Mechanisms of craniofacial pain

Chichorro, Juliana Geremias; Porreca, Frank; Sessle, Barry J.

doi:10.1177/0333102417704187

Cited by 125 publications

(120 citation statements)

References 108 publications

(156 reference statements)

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“…The ability of CNS areas to undergo neuroplastic changes represents an integral process underlying functions as seemingly diverse as memory, cognition, somatosensation and sensorimotor functions. Neuroplasticity occurring in a particular CNS area may be associated with plasticity of nonneural cells, such as glia (ie, "glioplasticity") and in fact glia can influence the expression of neuroplasticity, for example as shown in the case of processes underlying memory and in trigeminal central sensitisation which is a feature of acute or chronic oro-facial pain states (for review, see refs [61][62][63]. Given the focus of this article, the following centres on the role that plasticity in one particular CNS area, the sensorimotor cortex, play in oro-facial sensorimotor functions.…”

Section: Plasticity Of the Sensorimotor Cortex And Its Role In Adapmentioning

confidence: 99%

Can you be too old for oral implants? An update on ageing and plasticity in the oro‐facial sensorimotor system

Sessle

2019

J of Oral Rehabilitation

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This review focuses on the capacity of the brain for plasticity and the utility and efficacy of oral implants in helping to restore oro‐facial sensorimotor functions, especially in elderly patients. The review first outlines the components of the oro‐facial sensorimotor system which encompasses both oro‐facial tissues and a number of brain regions. One such region is the sensorimotor cortex that controls the activity of the numerous oro‐facial skeletal muscles. These muscles are involved in a number of functions including reflexes and the more complex sensorimotor functions of mastication, swallowing and speech. The review outlines the use by the brain of sensory inputs from oro‐facial receptors in order to provide for exquisite sensorimotor control of the activity of the oro‐facial muscles. It highlights the role in this sensorimotor control played by periodontal mechanoreceptors and their sensory inputs to the brain, and how oral implants in concert with the plastic capacity of the brain may, at least in part, compensate for reduced sensorimotor functioning when teeth are lost. It outlines findings of ageing‐related decrements in oro‐facial sensorimotor functions and control. The changes in oro‐facial tissues and the brain that underlie these ageing‐related functional alterations are also considered, along with adaptive and compensatory processes that utilise the brain's capacity for plasticity. The review also notes the evidence that rehabilitation that incorporates adjunctive approaches such as sensorimotor training paradigms in addition to oral prostheses such as implants may enhance these processes and help maintain or facilitate recovery of sensorimotor functioning in the elderly.

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Section: Plasticity Of the Sensorimotor Cortex And Its Role In Adapmentioning

confidence: 99%

Can you be too old for oral implants? An update on ageing and plasticity in the oro‐facial sensorimotor system

Sessle

2019

J of Oral Rehabilitation

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“…In addition, outputs from the thalamus can be directed to other cortical and limbic structures that are responsible for processing the cognitive, affective, and emotional components of pain. 1,12,13 In addition, the activation of mesencephalic and bulbar structures can modulate nociceptive processing. The main inhibitory descending pathway includes structures such as the periaqueductal gray matter (GM) and the rostral ventromedial medulla (RVM), which projects to the VBSNC where the nociceptive responses are modulated.…”

mentioning

confidence: 99%

Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

2020

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The trigeminal nerve (V) is the fifth and largest of all cranial nerves, and it is responsible for detecting sensory stimuli that arise from the craniofacial area. The nerve is divided into three branches: ophthalmic (V1), maxillary (V2), and mandibular (V3); their cell bodies are located in the trigeminal ganglia and they make connections with second-order neurons in the trigeminal brainstem sensory nuclear complex. Ascending projections via the trigeminothalamic tract transmit information to the thalamus and other brain regions responsible for interpreting sensory information. One of the most common forms of craniofacial pain is trigeminal neuralgia. Trigeminal neuralgia is characterized by sudden, brief, and excruciating facial pain attacks in one or more of the V branches, leading to a severe reduction in the quality of life of affected patients. Trigeminal neuralgia etiology can be classified into idiopathic, classic, and secondary. Classic trigeminal neuralgia is associated with neurovascular compression in the trigeminal root entry zone, which can lead to demyelination and a dysregulation of voltage-gated sodium channel expression in the membrane. These alterations may be responsible for pain attacks in trigeminal neuralgia patients. The antiepileptic drugs carbamazepine and oxcarbazepine are the first-line pharmacological treatment for trigeminal neuralgia. Their mechanism of action is a modulation of voltage-gated sodium channels, leading to a decrease in neuronal activity. Although carbamazepine and oxcarbazepine are the first-line treatment, other drugs may be useful for pain control in trigeminal neuralgia. Among them, the anticonvulsants gabapentin, pregabalin, lamotrigine and phenytoin, baclofen, and botulinum toxin type A can be coadministered with carbamazepine or oxcarbazepine for a synergistic approach. New pharmacological alternatives are being explored such as the active metabolite of oxcarbazepine, eslicarbazepine, and the new Nav1.7 blocker vixotrigine. The pharmacological profiles of these drugs are addressed in this review.

