To study the role of the metabotropic glutamate receptor 8 (mGluR8), mice lacking this receptor were generated by homologous recombination. Homozygous mGluR8-deficient mice are about 8% heavier than their wild-type age-matched controls after reaching 4 weeks of age. This weight difference is not caused by an altered food intake and is not exacerbated by feeding the animals a high-fat diet. Moreover, mGluR8-/- mice are mildly insulin resistant, possibly as a result of being overweight. Behavioral testing revealed a reduced locomotor activity of mGluR8-/- mice compared with wild-type mice during the first 3 days in a novel enclosed environment. However after 3 days, the locomotor activities of wild-type and mGluR8-/- mice were similar, suggesting a reduced exploratory behavior of mGluR8-/- mice in a novel enclosed environment. By contrast, there were no genotype differences in locomotor activity in the open field, plus maze, or in total time spent exploring objects during object recognition tests, indicating that there is a dissociation between effects of mGluR8 deficiency in exploratory activity in a novel safe enclosed environment vs. a more anxiogenic novel open environment. The absence of mGluR8 also leads to increased measures of anxiety in the open field and elevated plus maze. Whether the diverse phenotypic differences observed in mGluR8-/- mice result from the misregulation of a unique neural pathway, possibly in the thalamus or hypothalamus, or whether they are the consequence of multiple developmental and functional alterations in synaptic transmission, remains to be determined.
Perineal streptococcal dermatitis (PSD) is largely known to be caused by group A β-hemolytic Streptococcus (GAS). We would like to bring cases of non-GAS PSD to the attention of dermatologists, as there are implications for workup and therapy. We report 3 pediatric cases of PSD: 1 caused by GAS, 1 caused by group B β-hemolytic Streptococcus (GBS), and 1 associated with group C β-hemolytic Streptococcus (GCS). GBS and GCS are very rarely reported in pediatric cases of PSD. The literature on non-GAS PSD is reviewed, which additionally revealed several instances of PSD caused by group G β-hemolytic Streptococcus (GGS) and Staphylococcus aureus. GBS, GCS, GGS, and S aureus are significant causes of PSD to consider, particularly among adult patients, based on our encountered cases and the literature. If using rapid antigen tests to expedite the diagnosis of GAS, we recommend supplementing with a lesional swab for bacterial culture and sensitivity as the rapid antigen test does not detect non-GAS organisms. Therapy should be tailored to the microbiologic cause.
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