amygdala and the orbital PF cortex supports the ability to choose a new food, rather than the one on which the animal has become satiated. The lateral sector of the orbital PF cortex supports the ability to change behaviour depending on the outcome.


2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Vinicius M. Gadotti ◽  
Zizhen Zhang ◽  
Junting Huang ◽  
Gerald W. Zamponi

AbstractPeripheral nerve injury can lead to remodeling of brain circuits, and this can cause chronification of pain. We have recently reported that male mice subjected to spared injury of the sciatic nerve undergo changes in the function of the medial prefrontal cortex (mPFC) that culminate in reduced output of layer 5 pyramidal cells. More recently, we have shown that this is mediated by alterations in synaptic inputs from the basolateral amygdala (BLA) into GABAergic interneurons in the mPFC. Optogenetic inhibition of these inputs reversed mechanical allodynia and thermal hyperalgesia in male mice. It is known that the processing of pain signals can exhibit marked sex differences. We therefore tested whether the dysregulation of BLA to mPFC signaling is equally altered in female mice. Injection of AAV-Arch3.0 constructs into the BLA followed by implantation of a fiberoptic cannula into the mPFC in sham and SNI operated female mice was carried out, and pain behavioral responses were measured in response to yellow light mediated activation of this inhibitory opsin. Our data reveal that Arch3.0 activation leads to a marked increase in paw withdrawal thresholds and latencies in response to mechanical and thermal stimuli, respectively. However, we did not observe nerve injury-induced changes in mPFC layer 5 pyramidal cell output in female mice. Hence, the observed light-induced analgesic effects may be due to compensation for dysregulated neuronal circuits downstream of the mPFC.


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