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“…Previous studies have shown that the peptide EPQ(pY)EEIPIA may bind to the SH2 domain of SFKs and thereby activate the kinases (Liu et al, ; Xu, Doshi, Lei, Eck, & Harrison, ). Delivering 1 mM of the peptide into cultured neurons (Yu, Askalan, Keil, & Salter, ) or 5 mM of the peptide into hippocampal neurons in brain slice preparations (Chichorro, Porreca, & Sessle, ) significantly enhances SFK‐mediated neuronal activity. In this work, we investigated effects of the peptide EPQ(pY)EEIPIA delivered into neurons on the firing activity.…”

Section: Resultsmentioning

confidence: 99%

“…In this work, we investigated effects of the peptide EPQ(pY)EEIPIA delivered into neurons on the firing activity. Since the peptide EPQ(pY)EEIPIA is not membrane‐permeant (Liu et al, ; Xu et al, ), to examine the effect of direct activation of SFKs, the peptide was delivered into ARC neurons through recording electrodes filled with the internal solution containing the EPQ(pY)EEIPIA (1 mM) (Chichorro et al, ; Feng et al, ; Yu et al, ).…”

Section: Resultsmentioning

confidence: 99%

Regulation of the firing activity by PKA‐PKC‐Src family kinases in cultured neurons of hypothalamic arcuate nucleus

Sun

Wang

et al. 2019

J of Neuroscience Research

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The cAMP‐dependent protein kinase A family (PKAs), protein kinase C family (PKCs), and Src family kinases (SFKs) are found to play important roles in pain hypersensitivity. However, more detailed investigations are still needed in order to understand the mechanisms underlying the actions of PKAs, PKCs, and SFKs. Neurons in the hypothalamic arcuate nucleus (ARC) are found to be involved in the regulation of pain hypersensitivity. Here we report that the action potential (AP) firing activity of ARC neurons in culture was up‐regulated by application of the adenylate cyclase activator forskolin or the PKC activator PMA, and that the forskolin or PMA application‐induced up‐regulation of AP firing activity could be blocked by pre‐application of the SFK inhibitor PP2. SFK activation also up‐regulated the AP firing activity and this effect could be prevented by pre‐application of the inhibitors of PKCs, but not of PKAs. Furthermore, we identified that forskolin or PMA application caused increases in the phosphorylation not only in PKAs at T197 or PKCs at S660 and PKCα/βII at T638/641, but also in SFKs at Y416. The forskolin or PMA application‐induced increase in the phosphorylation of PKAs or PKCs was not affected by pre‐treatment with PP2. The regulations of the SFK and AP firing activities by PKCs were independent upon the translocation of either PKCα or PKCβII. Thus, it is demonstrated that PKAs may act as an upstream factor(s) to enhance SFKs while PKCs and SFKs interact reciprocally, and thereby up‐regulate the AP firing activity in hypothalamic ARC neurons.

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Mechanisms of craniofacial pain

Cited by 125 publications

References 108 publications

Can you be too old for oral implants? An update on ageing and plasticity in the oro‐facial sensorimotor system

Can you be too old for oral implants? An update on ageing and plasticity in the oro‐facial sensorimotor system

Trigeminal neuralgia: An overview from pathophysiology to pharmacological treatments

Regulation of the firing activity by PKA‐PKC‐Src family kinases in cultured neurons of hypothalamic arcuate nucleus

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