The increase of intrinsic excitability of layer V pyramidal cells in the prelimbic medial prefrontal cortex of adult mice after peripheral inflammation

Wu, Xiaobo; Liang, Biao; Gao, Yong‐Jing

doi:10.1016/j.neulet.2015.11.030

Cited by 24 publications

(24 citation statements)

References 30 publications

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“…These investigations showed that pharmacological deactivation of activity reduces chronic pain symptoms. In a study by Wu et al (2016) the excitability of prelimbic layer 5 pyramidal neuron was increased in a complete Freund’s adjuvant (CFA)-induced inflammatory pain model in mice, in contrast to the reduced intrinsic excitability (with enhanced glutamatergic transmission) of the layer 2/3 pyramidal neurons in CFA model rats ( Wang G.Q. et al, 2015 ).…”

Section: Activity Changes In the Mpfc In Chronic Pain Statesmentioning

confidence: 99%

Metabotropic Glutamate Receptor 5 in the Medial Prefrontal Cortex as a Molecular Determinant of Pain and Ensuing Depression

Chung

Kim

2018

Front. Mol. Neurosci.

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Pain and depression affect one another, and this bidirectional interaction implies the existence of common or interacting neural pathways. Among the neural circuits relevant to negative affection, the medial prefrontal cortex (mPFC) is known to be involved in both pain and depression. Persistent stress from physical pain and mental distress can evoke maladaptive changes in mPFC circuits to induce depression. Conversely, the unpleasant mood condition alters mPFC circuits to distort the appraisal of aversion and make individuals vulnerable to pain. In this article, recent findings regarding mPFC in chronic pain and/or depression are reviewed, with particular focus on the metabotropic glutamate receptor 5 (mGluR5). Although the involvement of mGluR5 within the mPFC in both pain and depressive disorders has been extensively studied, there are controversies regarding changes in the activity of the mPFC during chronic pain and depression, and the functional roles of mGluR5 on altered mPFC activity. We discuss alterations in the availability of mGluR5 in the mPFC in these disorders, its role in behavioral manifestations, and its possible influence on cellular subpopulations that mediate dysfunction in the mPFC. We also propose molecular mechanisms that may cause expressional changes in mGluR5 within the mPFC circuitry.

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Section: Activity Changes In the Mpfc In Chronic Pain Statesmentioning

confidence: 99%

Metabotropic Glutamate Receptor 5 in the Medial Prefrontal Cortex as a Molecular Determinant of Pain and Ensuing Depression

Chung

Kim

2018

Front. Mol. Neurosci.

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“…In addition, the firing activity of layer V prelimbic medial prefrontal cortex (mPFC) neurons by whole‐cell current–clamp recordings in brain slices following peripheral injection of complete Freund's adjuvant (CFA), a well‐characterized inflammatory pain model, has been carried out with the aim of assessing the effects of inflammatory pain in the brain. Results suggest that the electrophysiological properties of pyramidal cells in layer V prelimbic mPFC are significantly altered under peripheral inflammatory pain conditions (Wu et al, ).…”

Section: Neuroplasticity Of the Cortex With Neuropathic Pain And Inflmentioning

confidence: 99%

Neuroplasticity of Supraspinal Structures Associated with Pathological Pain

Boadas-Vaello

Homs

Reina

et al. 2017

The Anatomical Record

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Peripheral nerve and spinal cord injuries, along with other painful syndromes such as fibromyalgia, diabetic neuropathy, chemotherapeutic neuropathy, trigeminal neuralgia, complex regional pain syndrome, and/or irritable bowel syndrome, cause several neuroplasticity changes in the nervous system along its entire axis affecting the different neuronal nuclei. This paper reviews these changes, focusing on the supraspinal structures that are involved in the modulation and processing of pain, including the periaqueductal gray matter, red nucleus, locus coeruleus, rostral ventromedial medulla, thalamus, hypothalamus, basal ganglia, cerebellum, habenula, primary, and secondary somatosensory cortex, motor cortex, mammillary bodies, hippocampus, septum, amygdala, cingulated, and prefrontal cortex. Hyperexcitability caused by the modification of postsynaptic receptor expression, central sensitization, and potentiation of presynaptic delivery of neurotransmitters, as well as the reduction of inhibitory inputs, changes in dendritic spine, neural circuit remodeling, alteration of gray matter, and upregulation of proinflammatory mediators (e.g., cytokines) by reactivation of astrocytes and microglial cells are the main functional, structural, and molecular neuroplasticity changes observed in the above supraspinal structures, associated with pathological pain. Studying these changes in greater depth may lead to the implementation and improvement of new therapeutic strategies against pathological pain. Anat Rec, 300:1481-1501, 2017. © 2017 Wiley Periodicals, Inc.

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“…Indeed, although neuropathic pain inhibition was produced by a partial agonist of the NMDA receptor locally microinjected in the two divisions of mPFC, the PrL and infralimbic (IFL) cortexes, which are distinguished anatomically and functionally (Heidbreder & Groenewegen, ; Millecamps et al, ), bilateral mPFC lesions attenuated CFA‐induced hyperalgesia (Wang et al, ). Furthermore, the excitability of layer V pyramidal neurons in PrL mPFC proved to be facilitated in inflammatory pain conditions (Wu, Liang, Gao, ).…”

Section: Introductionmentioning

confidence: 99%

Characterization of the sensory, affective, cognitive, biochemical, and neuronal alterations in a modified chronic constriction injury model of neuropathic pain in mice

Medeiros

Freitas

Boccella

et al. 2019

J of Neuroscience Research

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The chronic constriction injury (CCI) of the sciatic nerve is a nerve injury-based model of neuropathic pain (NP). Comorbidities of NP such as depression, anxiety, and cognitive deficits are associated with a functional reorganization of the medial prefrontal cortex (mPFC). Here, we have employed an adapted model of CCI by placing one single loose ligature around the sciatic nerve in mice for investigating the alterations in sensory, motor, affective, and cognitive behavior and in electrophysiological and biochemical properties in the prelimbic division (PrL) of the mPFC. Our adapted model of CCI induced mechanical allodynia, motor, and cognitive impairments and anxietyand depression-like behavior. In the PrL division of mPFC was observed an increase in GABA and a decrease in d-aspartate levels. Moreover an increase in the activity of neurons responding to mechanical stimulation with an excitation, mPFC (+), and a decrease in those responding with an inhibition, mPFC (−), was found. Altogether these findings demonstrate that a single ligature around the sciatic nerve was able to induce sensory, affective, cognitive, biochemical, and functional alterations already observed in other neuropathic pain models and it may be an appropriate and easily reproducible model for studying neuropathic pain mechanisms and treatments. K E Y W O R D Saffective and cognitive behavior, chronic constriction injury, GABA and d-aspartate levels, ongoing-and mechanically evoked neural activity, prelimbic division of the medial prefrontal cortex | 339 MEDEIROS Et al.

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The increase of intrinsic excitability of layer V pyramidal cells in the prelimbic medial prefrontal cortex of adult mice after peripheral inflammation

Cited by 24 publications

References 30 publications

Metabotropic Glutamate Receptor 5 in the Medial Prefrontal Cortex as a Molecular Determinant of Pain and Ensuing Depression

Metabotropic Glutamate Receptor 5 in the Medial Prefrontal Cortex as a Molecular Determinant of Pain and Ensuing Depression

Neuroplasticity of Supraspinal Structures Associated with Pathological Pain

Characterization of the sensory, affective, cognitive, biochemical, and neuronal alterations in a modified chronic constriction injury model of neuropathic pain in mice

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