In estrogen-primed female rats, vaginal cervical stimulation (VCS) provided by male intromissions or by an experimenter enhances estrous behaviors exhibited by females during subsequent mating with a male. We tested the hypothesis that alpha(1)-adrenergic receptors, acting via the nitric oxide-cGMP-protein kinase G pathway, mediate VCS-induced facilitation of female reproductive behaviors. Ovariectomized, estradiol-primed rats received intracerebroventricular (icv) infusions of vehicle or pharmacological antagonists 15 or 60min before VCS. Estrous behaviors (lordosis and proceptivity) in the presence of a male were recorded immediately (0min), and 120min following VCS. First we verified that VCS, but not manual flank stimulation alone, enhanced estrous behaviors when females received icv infusion of the vehicles used to administer drugs. Increased estrous behavior was apparent immediately following VCS and persisted for 120min. We then infused prazosin, phenoxybenzamine (alpha(1)-adrenergic receptor antagonists), yohimbine, idaxozan (alpha(2)-adrenergic receptor antagonists), or propranolol (beta-adrenergic receptor antagonist) 15min prior to the application of VCS in females primed with 5mug estradiol benzoate. Only alpha(1)-adrenergic antagonists inhibited VCS facilitation of estrous behavior, apparent 120min after VCS. Finally, we administered specific inhibitors of soluble guanylyl cyclase, nitric oxide synthase or protein kinase G icv 15 or 60min before VCS. All three agents significantly attenuated VCS facilitation of estrous behavior. These data support the hypothesis that endogenously released norepinephrine, acting via alpha(1)-adrenergic receptors, mediates the facilitation of lordosis by VCS, and are consistent with a mechanism involving alpha(1)-adrenergic activation of the nitric oxide/cGMP/protein kinase G pathway.

We tested the hypothesis that GnRH, PGE 2 and db-cAMP act via the nitric oxide (NO)-cGMP and MAPK pathways to facilitate estrous behavior (lordosis and proceptivity) in estradiol-primed female rats. Estradiol-primed rats received intracerebroventricular (icv) infusions of pharmacological antagonists of NO synthase (L-NAME), NO-dependent soluble guanylyl cyclase (ODQ), protein kinase G (KT5823), or the ERK1/2 inhibitor PD98059 15 min before icv administration of 50 ng of GnRH, 1 μg of PGE 2 or 1 μg of db-cAMP. Icv infusions of GnRH, PGE 2 and db-cAMP enhanced estrous behavior at 1 and 2 hr after drug administration. Both L-NAME and ODQ blocked the estrous behavior induced by GnRH, PGE 2 and db-cAMP at some of the times tested. The protein kinase G inhibitor KT5823 reduced PGE 2 and db-cAMP facilitation of estrous behavior but did not affect the behavioral response to GnRH. In contrast, PD98059 blocked the estrous behavior induced by all three compounds. These data support the hypothesis that the NO-cGMP and ERK/MAPK pathways are involved in the lordosis and proceptive behaviors induced by GnRH, PGE 2 and db-cAMP. However, cGMP mediation of GnRH-facilitated estrous behavior is independent of protein kinase G.

Chondrocytes in the co-culture system or in enriched medium showed an increase in proliferation; only when osteoarthritis chondrocytes were cultured in enriched medium would they display a statistically significant increase in their proliferation rate and in their viability. When chondrocytes from the monolayer were analysed, differential mRNA expression of TGF-beta1 and IGF-1 was found during all passages, which suggests that these two growth factors might be involved in chondrocyte proliferation.

The aim of this work was to study the ontogeny of chondrocyte cell division using embryo, adult and osteoarthritic (OA) cartilage. We searched for mitosis phases and performed a comparative evaluation of mitotic index, basic fibroblast growth factor b (FGFb), transforming growth factor β1 (TGF-β1) receptors, cyclin dependent kinase (CDK1) and Cyclin-B expression in fetal, neonate, 3, 5, 8 weeks old rats and experimental OA. Our results showed that mitosis phases were observed in all normal cartilage studied, although, we found a decrease in mitotic index in relation to tissue development. No mitosis was detected in OA cartilage. We also found a statistical significant reduction in cell number in OA cartilage, compared with the normal tissue. Furthermore, FGFb and TGF-β1 receptors diminished in relation to tissue development, and were very scarce in experimental OA. Western blot assays showed CDK-1 expression in all cases, including human-OA cartilage. Similar results were observed for Cyclin-B, except for 8 weeks, when it was not expressed. Our results suggest that cell division seems to be scarce, if not absent within the OA cartilage studied. Nevertheless, the existence of factors essential for cell division leaves open the question concerning chondrocyte proliferation in OA cartilage, which is likely to be present in the early stages of the disease.

The aim of this study was to assess the levels of some persistent organic pollutants in the surface sediments from the Zahuapan and Atoyac rivers (Tlaxcala, Mexico), as well as to determine the genotoxic potential, by the micronucleus test in Vicia faba, of the sediments and agricultural soils irrigated with water from these rivers. This document is the first study on the presence of POPs in surface sediments of the above-mentioned rivers; among the compounds analyzed are the HCH isomers, DDT and its metabolite DDE, HCB, mirex, aldrin, and 41 PCB congeners. The concentrations of HCB, DDTs, HCHs, and PCBs ranged from 138-510, 45-450, 3-27, and 59-1876 μg kg −1 dry weight, respectively. The highest levels of HCB, HCH isomers, and PCB congeners were found in the Atoyac River, and these compounds have the potential for causing an environmental impact. On the other hand, biological testing shows that both sediments and agricultural soils possess a genotoxic potential, given that the micronuclei frequency in V. faba is increased.