scholarly journals Animal models in the study and treatment of orofacial pain

2019 ◽  
pp. 0-0
Author(s):  
MA Martinez-Garcia ◽  
BC Miguelanez-Medran ◽  
C Goicoechea
Keyword(s):  
Animal Models ◽  
Orofacial Pain

Animal Models of Orofacial Pain

2010 ◽  
pp. 93-104 ◽  
Author(s):  
Asma Khan ◽  
Kenneth M. Hargreaves
Keyword(s):  
Animal Models ◽  
Orofacial Pain

Chronic orofacial pain animal models - progress and challenges

2018 ◽  
Vol 13 (10) ◽  
pp. 949-964 ◽  
Author(s):  
Heitor G. Araújo-Filho ◽  
Erik W.M. Pereira ◽  
Adriana Rolim Campos ◽  
Lucindo J. Quintans-Júnior ◽  
Jullyana S.S. Quintans
Keyword(s):  
Animal Models ◽  
Orofacial Pain ◽  
Chronic Orofacial Pain

scholarly journals Potential Molecular Targets for Treating Neuropathic Orofacial Pain Based on Current Findings in Animal Models

2021 ◽  
Vol 22 (12) ◽  
pp. 6406
Author(s):  
Yukinori Nagakura ◽  
Shogo Nagaoka ◽  
Takahiro Kurose
Keyword(s):  
Animal Models ◽  
Trigeminal Nerve ◽  
Orofacial Pain ◽  
Signal Transmission ◽  
Molecular Targets ◽  
Biological Processes ◽  
Preclinical Research ◽  
Nerve Branch ◽  
Root Entry Zone ◽  
Trigeminal Root

This review highlights potential molecular targets for treating neuropathic orofacial pain based on current findings in animal models. Preclinical research is currently elucidating the pathophysiology of the disease and identifying the molecular targets for better therapies using animal models that mimic this category of orofacial pain, especially post-traumatic trigeminal neuropathic pain (PTNP) and primary trigeminal neuralgia (PTN). Animal models of PTNP and PTN simulate their etiologies, that is, trauma to the trigeminal nerve branch and compression of the trigeminal root entry zone, respectively. Investigations in these animal models have suggested that biological processes, including inflammation, enhanced neuropeptide-mediated pain signal transmission, axonal ectopic discharges, and enhancement of interactions between neurons and glial cells in the trigeminal pathway, are underlying orofacial pain phenotypes. The molecules associated with biological processes, whose expressions are substantially altered following trigeminal nerve damage or compression of the trigeminal nerve root, are potentially involved in the generation and/or exacerbation of neuropathic orofacial pain and can be potential molecular targets for the discovery of better therapies. Application of therapeutic candidates, which act on the molecular targets and modulate biological processes, attenuates pain-associated behaviors in animal models. Such therapeutic candidates including calcitonin gene-related peptide receptor antagonists that have a reasonable mechanism for ameliorating neuropathic orofacial pain and meet the requirements for safe administration to humans seem worth to be evaluated in clinical trials. Such prospective translation of the efficacy of therapeutic candidates from animal models to human patients would help develop better therapies for neuropathic orofacial pain.

scholarly journals Natural products assessed in animal models for orofacial pain – a systematic review

2017 ◽  
Vol 27 (1) ◽  
pp. 124-134 ◽  
Author(s):  
Pollyana S. Siqueira-Lima ◽  
Juliane C. Silva ◽  
Jullyana S.S. Quintans ◽  
Angelo R. Antoniolli ◽  
Saravanan Shanmugam ◽  
...  
Keyword(s):  
Systematic Review ◽  
Natural Products ◽  
Animal Models ◽  
Orofacial Pain

Comparison of antinociceptive effects of plain lidocaine versus lidocaine complexed with hydroxypropyl-β-cyclodextrin in animal models of acute and persistent orofacial pain

2019 ◽  
Vol 392 (5) ◽  
pp. 573-583
Author(s):  
Stéphani Batista de Oliveira ◽  
Erika Ivanna Araya ◽  
Eder Gambeta ◽  
Luiz Eduardo Nunes Ferreira ◽  
Michele Franz-Montan ◽  
...  
Keyword(s):  
Animal Models ◽  
Orofacial Pain ◽  
Antinociceptive Effects

The influence of orofacial pain on sleep pattern: A review of theory, animal models and future directions

2009 ◽  
Vol 10 (8) ◽  
pp. 822-828 ◽  
Author(s):  
Teresa C.B. Schütz ◽  
Monica L. Andersen ◽  
Sergio Tufik
Keyword(s):  
Animal Models ◽  
Orofacial Pain ◽  
Sleep Pattern ◽  
Future Directions

Inclusion complex between β-cyclodextrin and hecogenin acetate produces superior analgesic effect in animal models for orofacial pain

2017 ◽  
Vol 93 ◽  
pp. 754-762 ◽  
Author(s):  
Yasmim M.B.G. Carvalho ◽  
Paula P. Menezes ◽  
Bruna M.H. Sousa ◽  
Bruno S. Lima ◽  
Igor A.S. Trindade ◽  
...  
Keyword(s):  
Animal Models ◽  
Inclusion Complex ◽  
Analgesic Effect ◽  
Orofacial Pain ◽  
Hecogenin Acetate

Reductionist thinking and animal models in neuropsychiatric research

2019 ◽  
Vol 42 ◽  
Author(s):  
Nicole M. Baran
Keyword(s):  
Animal Models ◽  
Mental Disorders ◽  
Environmental Factors ◽  
Neuropsychiatric Disorders ◽  
Model Organisms ◽  
Developmental Genetic ◽  
Term Study ◽  
Genetic And Environmental Factors ◽  
Mechanisms Of Plasticity

AbstractReductionist thinking in neuroscience is manifest in the widespread use of animal models of neuropsychiatric disorders. Broader investigations of diverse behaviors in non-model organisms and longer-term study of the mechanisms of plasticity will yield fundamental insights into the neurobiological, developmental, genetic, and environmental factors contributing to the “massively multifactorial system networks” which go awry in mental disorders.

Inflammational Animal Models for Schizophrenia

2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel
Keyword(s):  
Animal Model ◽  
Animal Models ◽  
Immune Activation ◽  
Microglial Activation ◽  
Treatment Options ◽  
Early Adulthood ◽  
Brain Regions ◽  
Synaptic Connections ◽  
Preventive Interventions ◽  
Immunological System

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.

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