Perineuronal nets (PNNs) are condensed extracellular matrix (ECM) structures that enwrap the cell bodies and dendrites of specialized cells. Formation of PNNs is promoted by neuronal activity. Within the cortex and limbic structures, PNNs predominantly surround fast spiking parvalbumin positive GABAergic interneurons. As a core component of tetrapartite glutamatergic synapses, PNNs stabilize homeostatic synaptic plasticity, facilitate neuronal-glia communication, and provide a physical barrier protecting neurons from toxic molecules within the ECM. In adulthood, PNNs constrain plasticity by limiting receptor trafficking at synapses, acting as a scaffold for inhibitors of synaptic formation such as semaphorin A, and modifying synaptogenesis.
Dysregulated synaptic plasticity and excitatory inhibitory (E/I) imbalance are molecular hallmarks of multiple neuropsychiatric disorders. Pathological alterations in PNNs have been reported across several neuropsychiatric conditions ranging from major depressive disorder, chronic pain, and substance use disorder to autism and schizophrenia. Thus, restoration of normal PNN function has emerged as a potential therapeutic target for the remediation of several psychiatric disorders
This Research Topic aims to obtain an in-depth understanding of PNN impairment in neuropsychiatric disorders and highlight PNN components, such as hyaluronan, proteoglycans, tenascins, and Hapln proteins), which may serve as candidates for therapeutic intervention. Also, of relevance to these disorders are matrix metalloproteinase (MMPs), and other ECM molecules that degrade PNNs, and the inhibitors of these degradative proteinases (TIMP proteins).
We welcome manuscripts focused on but not limited to:
• Modification of PNN composition, integrity, and function in the context of neuropsychiatric disorders;
• PNNs or other ECM components as trait markers of dysregulated synaptic plasticity;
• PNNs or other ECM components as potential therapeutic targets for neuropsychiatric disorders.
Perineuronal nets (PNNs) are condensed extracellular matrix (ECM) structures that enwrap the cell bodies and dendrites of specialized cells. Formation of PNNs is promoted by neuronal activity. Within the cortex and limbic structures, PNNs predominantly surround fast spiking parvalbumin positive GABAergic interneurons. As a core component of tetrapartite glutamatergic synapses, PNNs stabilize homeostatic synaptic plasticity, facilitate neuronal-glia communication, and provide a physical barrier protecting neurons from toxic molecules within the ECM. In adulthood, PNNs constrain plasticity by limiting receptor trafficking at synapses, acting as a scaffold for inhibitors of synaptic formation such as semaphorin A, and modifying synaptogenesis.
Dysregulated synaptic plasticity and excitatory inhibitory (E/I) imbalance are molecular hallmarks of multiple neuropsychiatric disorders. Pathological alterations in PNNs have been reported across several neuropsychiatric conditions ranging from major depressive disorder, chronic pain, and substance use disorder to autism and schizophrenia. Thus, restoration of normal PNN function has emerged as a potential therapeutic target for the remediation of several psychiatric disorders
This Research Topic aims to obtain an in-depth understanding of PNN impairment in neuropsychiatric disorders and highlight PNN components, such as hyaluronan, proteoglycans, tenascins, and Hapln proteins), which may serve as candidates for therapeutic intervention. Also, of relevance to these disorders are matrix metalloproteinase (MMPs), and other ECM molecules that degrade PNNs, and the inhibitors of these degradative proteinases (TIMP proteins).
We welcome manuscripts focused on but not limited to:
• Modification of PNN composition, integrity, and function in the context of neuropsychiatric disorders;
• PNNs or other ECM components as trait markers of dysregulated synaptic plasticity;
• PNNs or other ECM components as potential therapeutic targets for neuropsychiatric disorders.
