Supplementing the medium with free cholesterol abrogated the effects of haloperidol on lipid-raft composition and functionality. LDL (low-density lipoprotein), a physiological vehicle
of cholesterol in plasma, was much less effective in preventing the effects of haloperidol, which is attributed to the drug’s inhibition of intracellular vesicular trafficking. These effects on cellular cholesterol homeostasis that ultimately result in the alteration of lipid-raft-dependent insulin signaling action may underlie some of the metabolic effects of this widely used antipsychotic. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Heterozygous mutations in CIC-2 have been associated in rare cases with increased susceptibility to generalized, idiopathic epilepsy. Initially, find more it was hypothesized that mutations in CIC-2 may be associated with epilepsy due to a direct
role for CIC-2 in the modification of hippocampal neuronal excitability. However, the absence of an overt seizure-susceptibility phenotype in young CIC-2 knockout CA3 manufacturer (KO) mice rendered this hypothesis- implausible. A recent study of older CIC-2 KO mice (>6 months) revealed abnormalities in the myelin of central axons and a subtle defect in the neuronal function in the central auditory pathway. These findings prompted us to re-examine hippocampal neuron morphology and excitability in older CIC-2 KO mice. Interestingly, electrocorticographic recordings obtained in older mice revealed spontaneous interictal spikes which are a marker CB-5083 mouse of perturbed hippocampal neurotransmission with a resultant increase in excitation. This electrophysiological defect was associated with astrocyte activation and evidence of neuronal degeneration in the CA3 region of the hippocampus of these older mice. Together, these findings raise the possibility that CIC-2 expression plays a subtle neuroprotective role in the aging hippocampus. (C) 2010 IBRO.
Published by Elsevier Ltd. All rights reserved.”
“We have recently identified hippocampal cell death and reduced neuronal and glial cells densities during adolescent nicotine and ethanol exposures and outcomes reduced in severity when nicotine and ethanol are co-administered during this developmental period. In the present study, we investigated the effects of adolescent nicotine and/or ethanol withdrawal on the following regions of the hippocampus: Granular layer of the Dentate Gyrus (GrDG), Molecular layer (Mol), CA1, CA2 and CA3. From the 30th to the 45th postnatal day (PN30-PN45), C57BL/6 male and female mice were exposed to nicotine free base (NIC) and/or ethanol (ETOH). Four groups were analyzed: (1) concomitant NIC (50 mu g/ml in 2% saccharin to drink) and ETOH (25%, 2 g/kg i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) vehicle.