ArticleFrontiers in molecular neuroscience2019
Malocclusion Generates Anxiety-Like Behavior Through a Putative Lateral Habenula-Mesencephalic Trigeminal Nucleus Pathway.
Article in Frontiers in molecular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Occlusal disharmony attenuates inhibitory synaptic transmission in the medial prefrontal cortex and contributes to anxiety.Biomedical journal · 2026Article
- Functional brain network alterations in a rat model of dental malocclusion.Frontiers in neuroscience · 2026Article
- The mesencephalic trigeminal neuron: electrophysiological insights into function and dysfunction.Frontiers in cellular neuroscience · 2026Review
- Mental Health and Malocclusion: A Comprehensive Review.Clinics and practice · 2025Review
- Foxg1 Modulation of the Prkcd Gene in the Lateral Habenula Mediates Trigeminal Neuralgia-Associated Anxiety-Like Behaviors in Mice.Molecular neurobiology · 2024Article
- Neurobiology of bruxism: The impact of stress (Review).Biomedical reports · 2024Review
- Article
- The ultrastructure of macaque mesencephalic trigeminal nucleus neurons.Experimental brain research · 2024Article
- Regulation of CeA-Vme projection in masseter hyperactivity caused by restraint stress.Frontiers in cellular neuroscience · 2024Article
- The neural substrates of bruxism: current knowledge and clinical implications.Frontiers in neurology · 2024Review
- Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review).Experimental and therapeutic medicine · 2023Review
- The Cognitive and Emotional Aspect in Fibromyalgia: The Importance of the Orofacial Sphere.Cureus · 2023Review
- Tachykinin receptor 3 in the lateral habenula alleviates pain and anxiety comorbidity in mice.Frontiers in immunology · 2023Article
- Spinal CCK1 Receptors Contribute to Somatic Pain Hypersensitivity Induced by Malocclusion via a Reciprocal Neuron-Glial Signaling Cascade.The journal of pain · 2022Article
- Occlusal Disharmony-A Potential Factor Promoting Depression in a Rat Model.Brain sciences · 2022Article
- Activation of the Mesencephalic Trigeminal Nucleus Contributes to Masseter Hyperactivity Induced by Chronic Restraint Stress.Frontiers in cellular neuroscience · 2022Article
- Activation of the VpdmFrontiers in cellular neuroscience · 2022Article
- Effect of dental malocclusion on cerebellar neuron activation via the dorsomedial part of the principal sensory trigeminal nucleus.European journal of oral sciences · 2021Article
- Animal Models of Temporomandibular Disorder.Journal of pain research · 2021Review
- Excitatory Impact of Dental Occlusion on Dorsal Motor Nucleus of Vagus.Frontiers in neural circuits · 2021Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malocclusion is an important risk factor for temporomandibular disorder (TMD), a series of disorders characterized by dysfunction in the orofacial region involving the temporomandibular joint (TMJ) and jaw muscles. We recently showed that experimental unilateral anterior crossbite (UAC) produced masseter hyperactivity through a circuit involving the periodontal proprioception, trigeminal mesencephalic nucleus (Vme), and trigeminal motor nucleus (Vmo). Anxiety is a common complication in patients with TMD. The lateral habenula (LHb) is involved in emotional modulation and has direct projections to the Vme. Therefore, the present research examined whether UAC facilitates excitatory input from the LHb to the Vme and, subsequently, anxiety-like behaviors in rats. The LHb activation was evaluated by the electrophysiological recording, assessment of vesicular glutamate transporter-2 (VGLUT2) mRNA expression, and measurement of anxiety-like behaviors. The effects of LHb activity on Vme were evaluated by electrophysiological recording from Vme neurons and local changes in VGLUT2 protein density. UAC produced anxiety in modeled rats and increased neuronal activity in the LHb. VGLUT2 mRNA expression was also increased in the LHb. Further, VGLUT2-positive boutons were observed in close apposite upon parvalbumin (PV)-labeled Vme neurons. VGLUT2 protein expression was also increased in the Vme. Significantly, injection of VGLUT2-targeted shRNA into the LHb reduced the expression of VGLUT2 protein in the Vme, attenuated UAC-associated anxiety-like behaviors, and attenuated electrophysiological changes in the Vme neurons. In conclusion, we show that UAC activates the LHb neurons as well as the periodontal proprioceptive pathway to provide excitatory input to the Vme and produce anxiety in rats. These findings provide a rationale for suppressing activity of the LHb to attenuate both the physical and psychological effects of TMD.
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