Temporomandibular inflammation mobilizes parvalbumin and FosB/deltaFosB neurons of amygdala and dorsal raphe

Nascimento, Glauce Crivelaro do; Paula, Bruna Balbino de; Lowry, Christopher A.; Leite–Panissi, Christie Ramos Andrade

doi:10.1590/1414-431x20209950

Cited by 5 publications

(5 citation statements)

References 39 publications

(48 reference statements)

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“…Similarly, imaging findings demonstrate that TMD patients display structural and functional changes in the brainstem associated with descending pain controls including the RVM [ 14 , 20 , 21 , 52 ]. Further, CFA-evoked TMJ inflammation for 10 days changes neural activities indicated by FosB/delta FosB expression in the amygdala and dorsal raphe nucleus [ 139 ]. These findings suggest that CFA model displays an altered neural function in the CNS associated with affective dimension of pain associated with deep craniofacial tissues.…”

Section: Neural Mechanisms For Pain In the Deep Craniofacial Tissues In Animalsmentioning

confidence: 99%

Preclinical models of deep craniofacial nociception and temporomandibular disorder pain

Okamoto

Hasegawa

Piriyaprasath

et al. 2021

Japanese Dental Science Review

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Section: Neural Mechanisms For Pain In the Deep Craniofacial Tissues In Animalsmentioning

confidence: 99%

Preclinical models of deep craniofacial nociception and temporomandibular disorder pain

Okamoto

Hasegawa

Piriyaprasath

et al. 2021

Japanese Dental Science Review

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“…Dorsal raphe nucleus (DR) serotonergic (5-HT)-neurons play well-characterized roles in stress adaptation and stress-related depressive disorders ( Hernández-Vázquez et al, 2019 ; Ohmura et al, 2020 ). The DR neurons show FOS and FOSB/ΔFOSB activation both in acute and chronic stress in rodents ( Ishida et al, 2002 ; Turek and Ryabinin, 2005 ; Kormos et al, 2016 ; Farkas et al, 2017 ; Kovács et al, 2018 ; Lopes et al, 2019 ; Nascimento et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Age-Dependent FOSB/ΔFOSB Response to Acute and Chronic Stress in the Extended Amygdala, Hypothalamic Paraventricular, Habenular, Centrally-Projecting Edinger-Westphal, and Dorsal Raphe Nuclei in Male Rats

Kovács

Füredi

Ujvári

et al. 2022

Front. Aging Neurosci.

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FOS proteins are early-responding gene products that contribute to the formation of activator protein-1. Several acute and chronic stimuli lead to Fos gene expression, accompanied by an increase of nuclear FOS, which appears to decline with aging. FOSB is another marker to detect acute cellular response, while ΔFOSB mirrors long-lasting changes in neuronal activity upon chronic stress. The notion that the occurrence of stress-related mood disorders shows some age dependence suggests that the brain’s stress sensitivity is also a function of age. To study age-dependent stress vulnerability at the immediate-early gene level, we aimed to describe how the course of aging affects the neural responses of FOSB/ΔFOSB in the acute restraint stress (ARS), and chronic variable mild stress (CVMS) in male rats. Fourteen brain areas [central, medial, basolateral (BLA) amygdala; dorsolateral- (BNSTdl), oval- (BNSTov), dorsomedial-, ventral- (BNSTv), and fusiform- (BNSTfu) divisions of the bed nucleus of the stria terminalis; medial and lateral habenula, hypothalamic paraventricular nucleus (PVN), centrally-projecting Edinger-Westphal nucleus, dorsal raphe nucleus, barrel field of somatosensory cortex (S1)] were examined in the course of aging. Eight age groups [1-month-old (M), 1.5 M, 2 M, 3 M, 6 M, 12 M, 18 M, and 24 M] of rats were exposed to a single ARS vs. controls. In addition, rats in six age groups (2, 3, 6, 12, 18, and 24 M) were subjected to CVMS. The FOSB/ΔFOSB immunoreactivity (IR) was a function of age in both controls, ARS- and CVMS-exposed rats. ARS increased the FOSB/ΔFOSB in all nuclei (except in BLA), but only BNSTfu, BNSTv, and PVN reacted throughout the examined lifespan. The CVMS did not increase the FOSB/ΔFOSB in BLA, BNSTov, BNSTdl, and S1. PVN showed a constantly maintained FOSB/ΔFOSB IR during the examined life period. The maximum stress-evoked FOSB/ΔFOSB signal was detected at 2–3 M periods in the ARS- and at 6 M, 18 M in CVMS- model. Corresponding to our previous observations on FOS, the FOSB/ΔFOSB response to stress decreased with age in most of the examined nuclei. Only the PVN exerted a sustained age-independent FOSB/ΔFOSB, which may reflect the long-lasting adaptation response and plasticity of neurons that maintain the hypothalamus-pituitary-adrenal axis response throughout the lifespan.

