Varicella Zoster Virus Associated Affective Pain

Infection with varicella zoster virus (VZV) resulting in chicken pox and after this initial infection the virus remains latent in sensory nerve ganglia until reactivation results in a painful disorder termed herpes zoster or shingles. studies in females indicated that during proestrus when estradiol is high there was a reducing response to VZV inducing pain versus diestrus when estradiol was low.

In an inflammatory temporomandibular joint (TMJ) model; rats giving a low diestrus level of estradiol had a greater nociceptive response in comparison to rats given a high proestrus dose of estradio; Estradiol effects neuronal activity within the thalamus; indicating sex hormones control neuronal function; and sex steroids like estrogen can increase activity in the thalamus of stressing in rats.

Varicella zoster virus

Sex steroids also influence the excitability of neurons by altering GABA amino decarboxylase (GAD) and GABAA receptor subunits expression. Thus, it was hypothesizing that estradiol attenuating herpes zoster induced pain by modulating GABA ergic signaling in the thalamus.

But the pERK activity within GAD; and glutaminase staining cells were quantitating within the thalamus to characterize the role of inhibitory; and excitatory neurons within the thalamus. Thalamic infusion of an estrogen receptor antagonist ICI was completing to identify if estradiol was inducing its action on behavior through the estrogen receptor.

RNA lipid tissue kit

But the RNA was isolating from thalamic tissue; punches obtaining from five randomly selecting animals per group in experiment  RNA extraction was performed using the RNA Lipid Tissue Kit from Qiagen; A high, physiological concentration of estradiol; reducing VZV associating affective pain and administration estrogen receptor antagonist ICI increasing the pain response; but suggesting a role for estrogen and the estrogen receptor in shingles pain.

GABA genes such as VGAT increasing their expression after treatment; with estradiol but decreased after treatment with estrogen receptor antagonist ICI; Thus, estrogen can modulate pain acting centrally through genomic or non-genomic receptors to alter gene expression, calcium levels and oxidative responses.