It was also examined whether the effects of neonatal CL treatment could be further modified by environmental conditions. In the present experiments, postweaning isolation rearing (Iso) was examined as an environmental condition, because postweaning Iso is reported to change the density of 5-HT axons in the rat brain. Unexpectedly, neonatal CL treatment alone had no effect on the density of 5-HT or NA axons or depressive behavior. Postweaning social Iso rearing reduced the density

of 5-HT axons in the central nucleus and basolateral nucleus of the amygdala and CA3 of the hippocampus. In the prelimbic area and infralimbic area of medial prefrontal cortex and the dentate gyrus of the hippocampus, the density of 5-HT axons was not affected by social Iso alone, but was reduced when buy Fedratinib animals were socially isolated after neonatal CL treatment. Postweaning Iso, but not neonatal CL treatment, increased immobility in the forced swim test in adolescence/early adulthood. These findings Selleckchem AZD5153 suggest that postweaning social Iso alters the density of monoaminergic axons, particularly 5-HT axons, and induces a possible model of depression, while neonatal

CL treatment alone has no effect on the density of NA or 5-HT axons or depressive behavior in adolescence/early adulthood. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Huntington’s disease (HD) is an inherited neurodegenerative disease

Oxaliplatin characterised by cell dysfunction and death in the basal ganglia and cortex. Currently there are no effective pharmacological treatments available. Loss of cannabinoid CB1 receptor ligand binding in key brain regions is detected early in HD in human postmortem tissue [Glass M, Dragunow M, Faull RL (2000) The pattern of neurodegeneration in Huntington's disease: a comparative study of cannabinoid, dopamine, adenosine and GABA(A) receptor alterations in the human basal ganglia in Huntington's disease. Neuroscience 97:505-519]. In HD transgenic mice environmental enrichment upregulates the CB1 receptors and slows disease progression [Glass M, van Dellen A, Blakemore C, Hannan AJ, Faull RL (2004) Delayed onset of Huntington's disease in mice in an enriched environment correlates with delayed loss of cannabinoid CB1 receptors. Neuroscience 123:207-212]. These findings, combined with data from lesion studies have led to the suggestion that activation of cannabinoid receptors may be protective. However, studies suggest that CB1 mRNA may be decreased early in the disease progression in HD mice, making this a poor drug target. We have therefore performed a detailed analysis of CB1 receptor ligand binding, protein, gene expression and levels of endocannabinoids just prior to motor symptom onset (12 weeks of age) in R6/1 transgenic mice.