The nucleus accumbens core (NAcc) is an important component of brain reward circuitry, but studies have revealed its involvement in pain circuitry also. However, its effect on trigeminal neuralgia (TN) and the mechanism underlying it are yet to be fully understood. Therefore, this study aimed to examine the outcomes of optogenetic stimulation of NAcc GABAergic neurons in an animal model of TN. Animals were allocated into TN, sham, and control groups. TN was generated by infraorbital nerve constriction and the optogenetic virus was injected into the NAcc. In vivo extracellular recordings were acquired from the ventral posteromedial nucleus of the thalamus. Alterations of behavioral responses during stimulation “ON” and “OFF” conditions were evaluated. In vivo microdialysis was performed in the NAcc of TN and sham animals. During optogenetic stimulation, electrophysiological recordings revealed a reduction of both tonic and burst firing activity in TN animals, and significantly improved behavioral responses were observed as well. Microdialysis coupled with liquid chromatography/tandem mass spectrometry analysis revealed significant alterations in extracellular concentration levels of GABA, glutamate, acetylcholine, dopamine, and citrulline in NAcc upon optic stimulation. In fine, our results suggested that NAcc stimulation could modulate the transmission of trigeminal pain signals in the TN animal model.

Excruciating trigeminal neuralgia (TN) management is very difficult and severely affects the patient’s quality of life. Earlier studies have shown that the trigeminal ganglion (TG) comprises several receptors and signal molecules that are involved in the process of peripheral sensitization, which influences the development and persistence of neuropathic pain. Targeting TG can modulate this sensitization pathway and mediate the pain-relieving effect. So far,there are few studies in which modulation approaches to TG itself have been suggested so far. “Trigeminal ganglion modulation” and “trigeminal neuralgia” were used as search phrases in the Scopus Index and PubMed databases to discover articles that were pertinent to the topic. In this review, we address the role of the trigeminal ganglion in TN and underlying molecules and neuropeptides implicated in trigeminal pain pathways in processing pathological orofacial pain. We also reviewed different modulation approaches in TG for TN management. Furthermore, we discuss the prospect of targeting trigeminal ganglion to manage such intractable pain.

Newcastle disease (ND) is one of the major viral diseases of poultry, remains a constant threat in poultry farms that causes huge economic losses every year. However, little is known regarding the potential risk factors of the disease in broiler. The study was undertaken to ascertain the potential risk factors and biosecurity measures in ND prevalent broiler farm. A total of 116 broiler farms were considered as a sample size from a different area of Barishal district of Bangladesh in which 19.83% ND prevalence was found. In the findings, the farmers (33.62%) who had training on poultry farming, were significantly less ND positive case (7.69%). Besides this, among the different risk factors and biosecurity measures only shed location, ventilation, vaccination status, feeder and waterer cleaning frequency, visitors accession, pets in the farm, use of disinfectant and seasonal variation had significant effect on ND outbreak. However, among all the factors only farmers training (OR=0.025; 95% CI: 0.001-0.509), shed location (OR=0.035; 95% CI: 0.003-0.390), vaccination against ND (OR=0.017; 95% CI: 0.001-0.435) and use of disinfectant daily (OR=0.011; 95% CI: 0.000-0.294) made a unique statistically significant contribution to the regression model and the predictors had approximately similar strength on reporting ND outbreak. In completion, ND can be reduced in broiler farms by improving the level of common biosecurity, farm management practices, and minimizing the potential risk factors through training of farmers, awareness build-up, and enforcement of these practices on the farms.

No optimum genetic rat Huntington model both neuropathological using an adeno-associated virus (AAV-2) vector vector has been reported to date. We investigated whether direct infection of an AAV2 encoding a fragment of mutant huntingtin (AV2-82Q) into the rat striatum was useful for optimizing the Huntington rat model. We prepared ten unilateral models by injecting AAV2-82Q into the right striatum, as well as ten bilateral models. In each group, five rats were assigned to either the 2×1012 genome copies (GC)/mL of AAV2-82Q (×1, low dose) or 2×1013 GC/mL of AAV2-82Q (×10, high dose) injection model. Ten unilateral and ten bilateral models injected with AAV-empty were also prepared as control groups. We performed cylinder and stepping tests 2, 4, 6, and 8 weeks after injection, tested EM48 positive mutant huntingtin aggregates. The high dose of unilateral and bilateral AAV2-82Q model showed a greater decrease in performance on the stepping and cylinder tests. We also observed more prominent EM48-positive mutant huntingtin aggregates in the medium spiny neurons of the high dose of AAV2-82Q injected group. Based on the results from the present study, high dose of AAV2-82Q is the optimum titer for establishing a Huntington rat model. Delivery of high dose of human AAV2-82Q resulted in the manifestation of Huntington behaviors and optimum expression of the huntingtin protein in vivo.