Although only few postmenopausal women exhibit biochemical signs of hypovitaminosis D, vitamin D insufficiency has been shown to have adverse effects on bone metabolism and could be an important risk factor for osteoporosis and fracture. We determined serum levels of 25-hydroxyvitamin D [25(OH)D], intact parathyroid hormone (iPTH), bone turnover markers, dietary calcium intake, and bone mineral density (BMD; measured by dual X-ray absorptiometry) in 161 consecutive ambulatory women, healthy except for osteoporosis, referred to a bone metabolic unit. The prevalence of vitamin D insufficiency [25(OH)D ≤ 15 ng/ml] was 39.1%. 25(OH)D was lower in the osteoporotic subjects (15.7 ± 5.3 ng/ml vs. 21.8 ± 9.7 ng/ml; p < 0.001). After controlling for all other variables, lumbar spine (LS) BMD was found to be significantly associated with 25(OH)D, body mass index (BMI), and years after menopause (YSM) (R2 = 0.253; p < 0.001). For femoral neck (FN), significant independent predictors of BMD were YSM, BMI, iPTH, and 25(OH)D (R2 = 0.368; p < 0.001). The probability of meeting osteoporosis densitometric criteria was higher in the vitamin D insufficiency group (odds ratio [OR], 4.17, 1.83-9.48) after adjusting by YSM, BMI, iPTH, and dietary calcium intake. Our study shows that vitamin D insufficiency in an otherwise healthy postmenopausal population is a common risk factor for osteoporosis associated with increased bone remodeling and low bone mass.

The present study examined the effects of strychnine on the tonic hyperpolarization and the changes in membrane properties of lumbar motoneurons that occur during active sleep. To carry out these studies, intracellular recordings from lumbar motoneurons were combined with the juxtacellular microiontophoretic application of strychnine in chronic, undrugged, normally respiring cats. During active sleep, compared to quiet sleep, motoneurons that were not exposed to strychnine exhibited tonic hyperpolarization, a decrease in cell excitability, and an increase in membrane conductance; they were also bombarded by high- frequency, large-amplitude IPSPs. In conjunction with the juxtacellular application of strychnine, there was a marked reduction in the degree of hyperpolarization during active sleep; motoneuron excitability was no longer suppressed, and there was a reduction in the increase in membrane conductance. In addition, the large-amplitude IPSPs were blocked. These results identify glycine as the neurotransmitter responsible for the state-dependent changes in membrane properties and the hyperpolarization of motoneurons that takes place during active sleep.