Given the fact that the nervous system is a complex neural network and many interconnected neurons constitute the cellular substrate for processing and transferring information, focusing on synchronous activities of clustered neurons, or neural circuits, is essential when discussing diverse neurophysiological functions.
Neural circuits are characterized by populations of neurons interconnected by synapses, and they can be activated to execute a specific function. In recent studies, neural circuits have been gradually found to play a critical role in the context of mood and behavioral regulation, therefore having therapeutic potential for neuropsychiatric disorders.
However, since extremely complex processes underlie the emotional and behavioral repertoires of both humans and animals, the neurophysiological and neuropathological mechanisms at the basis of neuropsychiatric disorders are still obscure.
For a long time, people looked at the pathogenesis of neuropsychological diseases, putting more emphasis on molecular modulators, such as monoamines, amino acids, steroids, and peptide hormones. However, this well-known hypothesis of neurological diseases caused by neurotransmitters and/or their receptors’ abnormalities, for example, the so-called “Monoamine Hypothesis” of depression, appears to be insufficient to explain the onset of behavioral and mood alterations.
Thanks to the rapid technological development, novel genetic, viral and optogenetic tools make it possible to detect the synchronous activity of different clusters of neurons interconnected by synapses. For example, technologies like Positron Emission Tomography (PET) and functional Magnetic Resonance Imaging (fMRI) revealed abnormal activity in specific brain regions in patients affected by mood disorders or neurodegenerative diseases.
In animal research, specific cell types or monosynaptic circuits, which are characterized by a single chemical synapse transmitting the signal, could be identified via optogenetics upon external stimuli. It has been shown for example that, under different conditions, the same neural circuit might affect different behavioral physiological processes. In particular, recent literature demonstrated that cannabinoid CB1 receptors in the amygdalar cholecystokinin glutamatergic afferents to the nucleus accumbens (NAc), which is an extensively studied reward circuit, can modulate depressive-like behavior.
In addition, it is known that neural circuits can affect physiological processes via different downstream targets. For example, entorhinal cortex glutamatergic afferents to the hippocampus were reported to potentiate learning and memory, and recent findings supplemented its antidepressant actions.
In this Research Topic, we invite contributions focusing on recent advances in the study of the neural circuitry involved in mood and behavioral regulation and their therapeutic potential for neurological diseases. We will welcome the submission of basic and translational Original Research, Review, and Mini-Review articles.
Potential topics will include, but won’t be limited to:
1. Optogenetic investigation of neural circuits in the context of mood disorders;
2. Sex differences in the neural circuits activated by stress hormones;
3. Amygdala circuits: implication of CB1-dependent LTD (Long-Term Depression) in the context of mood disorder;
4. Stress-induced neural activities in the medial prefrontal cortex projections to the basolateral amygdala;
5. The link between clinical depression and abnormal activity in the emotional brain circuitry;
6. The role of neural plasticity in depression: from the hippocampus to the prefrontal cortex.
Given the fact that the nervous system is a complex neural network and many interconnected neurons constitute the cellular substrate for processing and transferring information, focusing on synchronous activities of clustered neurons, or neural circuits, is essential when discussing diverse neurophysiological functions.
Neural circuits are characterized by populations of neurons interconnected by synapses, and they can be activated to execute a specific function. In recent studies, neural circuits have been gradually found to play a critical role in the context of mood and behavioral regulation, therefore having therapeutic potential for neuropsychiatric disorders.
However, since extremely complex processes underlie the emotional and behavioral repertoires of both humans and animals, the neurophysiological and neuropathological mechanisms at the basis of neuropsychiatric disorders are still obscure.
For a long time, people looked at the pathogenesis of neuropsychological diseases, putting more emphasis on molecular modulators, such as monoamines, amino acids, steroids, and peptide hormones. However, this well-known hypothesis of neurological diseases caused by neurotransmitters and/or their receptors’ abnormalities, for example, the so-called “Monoamine Hypothesis” of depression, appears to be insufficient to explain the onset of behavioral and mood alterations.
Thanks to the rapid technological development, novel genetic, viral and optogenetic tools make it possible to detect the synchronous activity of different clusters of neurons interconnected by synapses. For example, technologies like Positron Emission Tomography (PET) and functional Magnetic Resonance Imaging (fMRI) revealed abnormal activity in specific brain regions in patients affected by mood disorders or neurodegenerative diseases.
In animal research, specific cell types or monosynaptic circuits, which are characterized by a single chemical synapse transmitting the signal, could be identified via optogenetics upon external stimuli. It has been shown for example that, under different conditions, the same neural circuit might affect different behavioral physiological processes. In particular, recent literature demonstrated that cannabinoid CB1 receptors in the amygdalar cholecystokinin glutamatergic afferents to the nucleus accumbens (NAc), which is an extensively studied reward circuit, can modulate depressive-like behavior.
In addition, it is known that neural circuits can affect physiological processes via different downstream targets. For example, entorhinal cortex glutamatergic afferents to the hippocampus were reported to potentiate learning and memory, and recent findings supplemented its antidepressant actions.
In this Research Topic, we invite contributions focusing on recent advances in the study of the neural circuitry involved in mood and behavioral regulation and their therapeutic potential for neurological diseases. We will welcome the submission of basic and translational Original Research, Review, and Mini-Review articles.
Potential topics will include, but won’t be limited to:
1. Optogenetic investigation of neural circuits in the context of mood disorders;
2. Sex differences in the neural circuits activated by stress hormones;
3. Amygdala circuits: implication of CB1-dependent LTD (Long-Term Depression) in the context of mood disorder;
4. Stress-induced neural activities in the medial prefrontal cortex projections to the basolateral amygdala;
5. The link between clinical depression and abnormal activity in the emotional brain circuitry;
6. The role of neural plasticity in depression: from the hippocampus to the prefrontal cortex.
