PURPOSE: To assess the clinical and functional outcome of the patients who underwent percutaneous vertebroplasty with bone cement for the osteoporotic compression fracture and who had been followed up for minimum 1 year. MATERIALS AND METHODS: Among 110 patients who had been undergone percutaneous vertebroplasty with bone cement for osteoporotic compression fracture in Gangneung Asan Hospital from January 2001 to August 2002, 75 patients who had been followed up for more than 1 year were selected. And retrospectively, we analyzed the clinical and radiographic finding of 1 year, 2 year and 3 year follow-up. The patients were divided into 3 groups, the first group who have follow-up period of the from 1 to 2 years had 75 patients, the second group who the from 2 to 3 years, 49 patients, and the third group who the more than 3 years, 20 patients. We graded the clinical results to excellent, good, normal, fair and poor. Also, we assessed the height of vertebral body, the adjacent vertebral body fracture and the leakage of bone cement. RESULTS: 74 patients (98.6%) had the excellent or good results postoperatively. 69 patients (92%) of the first group, 46 patients (93.8%) of the second group and 16 patients (80%) of the third group had excellent or good results at last follow-up. There was no statistical correlation of each groups (p>0.05). In first group, the average height of body was 71.1% preoperatively, 73.5% postoperatively and 73.5% at follow-up. In second group, 71.5%, 75.5%, and 73.1%. In third group, 71.2%, 78.0% and 77.8%. There was no significant statistical correlation of each groups (p>0.05). 47cases (38.8%) had some leakage of cement immediate postoperatively. In 4 cases (7 vertebra), there were adjacent vertebral body fractures. CONCLUSION: Based on the results of our study, percutaneous vertebroplasty is a useful method in the treatment for the osteoporotic compression fracture of vertebra body.
Chungcheongnam-do ; Follow-Up Studies* ; Fractures, Compression* ; Gangwon-do ; Humans ; Retrospective Studies ; Spine ; Vertebroplasty*

Like neurons, astrocytes produce and release GABA to influence neuronal signaling. At the perforant path to dentate gyrus granule neuron synapse, GABA from astrocyte was found to be a strong inhibitory factor, which impairs synaptic transmission, synaptic plasticity and memory in Alzheimer's disease. Although astrocytic GABA is observed in many brain regions, its physiological role has not been clearly demonstrated yet. Here, we show that astrocytic GABA exerts disinhibitory action to dentate granule neurons by targeting GABA(B) receptors of GABAergic interneurons in wild-type mice. This disinhibitory effect is specific to a low intensity of electrical stimulation at perforant path fibers. Inversely in Alzheimer's disease model mice, astrocytic GABA targets GABA(A) receptors and exerts inhibitory action by reducing release probability of glutamatergic perforant path terminals. These results suggest that astrocytic GABA differentially modulates the signaling from cortical input to dentate gyrus under physiological and pathological conditions.
Alzheimer Disease* ; Animals ; Astrocytes ; Brain ; Dentate Gyrus* ; Electric Stimulation ; gamma-Aminobutyric Acid* ; Interneurons ; Memory ; Mice ; Neurons* ; Perforant Pathway* ; Plastics ; Receptors, GABA-A ; Synapses* ; Synaptic Transmission

µ-opioid receptor (MOR) is a class of opioid receptors with a high affinity for enkephalins and beta-endorphin. In hippocampus, activation of MOR is known to enhance the neuronal excitability of pyramidal neurons, which has been mainly attributed to a disinhibition of pyramidal neurons via activating Gαi subunit to suppress the presynaptic release of GABA in hippocampal interneurons. In contrast, the potential role of MOR in hippocampal astrocytes, the most abundant cell type in the brain, has remained unexplored. Here, we determine the cellular and subcellular distribution of MOR in different cell types of the hippocampus by utilizing MOR-mCherry mice and two different antibodies against MOR. Consistent with previous findings, we demonstrate that MOR expression in the CA1 pyramidal layer is co-localized with axon terminals from GABAergic inhibitory neurons but not with soma of pyramidal neurons. More importantly, we demonstrate that MOR is highly expressed in CA1 hippocampal astrocytes. The ultrastructural analysis further demonstrates that the astrocytic MOR is localized in soma and processes, but not in microdomains near synapses. Lastly, we demonstrate that astrocytes in ventral tegmental area and nucleus accumbens also express MOR. Our results provide the unprecedented evidence for the presence of MOR in astrocytes, implicating potential roles of astrocytic MOR in addictive behaviors.
Animals ; Antibodies ; Astrocytes* ; Behavior, Addictive ; beta-Endorphin ; Brain ; Carisoprodol ; Enkephalins ; gamma-Aminobutyric Acid ; Hippocampus ; Interneurons ; Mice ; Microscopy, Electron ; Neurons ; Nucleus Accumbens ; Presynaptic Terminals ; Pyramidal Cells ; Receptors, Opioid ; Synapses ; Ventral Tegmental Area