Various forms of reproductive suppression are displayed within this family: in the solitary species, breeding is suspended for part of the year and in the social species, reproduction is suppressed in subordinate animals. This study investigated the gonadotrophin-releasing hormone 1 (GnHR-1) systems of breeding and non-breeding solitary Cape mole-rats and social Natal mole-rats for possible inter-and/or intra-species differences. In both species, GnRH-1 cell bodies are predominantly in the medial septum region of the diagonal band or the preoptic

area, with relatively few in the mediobasal hypothalamus; a dense concentration of GnRH1-immunoreactive (ir) processes is present in the region of the organum vasculosum of the lamina terminalis. In Cape mole-rats, GnRH-1-ir processes are particularly dense within the E7080 purchase lateral margins of the median eminence, which is enfolded by a large pars tuberalis of the pituitary gland. Natal mole-rats display GnRH-1-ir processes across the breadth of the median eminence, which is abutted by a relatively small pars tuberalis. There are more GnRH-1-ir cell bodies in Natal mole-rats than in Cape mole-rats (similar to 720 vs. similar to 420). No significant

differences were found in the number, www.selleckchem.com/products/Pazopanib-Hydrochloride.html distribution or size of GnRH-1-ir cell bodies according to season in Cape mole-rats or PS-341 ic50 according to reproductive status or sex in Natal mole-rats. In female and male Natal mole-rats, GnRH-1-immunoreactivity in the median eminence is less dense in the reproductive animals; no such difference was found in Cape mole-rats between the breeding and non-breeding seasons. These immunohistochemical results are discussed in the light of earlier studies which identified no functional neuroendocrine impediments

underlying regulated reproduction in either Cape or Natal mole-rats. The cumulative findings suggest that the principal factors determining seasonal or socially induced suppression of reproduction in these species are behavioral rather than neuroendocrine. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The mechanism(s) by which herpes simplex virus type 1 (HSV-1) latency is established in neurons is not known. In this study, we examined the effect of dendritic cells (DCs) on the level of HSV-1 latency in trigeminal ganglia (TGs) of ocularly infected BALB/c and C57BL/6 mice. We found that immunization of wild-type mice with FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which increases the number of DCs, increased the amount of latency in infected mice. Conversely, depletion of DCs was associated with reduced latency. Latency was also significantly reduced in Flt3L(-/-) and CD8(-/-) mice. Interestingly, immunization of Flt3L(-/-) but not CD8(-/-) mice with Flt3L DNA increased latency.