Growth hormone-releasing hormone depletion in the female rat: similarities to aging.

The age-related decline in growth hormone (GH) secretion has been largely attributed to age-related degeneration of hypothalamic growth hormone-releasing hormone (GHRH)-producing neurons. GH decline has recently been linked to age-related bone changes in humans. Bone loss and decreased bone strength are common in aging rats and humans, but density of remaining mineral tissue is known to be increased. The effect of induced hypothalamic GHRH deficiency on bone was assessed, and similarities between bone changes encountered and those taking place in aging were identified. Female rats received monosodium glutamate (MSG) following birth, and they were euthanized at 19 weeks of age. Femurs from MSG-treated rats had greater mineral density (p < .05), greater mineral/matrix ratio (p < .01), lower mineral apposition rate (p < .005), and lower bone formation rate (p < .05). These results suggest that hypothalamic GHRH decline plays a substantial role in the development of bone pathology similar to that observed in aging individuals.

Behavioral and physiological sex differences observed in an animal model of fulminant hepatic encephalopathy in the rat.

Hepatic encephalopathy is characterized by a number of neuropsychiatric and motor disturbances observed in patients with liver dysfunction. The purpose of this study is to fully characterize behavioral and physiological sex differences in an animal model of fulminant hepatic encephalopathy (FHE). Male and female rats were administered thioacetamide (600 mg/kg) via i.p. (intraperitoneal) injection at Hours 0 and 24 and allowed to progress into the four stages of FHE. Male rats reached all four stages of FHE significantly earlier than female rats (p < 0.05). The performance of the male rats deteriorated more quickly (p < 0.05) than that of the females in all of the sensory and motor behavioral tests. Sex differences were observed in the liver enzymes of the FHE rats. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase were significantly greater (p < 0.05) in male rats in all four stages of FHE. Significant increases were also observed in the levels of direct and total bilirubin (p < 0.05). Neuronal damage was observed in the CA1 and CA2 regions of the hippocampus. In the CA1 region, male rats displayed greater pathological changes in Stages III and IV (p < 0.05) than female rats. The damage in the CA2 region was only observed in Stage IV male rats. Our data indicate that observable behavioral and physiological sex differences occur in thioacetamide-induced FHE in the rat.

Multiple enamel pearls in two siblings detected by volumetric computed tomography.

A rare case of multiple enamel pearl formation is presented involving the maxillary molars in two siblings incidentally recognized during volumetric CT examination. Although the pathogenesis of ectopic enamel formation is not known, possible mechanisms to account for this phenomenon are discussed in the context of current knowledge regarding root genesis. The radiographic presentation of enamel pearls and its clinical significance is also discussed. The observation of multiple enamel pearls in two siblings raises the possibility of a hereditary association in the formation of enamel pearls.

Is glutamate-induced reduction in growth hormone-releasing hormone a neuroendocrine model of aging in the rat?

Decreases in serum growth hormone (GH) associated with aging may be a result of age-related degenerative changes in neurons of the hypothalamus resulting in a decrease of growth hormone-releasing hormone (GHRH). This study tests the utility of glutamate-induced hypothalamic neuronal degeneration in the rat as a neuroendocrine model of aging. Sprague-Dawley female rats received three 4-mg/g monosodium glutamate (MSG) subcutaneous injections during the first 5 days following birth. Animals were anesthetized at 60 days of age and challenged with GHRH. Blood samples were assayed for GH. Serum GH levels following GHRH challenge in the MSG-treated group rose more slowly and to a lower peak than in controls (P < 0.05). There was no difference in total GH release over the 1-hr interval following challenge. MSG-treatment of animals resulted in lower gross body (P < 0.05) and kidney (P < 0.05) weights with no difference in ovary or adrenal weights. There were also no differences in pituitary GH or total protein content between the groups. Analysis of femurs in the MSG animals revealed both a lower bone strength (P < 0.05) and maximum mid-shaft diameter (P < 0.05), but no difference in length, mineral/matrix ratio, or tissue density. Our data suggest that the degree of neuroendocrine disruption resulting from neonatal MSG administration mimics in part systemic changes commonly observed in aged animals. Hence, definite similarities exist between MSG treatment and the documented aging-related changes in hypothalamic GHRH content and GH regulation in the rat.

A quantitative evaluation of magnetic resonance image signal changes of the brain in chronic hepatic encephalopathy.

Hyperintensity in the basal ganglia of patients with serious liver disease is a common finding on T1-weighted magnetic resonance images. In this study, we used optical densitometry to quantitatively evaluate the hyperintense magnetic resonance image signal changes in the various regions of the brain of patients with chronic hepatic encephalopathy. The incidence and morphological distribution of the magnetic resonance signal changes were evaluated from T1-weighted magnetic resonance images of the brain from seven non-alcoholic patients and six healthy controls. Significant differences (p < 0.05) between the patient group and controls were found in the limbic system (hippocampus, temporal lobe, cingulate gyrus, and fornix), extrapyramidal system and associated myelinated pathways (lentiform nucleus, tectum, tegmentum, cerebral peduncles, internal capsule and the corpus callosum). No measurable differences were observed in the frontal, parietal, and occipital cortex, or the dorsomedial thalamus. The presence of the high signal intensity changes on T1-weighted magnetic resonance image suggests that characteristics alterations occur in functional regions of the brain in chronic hepatic encephalopathy.