Prefrontal cortical areas are known to support goal-directed behaviors in humans, mediating a variety of functions that lead to behavioral flexibility/adaptability in response to continuously varying environmental demands. Normal prefrontal function relies on interconnectivity with subcortical brain structures, including the striatum and amygdala, as well as dopaminergic innervation and dopamine release from the ventral tegmental area.
Dysregulation of prefrontal connectivity or abnormal dopamine release at the level of the prefrontal cortex (PFC) can contribute to a variety of psychopathologies and mood disorders, including schizophrenia, bipolar disorder, attentional deficits, anxiety disorders, eating disorders, and compulsive drug-seeking. More recently, neuroinflammatory processes have been shown to alter dopamine release and neuroinflammation is associated with many of these etiologies.
While aspects of the circuits discussed above have been extensively studied, the field still lacks knowledge about the anatomical and functional interconnectivity between these systems. Importantly, the role of neuroinflammation across these regions and its contribution to corticolimbic circuit dysfunction and behavioral abnormalities is largely unknown. Moreover, studies examining single-cell phenomena pertinent to regional functions and intraregional connectivity, as well as the role of immunomodulatory mechanisms that regulate these phenomena, are sparce.
Exploring the links between changes in the neurophysiological properties of these cellular networks and psychopathological behavioral outcomes will advance the field’s current understanding.
With the continuous advancement of targeted techniques such as chemogenetics and optogenetics, precise control and dissection of neuronal underpinnings of these disease states have enhanced our ability to design targeted pharmacotherapies. Additionally, techniques and antibodies targeting neuroinflammatory markers provide an understanding of how neuroinflammation can contribute to particular disease states, and their usage may shed light on future treatment options in these individuals.
This Research Topic aims to further our knowledge on novel aspects of the neurophysiological and behavioral underpinnings of neuropsychiatric disorders linked to abnormalities in PFC network functionality. In particular, this Research Topic aims to expand our current understanding of neuroimmune mechanisms that play a vital role in shaping PFC network structure and function.
Towards these aims, this Research Topic welcomes articles addressing, but not limited to, the following topics:
• Single-cell physiology and gene expression within the prefrontal cortex and mesocorticolimbic structures associated with disease states and their relevance to regional connectivity.
• The use cell type-specific manipulation techniques (e.g., optogenetics, chemogenetics) to identify the role of single neuronal subtypes or glia in the behavioral aspects of disease states.
• Identification of neuroimmune biomarkers of pathology within mesocorticolimbic circuitry.
• Application of novel anatomical tracers to explore neuronal pathways between prefrontal cortical layers and reward-associated regions.
• High-resolution imaging of neuronal and glial cell structure to examine morphological alterations in disease states.
Prefrontal cortical areas are known to support goal-directed behaviors in humans, mediating a variety of functions that lead to behavioral flexibility/adaptability in response to continuously varying environmental demands. Normal prefrontal function relies on interconnectivity with subcortical brain structures, including the striatum and amygdala, as well as dopaminergic innervation and dopamine release from the ventral tegmental area.
Dysregulation of prefrontal connectivity or abnormal dopamine release at the level of the prefrontal cortex (PFC) can contribute to a variety of psychopathologies and mood disorders, including schizophrenia, bipolar disorder, attentional deficits, anxiety disorders, eating disorders, and compulsive drug-seeking. More recently, neuroinflammatory processes have been shown to alter dopamine release and neuroinflammation is associated with many of these etiologies.
While aspects of the circuits discussed above have been extensively studied, the field still lacks knowledge about the anatomical and functional interconnectivity between these systems. Importantly, the role of neuroinflammation across these regions and its contribution to corticolimbic circuit dysfunction and behavioral abnormalities is largely unknown. Moreover, studies examining single-cell phenomena pertinent to regional functions and intraregional connectivity, as well as the role of immunomodulatory mechanisms that regulate these phenomena, are sparce.
Exploring the links between changes in the neurophysiological properties of these cellular networks and psychopathological behavioral outcomes will advance the field’s current understanding.
With the continuous advancement of targeted techniques such as chemogenetics and optogenetics, precise control and dissection of neuronal underpinnings of these disease states have enhanced our ability to design targeted pharmacotherapies. Additionally, techniques and antibodies targeting neuroinflammatory markers provide an understanding of how neuroinflammation can contribute to particular disease states, and their usage may shed light on future treatment options in these individuals.
This Research Topic aims to further our knowledge on novel aspects of the neurophysiological and behavioral underpinnings of neuropsychiatric disorders linked to abnormalities in PFC network functionality. In particular, this Research Topic aims to expand our current understanding of neuroimmune mechanisms that play a vital role in shaping PFC network structure and function.
Towards these aims, this Research Topic welcomes articles addressing, but not limited to, the following topics:
• Single-cell physiology and gene expression within the prefrontal cortex and mesocorticolimbic structures associated with disease states and their relevance to regional connectivity.
• The use cell type-specific manipulation techniques (e.g., optogenetics, chemogenetics) to identify the role of single neuronal subtypes or glia in the behavioral aspects of disease states.
• Identification of neuroimmune biomarkers of pathology within mesocorticolimbic circuitry.
• Application of novel anatomical tracers to explore neuronal pathways between prefrontal cortical layers and reward-associated regions.
• High-resolution imaging of neuronal and glial cell structure to examine morphological alterations in disease states.
