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The properties of D-β-hydroxybutyrate dehydrogenase (BDH) from rat liver and brain mitochondria were compared to determine if isozymes of this enzyme exist in these tissues. The BDHs from these tissues behaved similarly during the purification process. The enzymes were indistinguishable by sodium dodecyl sulfate – polyacrylamide or acid-urea – polyacrylamide gel electrophoresis and they had identical isoelectric points. The BDHs from rat liver and brain were also quite similar in functional parameters determined by kinetic analysis and phospholipid activation of apo-BDH (i.e., the lipid-free enzyme). Antiserum against rat liver BDH inhibited both enzymes to an equivalent extent in a titration assay. The enzymes had similar patterns of peptide mapping by partial digestion with Staphylococcus aureus V8 protease, followed by immunoblotting using antiserum against the liver enzyme. These results suggest that the BDHs in rat liver and brain are very similar and possibly identical.Key words: D-β-hydroxybutyrate dehydrogenase, membrane-bound enzyme, lipid activation.

Vascular changes in the cerebral arterioles (150 - 500 mu) were demonstrated by means of magnification serial cerebral angiography (focal spot 0.15 mm) in a consecutive series of 25 hypertensive patients of advanced age suffering from cerebrovascular disease. The changes identified were: (a) arteriosclerotic lesions, (b) arteriolar occlusion, and (c) miliary aneurysms. The enhancement of vascular details obtained is essential to arrive at exact diagnosis and accurate clinical management.

It has been proposed that the small volume of a dendritic spine can amplify Ca2+signals during synaptic transmission. Accordingly, we have performed calculations to determine whether the activation of N-methyl-D-aspartate (NMDA) type glutamate receptors during synaptic transmission results in significant elevation in intracellular Ca2+levels, permitting optical detection of synaptic signals within a single spine. Simple calculations suggest that the opening of even a single NMDA receptor would result in the influx of ~ 310 000 Ca2+ions into the small volume of a spine, producing changes in Ca2+levels that are readily detectable using high affinity Ca2+indicators such as fura-2 or fluo-3. Using fluorescent Ca2+indicators, we have imaged local Ca2+transients mediated by NMDA receptors in spines and dendritic shafts attributed to spontaneous miniature synaptic activity. Detailed analysis of these quantal events suggests that the current triggering these transients is attributed to the activation of <10 NMDA receptors. The frequency of these miniature synaptic Ca2+transients is not randomly distributed across synapses, as some synapses can display a >10-fold higher frequency of transients than others. As expected for events mediated by NMDA receptors, miniature synaptic Ca2+transients were suppressed by extracellular Mg2+at negative membrane potentials; however, the Mg2+block could be removed by depolarization.Key words: miniature release, N-methyl-D-aspartate (NMDA), calcium, glutamate, spine.

The neuropeptide galanin is implicated in regulation of affective behavior, including modulation of 5-HT signaling. Here, we investigated, by use of microdialysis in freely moving rats, the effects of intracerebral (i.c.) and intracerebroventricular (i.c.v.) infusions of galanin on basal extracellular 5-HT levels in medial prefrontal cortex (mPFC), CA1 area of ventral hippocampus (vHPC), central amygdaloid nucleus (CeA), ventromedial hypothalamic nucleus ventrolateral part (VMHvl), and ventromedial caudate putamen (CPu). These results were compared with a parallel immunohistochemical analysis of the distribution of galanin, 5-HT, and noradrenaline (NA) nerve terminals, and with data on galanin receptors. Galanin i.c.v. significantly decreased the 5-HT levels in mPFC to 79% and in vHPC to 72%. Local infusions of galanin caused a long-lasting decrease in 5-HT levels in vHPC to 88%, and a moderate decrease in CeA, whereas the 5-HT levels in mPFC significantly increased to 121%. These effects of i.c. galanin correlated well with the density of 5-HT and galanin nerve terminals and galanin receptors autoradiography in mPFC, vHPC, and CeA. No effects of i.c. or i.c.v. galanin on 5-HT levels were observed in CPu or VMHvl, in agreement with the low numbers of galanin-positive terminals and low/moderate galanin receptor density. Galanin was often found to coexist in NA, but could never be detected in 5-HT terminals. Together the results show a neuroanatomical correlation between the effects of galanin infusions on 5-HT release and distribution of galanin and its receptors, and that i.c.v. and i.c. administration can give opposite effects on 5-HT release.

We hypothesized that very brief episodes of hypoxia (<1 min) would evoke long-term facilitation (LTF) in individuals free of inspiratory flow limitation (IFL). We studied 12 healthy participants who were self-reported non-snorers and confirmed the absence of IFL. We induced 15 brief episodes of hypoxia during non-REM sleep, reducing arterial oxygen saturation to 84–85%, followed by 1 min of room air. Ventilatory variables and resistance were measured during the control period, hypoxic trials, room air controls, and for 20 min following the last hypoxic episode. There was a significant increase in minute ventilation (108 ± 1.3% of control, P < 0.05) and tidal volume (105 ± 1.7% of control, P < 0.05) and a significant decrease in upper airway resistance (88 ± 9.8% control, P < 0.05) during the recovery period. However, there were no significant changes in any variable during sham studies. We have shown for the first time that LTF can be elicited in sleeping humans free of IFL.

Brain morphological alterations in schizophrenic patients have led to the neurodevelopmental hypothesis of schizophrenia. On the other hand, a progressive neurodegenerative process has also been suggested and some follow-up studies have shown progressive morphological changes in schizophrenic patients. Several neurotransmitter systems have been suggested to be involved in this disorder and some of them could lead to neuronal death under certain conditions. This review discusses some of the biochemical pathways that could lead to neurodegeneration in schizophrenia showing that neuronal death may have a role in the etiology or natural course of this disorder.