Congenital deafness affects deep layers in primary and secondary auditory cortex.

Congenital deafness leads to functional deficits in the auditory cortex for which early cochlear implantation can effectively compensate. Most of these deficits have been demonstrated functionally. Furthermore, the majority of previous studies on deafness have involved the primary auditory cortex; knowledge of higher-order areas is limited to effects of cross-modal reorganization. In this study, we compared the cortical cytoarchitecture of four cortical areas in adult hearing and congenitally deaf cats (CDCs): the primary auditory field A1, two secondary auditory fields, namely the dorsal zone and second auditory field (A2); and a reference visual association field (area 7) in the same section stained either using Nissl or SMI-32 antibodies. The general cytoarchitectonic pattern and the area-specific characteristics in the auditory cortex remained unchanged in animals with congenital deafness. Whereas area 7 did not differ between the groups investigated, all auditory fields were slightly thinner in CDCs, this being caused by reduced thickness of layers IV-VI. The study documents that, while the cytoarchitectonic patterns are in general independent of sensory experience, reduced layer thickness is observed in both primary and higher-order auditory fields in layer IV and infragranular layers. The study demonstrates differences in effects of congenital deafness between supragranular and other cortical layers, but similar dystrophic effects in all investigated auditory fields.

ATP-sensitive K(+) channels (Kir6.1/SUR1) regulate gap junctional coupling in cochlear-supporting cells.

Using the double whole-cell patch-clamp technique, we found that the absence of intracellular ATP led to gap junction uncoupling in cochlear-supporting Hensen cells. The uncoupling was observed as a progressive reduction of the gap junctional electrical conductance from a starting value of approximately 40 nS to less than 0.04 nS within 10-20 min. The conductance rundown was partly avoided by at least 3 mM ATP and completely suppressed by 5 mM ATP or 5'-adenylyl-imidodiphosphate (AMP-PNP), the non-hydrolysable ATP analog, in the pipette filling solution, suggesting that ATP was needed as ligand and not as a hydrolysable energy supplier or substrate for enzymatic reactions. The effect of intracellular ATP was mimicked by the external application of barium, a nonselective blocker of inwardly rectifying K(+) (Kir) channels, and glibenclamide, an inhibitor of the ATP-sensitive Kir channels (KATP). Moreover a Ba(2+)-sensitive whole-cell inward current was observed in absence of internal ATP. We propose that the internal ATP kept the KATP channels in a closed state, thereby maintaining the gap junction coupling of Hensen cells. The immunostaining of guinea pig cochlear tissue revealed for the first time the expression of the KATP channel subunits Kir6.1 and SUR1 in Hensen cells and supported the proposed hypothesis. The results suggest that KATP channels, as regulator of the gap junction coupling in Hensen cells, could be the physiological link between the metabolic state of the supporting cells and K(+) recycling in the organ of Corti.

Psychosocial determinants of quality of life in parents of obese children seeking inpatient treatment.

PURPOSE: To examine and identify predictors of parental health-related quality of life (HRQoL) in a sample of obese and very obese children participating in an inpatient program for treating obesity. METHODS: Data are part of a prospective multicenter randomized-controlled intervention trial. Parents (n = 463) of obese and very obese children (7-13 years) completed standardized questionnaires assessing their own and their child's HRQoL, psychosocial functioning, demographics and parental weight-specific self-efficacy on the child's admission to an inpatient pediatric weight management program. Weight and height of the children were measured by trained personnel; parental weight was assessed via self-report. RESULTS: Parents reported lower mental HRQoL compared to healthy adults and even lower than reference values for acute or chronic illness. With respect to physical HRQoL, parents of obese children reported higher scores than both groups. Effect sizes were small to medium. Overweight parents reported a lower physical HRQoL. Mental HRQoL was higher for married parents with a higher educational level and a higher self-efficacy and for those whose children depicted fewer behavioral problems and reported a higher HRQoL. Hierarchical regression analyses revealed that weight-specific self-efficacy explained 3% of variance in mental HRQoL in addition to the demographic and child psychosocial variables. Parental self-efficacy also partially mediated the association between the child's HRQoL and parental mental HRQoL. CONCLUSION: Childhood obesity is associated with reduced parental HRQoL. Interventions for obesity in children should consider the parents' psychosocial situation as well. Enhancing parental self-efficacy may be a promising approach.