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The distribution pattern of calbindin (CB)-D28k-expressing neurons results to be altered in several brain regions of chronic morphine exposed adult mice. In this study, the influence of chronic maternal exposure to morphine on the distribution pattern of CB-D28k-expressing neurons in the brain of mouse offspring was investigated. Females of CD-1 mice were daily administered with saline or morphine for 7 days before mating, during the whole gestation period, and until 21 day post-partum. Their offspring were sacrificed on postnatal day 18, and the brains were examined by histology using cresyl violet and by immunohistochemistry using a rabbit polyclonal anti-CB-D28k antibody. Histology revealed no significant differences in the distribution pattern and the number of neurons between the offspring forebrain of the control group of mice and the two groups of mice treated with different doses of morphine. However, immunohistochemical analysis revealed that the number of CB-D28k-immunoreactive neurons remarkably decreased in the cingulate cortex, in the layers II-IV of the parietal cortex and in all regions of the hippocampus, while it increased in the layers V-VI of the parietal cortex and in the subicular region of the offspring brain of morphine treated mice. Overall, our findings demonstrate that maternal exposure to morphine alters the pattern of CB-D28k-expressing neuron pattern in specific regions of murine developing brain, in a layer- and dose-dependent way, thus suggesting that these alterations might represent a mechanism by which morphine modifies the functional aspects of developing brain.

Introduction: 2,3,7,8-tetrachlorodibenzo-pdioxin (TCDD) influences infection of bovine cells (MDBK) with Bovine Herpesvirus 1 (BHV- 1) by increasing virus replication (Fiorito et al., 2008a) and anticipating BHV-1-induced apoptosis (Fiorito et al., 2008b). Moreover, TCDD accelerates the down-regulation of telomerase activity when virus-induced apoptosis occurred (Fiorito et al., 2014), anticipates the presence of bICP0 in the cytoplasm (Fiorito et al., 2010), and enhances the free intracellular iron availability (Fiorito et al., 2013). Several viruses control key cellular signaling pathways to facilitate the infection. For example, BHV-1 increases p53 levels during infection (Devireddy and Jones, 1999), and activates both phosphatidylinositol 3-kinase (PI3K)/Akt and mitogen activated protein kinases/extracellular signalregulated kinase 1/2 (MAPK/Erk1/2) signaling pathways (Zhu et al., 2011). Here to elucidate the influence of TCDD on BHV-1-infection we examined Akt/mTOR, ERK pathways and their downstream effectors including FOXO3, a transcription factor involved in promoting virus-induced apoptosis, as in canine coronavirus type II infection (Marfè et al., 2011).

Feline herpesvirus 1 (FHV-1) is a widespread cat pathogen inducing rhinitis, conjunctivitis and corneal ulcers. To alleviate acute FHV-1-induced disease, antiviral agents are used often with antibiotics. But sometimes, these treatments, as well as conventional doses of cytokines have moderate efficacy and/or collateral effects. Herein we have investigated the effects of low dose interleukin (IL)-12 plus interferon (IFN)-gamma, prepared by Sequential Kinetic Activated (SKA), on the treatment of FHV-1 infection. Twenty-five, unvaccinated FHV-1-positive cats were recruited into a prospective, randomized, placebo-controlled, double-blinded clinical trial. Fifteen cats were treated for 6 months with oral low doses of SKA IL-12 plus IFN-gamma and 10 cats were treated with placebo. At 1, 6 and 12 months (follow-up) after the beginning of treatment, clinical assessment, PCR assay and blood count were carried out. At follow-up, in treated group, we observed significant (p