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“…Nrxn3α is important for presynaptic GABA release (Aoto et al, 2015) and because parabrachial GABA release inhibits neuronal signals ascending from the trigeminal nucleus and trigeminal ganglia (Rodriguez et al, 2017;Raver et al, 2020) it is likely that by reducing Nrxn3 expression within amygdala that ascending pain signals would be enhanced. Consistent with this idea the amygdala has been shown to control orofacial affective pain responses (Nascimento et al, 2020;Askari-Zahabi et al, 2022). Moreover, GABAergic neurons within the central amygdala can regulate pain by inhibiting activity within the lateral parabrachial (Raver et al, 2020).…”

Section: Discussionmentioning

confidence: 80%

“…The parabrachial is known to control orofacial pain signals ( Rodriguez et al, 2017 ; Raver et al, 2020 ) and the amygdala controls affective orofacial pain ( Nascimento et al, 2020 ; Askari-Zahabi et al, 2022 ). Neurexin 3α (Nrxn3α) is important for presynaptic γ-Aminobutyric acid (GABA) release ( Aoto et al, 2015 ) and parabrachial GABA release inhibits neuronal signals ascending from the trigeminal nucleus and trigeminal ganglia ( Rodriguez et al, 2017 ; Raver et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Sex Differences in the Role of Neurexin 3α in Zoster Associated Pain

Kramer

Umorin

Hornung

et al. 2022

Front. Integr. Neurosci.

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Varicella zoster virus (VZV) induces orofacial pain and female rats show greater pain than male rats. During the proestrus phase of the estrous cycle the VZV induce pain response is attenuated in female rats. A screen of gene expression changes in diestrus and proestrus female rats indicated neurexin 3α (Nrxn3α) was elevated in the central amygdala of proestrus rats vs. diestrus rats. GABAergic neurons descend from the central amygdala to the lateral parabrachial region and Nrxn3α is important for presynaptic γ-Aminobutyric acid (GABA) release. Thus, we hypothesized that the reduced orofacial pain in male rats and proestrus female rats is the result of increased Nrxn3α within the central amygdala that increases GABA release from axon terminals within the parabrachial and inhibits ascending pain signals. To test this hypothesis Nrxn3 α expression was knocked-down by infusing shRNA constructs in the central amygdala. Then GABA release in the parabrachial was quantitated concomitant with measuring the pain response. Results revealed that knockdown of Nrxn3α expression significantly increases the pain response in both male rats and proestrus female rats vs. diestrus rats. GABA release was significantly reduced in the parabrachial of male and proestrus female rats after Nrxn3α knockdown. Neuronal activity of excitatory neurons was significantly inhibited in the parabrachial after Nrxn3α knockdown. These results are consistent with the idea that Nrxn3 within the central amygdala controls VZV associated pain by regulating GABA release in the lateral parabrachial that then modulates ascending orofacial pain signals.

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Temporomandibular inflammation mobilizes parvalbumin and FosB/deltaFosB neurons of amygdala and dorsal raphe

Cited by 5 publications

References 39 publications

Preclinical models of deep craniofacial nociception and temporomandibular disorder pain

Preclinical models of deep craniofacial nociception and temporomandibular disorder pain

Age-Dependent FOSB/ΔFOSB Response to Acute and Chronic Stress in the Extended Amygdala, Hypothalamic Paraventricular, Habenular, Centrally-Projecting Edinger-Westphal, and Dorsal Raphe Nuclei in Male Rats

Sex Differences in the Role of Neurexin 3α in Zoster Associated Pain

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