Mothering from the Inside Out: results of a pilot study testing a mentalization-based therapy for mothers enrolled in mental health services.

Mothers who are involved with mental health services (for themselves or their children) rarely receive adequate support for their role as parents. Mental illness in a parent or child often exacerbates the challenges of managing psychological distress that is germane to the parenting roll. Mentalization-based approaches to psychotherapy for parents have the potential to address challenges of emotional regulation in parents by supporting their capacity to recognize and modulate negative affect during stressful parenting situations. In this study, we piloted Mothering from the Inside Out (MIO) with 17 mothers receiving services at a community-based mental health clinic. MIO is a 12-week, mentalization-based parenting intervention that demonstrated efficacy in two previous randomized controlled trials with substance using mothers. In this study, we were interested in determining whether community-based clinicians could deliver MIO with sustained fidelity. We were also interested in examining the preliminary feasibility, acceptability and efficacy of MIO when delivered by clinicians in a community mental health center. Finally, we were interested in replicating prior tests of the proposed treatment mechanisms. Treatment outcomes included maternal reflective functioning, psychiatric and parenting stress, and mother-child interaction quality. Our findings indicated that MIO was feasible and acceptable when delivered in the community-based setting and that all maternal indices improved. However, no improvement in mother-child interaction quality was found, possibly because of insufficient time for these changes to consolidate.

Protein kinase Cdelta regulates ethanol intoxication and enhancement of GABA-stimulated tonic current.

Ethanol alters the distribution and abundance of PKCdelta in neural cell lines. Here we investigated whether PKCdelta also regulates behavioral responses to ethanol. PKCdelta(-/-) mice showed reduced intoxication when administered ethanol and reduced ataxia when administered the nonselective GABA(A) receptor agonists pentobarbital and pregnanolone. However, their response to flunitrazepam was not altered, suggesting that PKCdelta regulates benzodiazepine-insensitive GABA(A) receptors, most of which contain delta subunits and mediate tonic inhibitory currents in neurons. Indeed, the distribution of PKCdelta overlapped with GABA(A) delta subunits in thalamus and hippocampus, and ethanol failed to enhance tonic GABA currents in PKCdelta(-/-) thalamic and hippocampal neurons. Moreover, using an ATP analog-sensitive PKCdelta mutant in mouse L(tk(-)) fibroblasts that express alpha4beta3delta GABA(A) receptors, we found that ethanol enhancement of GABA currents was PKCdelta-dependent. Thus, PKCdelta enhances ethanol intoxication partly through regulation of GABA(A) receptors that contain delta subunits and mediate tonic inhibitory currents. These findings indicate that PKCdelta contributes to a high level of behavioral response to ethanol, which is negatively associated with risk of developing an alcohol use disorder in humans.