About this Research Topic
The involvement of the prefrontal cortex in complex psycho-affective disorders is very well established. Brain imaging and post-mortem studies have revealed abnormal synaptic activity and impaired homeostasis and neuroplasticity in prefrontocortical networks that regulate executive function and stress adaptation.
However, we are only beginning to uncover the precise cortical neural circuitry and systems crucial to underlying neurodevelopmental and stress-related pathophysiologies. These cortical systems comprise the bipartite default mode and executive networks. Human studies and counterpart animal work have suggested a well-coordinated oftentimes antagonistic interplay between these cortical networks as they concertedly control subcortical processes related to emotion regulation and action selection, respectively.
It is now evident that these top-down cognitive influences rely greatly in the filtering and fine-tuning of information along well-defined excitatory units (pyramidal neurons) and inhibitory units (e.g. parvalbumin-, somatostatin- and cholecystokinin-expressing interneurons) topographically organized across the cortical layers. There is a growing body of evidence highlighting the vulnerability of excitatory-inhibitory homeostasis in these circuits as a consequence of early life adversity, chronic stress, drug exposure, neuroinflammation, immune-compromising events and epigenetic mechanisms, especially crucial during critical development periods.
Their impact on prefrontal-subcortical regulation are powerful predictors of the onset, trajectory and time course of psycho-affective disorders, including depression, attention-deficit hyperactivity disorder and schizophrenia. Indeed, novel putative rapid-acting therapeutics and preventive interventions have been shown to correct prefrontocortical plasticity dysregulation in a circuit-specific and sometimes cell unit-selective manner. Further investigation into mechanisms at the circuit and cell unit levels could pave the way to better therapeutic outcomes with prefrontal-targeted treatment modalities.
We welcome article contributions focusing on prefrontocortical mechanisms and their involvement in the pathogenesis and pathophysiology of neurodevelopmental, cognitive and affective disorders. We welcome submissions that highlight basic and preclinical studies, especially those with strong translational implications. These could include investigations scrutinizing the effects of stress-related and neurodevelopmental factors on prefrontocortical circuit dynamics and plasticity in normal and disease states.
However, we are only beginning to uncover the precise cortical neural circuitry and systems crucial to underlying neurodevelopmental and stress-related pathophysiologies. These cortical systems comprise the bipartite default mode and executive networks. Human studies and counterpart animal work have suggested a well-coordinated oftentimes antagonistic interplay between these cortical networks as they concertedly control subcortical processes related to emotion regulation and action selection, respectively.
It is now evident that these top-down cognitive influences rely greatly in the filtering and fine-tuning of information along well-defined excitatory units (pyramidal neurons) and inhibitory units (e.g. parvalbumin-, somatostatin- and cholecystokinin-expressing interneurons) topographically organized across the cortical layers. There is a growing body of evidence highlighting the vulnerability of excitatory-inhibitory homeostasis in these circuits as a consequence of early life adversity, chronic stress, drug exposure, neuroinflammation, immune-compromising events and epigenetic mechanisms, especially crucial during critical development periods.
Their impact on prefrontal-subcortical regulation are powerful predictors of the onset, trajectory and time course of psycho-affective disorders, including depression, attention-deficit hyperactivity disorder and schizophrenia. Indeed, novel putative rapid-acting therapeutics and preventive interventions have been shown to correct prefrontocortical plasticity dysregulation in a circuit-specific and sometimes cell unit-selective manner. Further investigation into mechanisms at the circuit and cell unit levels could pave the way to better therapeutic outcomes with prefrontal-targeted treatment modalities.
We welcome article contributions focusing on prefrontocortical mechanisms and their involvement in the pathogenesis and pathophysiology of neurodevelopmental, cognitive and affective disorders. We welcome submissions that highlight basic and preclinical studies, especially those with strong translational implications. These could include investigations scrutinizing the effects of stress-related and neurodevelopmental factors on prefrontocortical circuit dynamics and plasticity in normal and disease states.
Keywords: Prefrontal cortex, Psycho-affective disorder, Neuroplasticity, Subcortical regulation, Network homeostasis
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