NMDA receptors and synaptic plasticity in the anterior cingulate cortex

Chen, Qi-Yu; Li, Xu Hui; Zhuo, Min

doi:10.1016/j.neuropharm.2021.108749

Cited by 56 publications

(41 citation statements)

References 68 publications

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“…Stimulation protocols for the induction of LTD are typically lower in frequency and longer in duration compared to LTP induction protocols. For example, pairing presynaptic stimulation with postsynaptic depolarization or using TBS induces NMDAR-dependent LTP in the ACC in whole-cell recordings, whereas low-frequency stimulation (1 Hz) may trigger GluN2B subunit-containing NMDAR-dependent LTD [ 83 , 84 , 85 ]. The modulation of AMPARs is also involved in the induction but perhaps not the maintenance of LTD, as the application of an exogenous PKC activator led to the internalization of the GluA2 subunit-containing AMPARs leading to LTD [ 86 ].…”

Section: Long-term Depression (Ltd)mentioning

confidence: 99%

Synaptic Plasticity in the Pain-Related Cingulate and Insular Cortex

2022

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Cumulative animal and human studies have consistently demonstrated that two major cortical regions in the brain, namely the anterior cingulate cortex (ACC) and insular cortex (IC), play critical roles in pain perception and chronic pain. Neuronal synapses in these cortical regions of adult animals are highly plastic and can undergo long-term potentiation (LTP), a phenomenon that is also reported in brain areas for learning and memory (such as the hippocampus). Genetic and pharmacological studies show that inhibiting such cortical LTP can help to reduce behavioral sensitization caused by injury as well as injury-induced emotional changes. In this review, we will summarize recent progress related to synaptic mechanisms for different forms of cortical LTP and their possible contribution to behavioral pain and emotional changes.

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Section: Long-term Depression (Ltd)mentioning

confidence: 99%

Synaptic Plasticity in the Pain-Related Cingulate and Insular Cortex

2022

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“…Recent studies have found that some intracellular proteins may be involved in NMDAR transport, synaptic localization, and activity regulation through interaction with NMDARs. Postsynaptic density protein-95 (PSD-95) is a scaffold protein that can cause a series of downstream molecular events that can cause pain by interacting with NMDARs (Chen et al, 2021a , b ). It is generally believed that PSD-95 couples nNOS to NMDARs through the PDZ domain to form an NMDAR-PSD95-nNOS complex, which produces NO and leads to central sensitization (Lee et al, 2015 ; Li J. et al, 2021 ).…”

Section: The Regulation In the Expression And Activation Of Nmdarsmentioning

confidence: 99%

NMDARs mediate peripheral and central sensitization contributing to chronic orofacial pain

Liu

Fang

et al. 2022

Front. Cell. Neurosci.

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Peripheral and central sensitizations of the trigeminal nervous system are the main mechanisms to promote the development and maintenance of chronic orofacial pain characterized by allodynia, hyperalgesia, and ectopic pain after trigeminal nerve injury or inflammation. Although the pathomechanisms of chronic orofacial pain are complex and not well known, sufficient clinical and preclinical evidence supports the contribution of the N-methyl-D-aspartate receptors (NMDARs, a subclass of ionotropic glutamate receptors) to the trigeminal nociceptive signal processing pathway under various pathological conditions. NMDARs not only have been implicated as a potential mediator of pain-related neuroplasticity in the peripheral nervous system (PNS) but also mediate excitatory synaptic transmission and synaptic plasticity in the central nervous system (CNS). In this review, we focus on the pivotal roles and mechanisms of NMDARs in the trigeminal nervous system under orofacial neuropathic and inflammatory pain. In particular, we summarize the types, components, and distribution of NMDARs in the trigeminal nervous system. Besides, we discuss the regulatory roles of neuron-nonneuronal cell/neuron-neuron communication mediated by NMDARs in the peripheral mechanisms of chronic orofacial pain following neuropathic injury and inflammation. Furthermore, we review the functional roles and mechanisms of NMDARs in the ascending and descending circuits under orofacial neuropathic and inflammatory pain conditions, which contribute to the central sensitization. These findings are not only relevant to understanding the underlying mechanisms, but also shed new light on the targeted therapy of chronic orofacial pain.

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“…Under normal physiological conditions, glutamate is involved in synaptic plasticity, sensory, movement, emotional, memory and other brain functions by acting on synaptic N-methyl-D-aspartate receptors (NMDARs) and other receptors [9]. For example, NMDAR-dependent long-term potentiation (LTP) in the hippocampus participates in the formation of long-term memory [10]. Besides some researches revealed the involvement of glutamate-related genes in risk for mood disorders [11].…”

Section: Introductionmentioning

confidence: 99%

Activation of CREB-BDNF Pathway in Pyramidal Neurons in the Hippocampus Improves the Neurological Outcome of Mice with Ischemic Stroke

et al. 2022

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Cerebral ischemia is characterized by several pathological reaction evolving over time. Hyperactivation of glutamatergic neurons is the main factor leading to excitotoxicity which potentiates oxidative stress and triggers the mechanisms of neural apoptosis after cerebral ischemia. However, it is unclear whether glutamate in the ventral hippocampal Cornus Ammonis 1 (vCA1) acts a part in neurological de cits, pain perception, anxiety and depression induced by ischemic-stroke. We investigated the effects of chemogenetic inhibition or activation of vCA1 pyramidal neurons which are mainly glutamatergic neurons on sequelae induced by cerebral ischemia. Our results revealed that inhibition of vCA1 pyramidal neurons by chemogenetics alleviated neurological de cits, pain perception, anxiety and depression caused by cerebral ischemia in mice, but activation of vCA1 pyramidal neurons had limited effects. Moreover, we found that stroke was accompanied by decreased levels of cAMP-response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in vCA1, which are modulated by glutamate.In this study, overexpression of CREB protein in pyramidal neurons in vCA1 by AAV virus signi cantly upregulated the content of BDNF and ameliorated the dysfunction induced by ischemic-stroke. Our results demonstrated activation of CREB-BDNF pathway in vCA1 pyramidal neurons signi cantly improved neurological de cits, pain perception, anxiety and depression induced by ischemic-stroke.

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NMDA receptors and synaptic plasticity in the anterior cingulate cortex

Cited by 56 publications

References 68 publications

Synaptic Plasticity in the Pain-Related Cingulate and Insular Cortex

Synaptic Plasticity in the Pain-Related Cingulate and Insular Cortex

NMDARs mediate peripheral and central sensitization contributing to chronic orofacial pain

Activation of CREB-BDNF Pathway in Pyramidal Neurons in the Hippocampus Improves the Neurological Outcome of Mice with Ischemic Stroke

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