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Trigeminal cardiac reflex in post-operative spheno-orbital meningioma
Published in Cut Adeya Adella, Stem Cell Oncology, 2018
The proposed mechanism for the development of TCR is that the sensory nerve endings of the trigeminal nerve send neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc (Schaller et al., 1999; Schaller, 2004). This afferent pathway continues along the short internuncial nerve fibres in the reticular formation to connect with the efferent pathway in the motor nucleus of the vagus nerve. Several lines of experimental evidence demonstrate that trigeminally induced cardiovascular reflexes could be mediated initially in the trigeminal nucleus caudalis and subsequently in the parabrachial nucleus, the rostral ventrolateral medulla oblongata, the dorsal medullary reticular field, and the paratrigeminal nucleus in animal models (Schaller et al., 2009).
Static electric field exposure decreases white blood cell count in peripheral blood through activating hypothalamic–pituitary–adrenal axis
Published in International Journal of Environmental Health Research, 2022
Jiahong Wu, Li Dong, Junli Xiang, Guoqing Di
One significant mechanism for HPA axis habituation is CORT-mediated negative feedback (Tasker and Herman 2011). As the main sites of CORT-mediated negative feedback, both the hypothalamus and the pituitary contain abundant GRs, which allows them to respond to excessive CORT by forming a CORT-GR complex (Laryea et al. 2015). In the parvocellular neurons of the hypothalamus, the CORT-GR complex could repress the expression of CRH gene by binding to the negative glucocorticoid response element (nGRE) in the CRH promoter (Webster and Cidlowski 1999). The inhibition of CRH gene expression would reduce its own subsequent synthesis (Kim and Iremonger 2019). In the basophilic cells of the pituitary, the CORT-GR complex could suppress the expression of Proopiomelanocortin (POMC) gene by binding to the nGRE in the POMC promoter (Webster and Cidlowski 1999). Since POMC is the precursor of ACTH (Pecori et al. 2011), the inhibition of POMC gene expression can reduce the synthesis of ACTH (Grissom and Bhatnagar 2009). With the synthesis of CRH and ACTH recovered, the stimulatory effect of ACTH on CORT synthesis was attenuated, and the HPA axis activation magnitude declined (Kim and Iremonger 2019). The regulation of stress-related neural circuitry is another important mechanism of HPA axis habituation (Grissom and Bhatnagar 2009). Among the stress-related neural circuitry, the posterior paraventricular thalamus (pPVT) is a key structure of HPA axis habituation under the condition of chronic stress (Hsu et al. 2014). The pPVT could receive afferent inputs originating from the parabrachial nucleus, locus coeruleus, dorsal raphe and the periaqueductal gray. Through integrating these afferent inputs, the pPVT could judge whether the stressor is a homotypic stressor or a heterotypic stressor (Mccarty 2016). Once the pPVT identifies that the stressor is a homotypic stressor, it projects signals to the medial prefrontal cortex and the ventricular subiculum. The signals of these two regions could be integrated by the bed nucleus of the stria terminalis and then projected to the paraventricular nucleus of the hypothalamus (PVN). As the control center of HPA axis activity, the PVN decreases the HPA axis activation magnitude. On the basis of the analysis above, it is concluded that the HPA axis habituation to SEF exposure in this study involves multiple mechanisms including CORT-mediated negative feedback and the regulation of stress-related neural circuitry.