Expression of estrogen receptors α and β in the trigeminal mesencephalic nucleus of adult women and men

Alimy-Allrath, Tahmina; Ricken, Albert; Bechmann, Ingo

doi:10.1016/j.aanat.2014.06.003

Cited by 8 publications

(1 citation statement)

References 41 publications

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“…CGRP is a 37-amino acid neuropeptide and has shown sex differences in expression, regulation, function, and behavior [25][26][27]. Past research has indicated that female sex hormones have the capacity to initiate the activation of the trigeminovascular system, leading to the subsequent release of CGRP [28][29][30][31][32][33]. Furthermore, these hormones exert their in uence on sensory neurons in both the central and peripheral nervous systems, thereby playing a contributory role in CGRP release [34,35].…”

Section: Introductionmentioning

confidence: 99%

CGRP as a potential mediator for the sexually dimorphic responses to traumatic brain injury

Li,

Ajmal,

Khaled

et al. 2024

Preprint

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Background The outcomes of traumatic brain injury (TBI) exhibit variance contingent upon biological sex. Although female sex hormones exert neuroprotective effects, the administration of estrogen and progesterone has not yielded conclusive results. Hence, it is conceivable that additional mediators, distinct from female sex hormones, merit consideration due to their potential differential impact on TBI outcomes. Calcitonin gene-related peptide (CGRP) exhibits sexually dimorphic expression and demonstrates neuroprotective effects in acute brain injuries. In this study, we aimed to examine sex-based variations in TBI structural and functional outcomes with respect to CGRP expression. Methods Male and female Sprague Dawley rats were exposed to controlled cortical impact to induce severe TBI, followed by interventions with and without CGRP inhibition. In the acute phase of TBI, the study centered on elucidating the influence of CGRP on oxidative stress, nuclear factor erythroid 2-related factor 2 (Nrf2) and endothelial nitric oxide synthase (eNOS) signaling in the peri-impact tissue. Subsequently, during the chronic phase of TBI, the investigation expanded to evaluate CGRP expression in relation to lesion volume, microvascular dysfunction, and white matter injury, as well as working and spatial memory, anxiety-like, and depression-like behaviors in subjects of both sexes. Results Female rats exhibited elevated levels of CGRP in the peri-impact brain tissue during both baseline conditions and in the acute and chronic phases of TBI, in comparison to age-matched male counterparts. Enhanced CGRP levels in specific brain sub-regions among female rats correlated with superior structural and functional outcomes following TBI compared to their male counterparts. CGRP inhibition induced heightened oxidative stress and a reduction in the expression of Nrf2 and eNOS in both male and female rats, with the observed alteration being more pronounced in females than in males. Conclusions This study marks the inaugural identification of CGRP as a downstream mediator contributing to the sexually dimorphic response observed in TBI outcomes.

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