ReviewFrontiers in neural circuits2021
Differential Rearrangement of Excitatory Inputs to the Medial Prefrontal Cortex in Chronic Pain Models.
Review in Frontiers in neural circuits, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- The Wnt5a-PKCδ-GluA1 axis controls synapse-specific plasticity in HIV-1 gp120-induced pain pathogenesis.Brain : a journal of neurology · 2026Article
- Concordance between the fast and efficient mixed-effects algorithm (FEMA) and conventional mixed-effects modeling for whole-brain connectivity in longitudinal chronic pain.bioRxiv : the preprint server for biology · 2026Article
- CDK5-Induced HCN2 Channel Dysfunction in the Prelimbic Cortex Drives Allodynia and Anxiety-Like Behaviors in Neuropathic Pain.Neuroscience bulletin · 2025Article
- Article
- Increased mGluR5 in somatostatin-positive interneurons mediates deactivation of the mPFC in a mouse model of neuropathic pain.Experimental & molecular medicine · 2025Article
- The Selective 5HTSynapse (New York, N.Y.) · 2025Article
- Chronic Pain and Comorbid Emotional Disorders: Neural Circuitry and Neuroimmunity Pathways.International journal of molecular sciences · 2025Review
- AMPA/kainate receptor activation within the prelimbic cortex is necessary for incubated cocaine-craving.Frontiers in psychiatry · 2025Article
- Advances in Neuroimaging of Breast Cancer Pain: An Overview.Journal of pain research · 2025Review
- Neuropeptidergic systems in psychiatric disorders.Frontiers in endocrinology · 2025Review
- A mesocortical glutamatergic pathway modulates neuropathic pain independent of dopamine co-release.Nature communications · 2024Article
- Spatial transcriptomics reveals the distinct organization of mouse prefrontal cortex and neuronal subtypes regulating chronic pain.Nature neuroscience · 2023Article
- Article
- Global Cerebral Ischemia-induced Depression Accompanies Alteration of Neuronal Excitability in the Infralimbic Cortex Layer 2/3 Pyramidal Neurons.Experimental neurobiology · 2023Article
- Article
- The role of ketamine in major depressive disorders: Effects on parvalbumin-positive interneurons in hippocampus.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Impaired muscarinic modulation of the rat prelimbic cortex in neuropathic pain is sexually dimorphic and associated with cold allodynia.Frontiers in cellular neuroscience · 2023Article
- A Possible Mechanism for Development of Working Memory Impairment in Male Mice Subjected to Inflammatory Pain.Neuroscience · 2022Article
- Targeting 5-HTNeuroscience letters · 2022Article
- Cholinergic basal forebrain nucleus of Meynert regulates chronic pain-like behavior via modulation of the prelimbic cortex.Nature communications · 2022Article
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Authors and funding
3 authors.
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Abstract
Chronic pain patients suffer a disrupted quality of life not only from the experience of pain itself, but also from comorbid symptoms such as depression, anxiety, cognitive impairment, and sleep disturbances. The heterogeneity of these symptoms support the idea of a major involvement of the cerebral cortex in the chronic pain condition. Accordingly, abundant evidence shows that in chronic pain the activity of the medial prefrontal cortex (mPFC), a brain region that is critical for executive function and working memory, is severely impaired. Excitability of the mPFC depends on the integrated effects of intrinsic excitability and excitatory and inhibitory inputs. The main extracortical sources of excitatory input to the mPFC originate in the thalamus, hippocampus, and amygdala, which allow the mPFC to integrate multiple information streams necessary for cognitive control of pain including sensory information, context, and emotional salience. Recent techniques, such as optogenetic methods of circuit dissection, have made it possible to tease apart the contributions of individual circuit components. Here we review the synaptic properties of these main glutamatergic inputs to the rodent mPFC, how each is altered in animal models of chronic pain, and how these alterations contribute to pain-associated mPFC deactivation. By understanding the contributions of these individual circuit components, we strive to understand the broad spectrum of chronic pain and comorbid pathologies, how they are generated, and how they might be alleviated.
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