Synapsin I has been proposed to be involved in the modulation of neurotransmitter release by controlling the availability of synaptic vesicles for exocytosis. To further understand the role of synapsin I in the function of adult nerve terminals, we studied synapsin I-deficient mice generated by homologous recombination. The organizaition of synaptic vesicles at presynaptic terminals of synapsin I-deficient mice was markedly altered: densely packed vesicles were only present in a narrow rim at active zones, whereas the majority of vesicles were dispersed throughout the terminal area. A great deal of evidence has implicated the synapsins in the regulation of synaptogenesis and in the modulation of neurotransmitter release from adult nerve terminals (1-4). To further assess the possible roles of synapsin I in the regulation of these processes, we have generated synapsin I-deficient mice by homologous recombination. In an accompanying paper (5), we report that axonal outgrowth and synaptogenesis are severely impaired in these mutant mice. Herein we present evidence that synapses of the adult synapsin I mutant mice manifest a variety of structural and physiological abnormalities. MATERIALS AND METHODSSynapsin I-Deficient Mice. Synapsin I mutant mice were generated by homologous recombination (5). Littermates of wild-type and synapsin I mutant mice were used in all of the analyses. Only male mice were used to avoid any variation caused by the estrous cycle of female mice. Except for glutamate release assays, all analyses were carried out by investigators without any knowledge of the genotype of the animal.Electron Microscopy. Wild-type (n = 2) and synapsin I-deficient mice (n = 3) were anesthetized with pentobarbital (40 mg/kg; i.p.) and perfused transcardially with Tyrode's solution followed by 3% (vol/vol) glutaraldehyde/0.5% paraformaldehyde in 0.1 M sodium phosphate-buffered saline (pH 7.4). Spinal cords and brains were dissected and postfixed in the same fixative for 4 h. Segments L4 and L5 of the spinal cord were cut into 60-to 100-,um transverse sections and hippocampi were cut into longitudinal sections. The sections were postfixed in 1% osmium tetroxide, dehydrated in alcohol, and embedded in Durcupan. Semithin (1 ,um) and ultrathin ("silver") sections were cut from the tissue blocks on an ultratome. The semithin sections were mounted on glass slides and counterstained with cresyl violet for light microscopic analysis. The ultrathin sections were mounted on Formvarcoated copper grids, counterstained with uranyl acetate and lead citrate, and examined in a Philips CM12 electron microscope. To compare the structural organization of synapses between the two groups of animals, we focused on one
We have analyzed blood vessel distribution in the primary and secondary visual cortices of the squirrel monkey in relation to cortical modules, laminae, and cytoarchitectonic areas. Measurements of microvessel length in tangential sections through the primary visual cortex showed that blobs are more richly vascularized than intervening cortical regions. Thus, the mean total length of microvessel profiles per unit was 42% greater within these cortical modules than within adjacent (interblob) areas. Total microvessel length per unit area in another class of module, the stripes in the secondary visual cortex, was 27% greater than in interstripe regions. Microvessel distribution also varied systematically from layer to layer in the primary visual cortex, being greatest in lamina IVc. Finally, the overall microvessel length per unit area in sections of the primary visual cortex was 26% greater than that in the secondary visual cortex. These observations indicate that the modular, laminar, and regional organization of the primate visual cortex is reflected in the underlying distribution of cortical microvessels. These vascular patterns should be discernable in living animals with vascular contrast agents and appropriate imaging techniques.
We have examined relative levels of metabolic and electrical activity across layer IV in the primary somatic sensory cortex (S1) of the rat in relation to regions of differential postnatal cortical growth. Each of several indices used--mitochondrial enzyme histochemistry, microvessel density, Na+/K+ pump activity, action potential frequency, and deoxyglucose uptake--indicate regional variations of metabolic and electrical activity in this part of the brain in both juvenile (1-week-old) and adult (10-12-week-old) animals. At both ages, areas of the somatic sensory map related to special sensors such as whiskers and digital pads showed evidence of the most intense activity. Thus, mitochondrial enzyme staining, blood vessel density, and Na+/K+ ATPase activity were all greatest in the barrels and barrel-like structures within S1, and least in the adjacent interbarrel cortex and the cortex surrounding S1. Multiunit recordings in and around the posteromedial barrel subfield of anesthetized animals also showed that the average ratio of evoked to spontaneous activity was greater in barrels than in the surrounding, metabolically less active cortex. Furthermore, autoradiograms of labeled deoxyglucose accumulation in awake behaving animals indicated systematic differences in neural activity across S1 barrels and barrel-like structures showed more deoxyglucose accumulation than interbarrel, nonbarrel, or peri-S1 cortex. These regional differences in neural activity correspond to regional differences in neocortical growth (Riddle et al., 1992). The correlation of greater electrical activity, increased metabolism, and enhanced cortical growth during postnatal maturation suggests that neural activity foments the elaboration of circuitry in the developing brain.
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