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Results for “Presynaptic Terminals”

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At least 181 records · Page 10Linked to original sources
PubMed1993

A complex of rab3A, SNAP-25, VAMP/synaptobrevin-2 and syntaxins in brain presynaptic terminals.

Two monoclonal antibodies (SPM-1 and SPM-2) immunoprecipitate brain N-type calcium channels. On immunoaffinity chromatography of digitonin extracts of bovine brain membranes on SPM-1- and SPM-2-Sepharose, proteins of 36 (syntaxins A and B), 28 and 19 kDa are specifically retained by both columns. Here we show that the 19 and 28 kDa bands contain VAMP/synaptobrevin-2, and rab3A/smg25A and SNAP-25, respectively. Since SPM-1 and SPM-2 recognize only syntaxins and the 28 kDa band (rab3A/sm25A and SNAP-25), respectively, the results indicate that all these proteins form a complex. Our results suggest tight linkage between the components involved in neurotransmitter release.

Amino Acid Sequence↗
PubMed1989

Are there morphological changes in presynaptic terminals of kindled rats?

Excitatory synapses were studied in the hippocampal dentate gyrus ipsilateral to the stimulated entorhinal cortex in fully kindled rats 2 weeks after the last (3rd) stage 5 seizure. No change was observed in the absolute number of synaptic vesicles. On the other hand, marked redistribution of the vesicles in the synaptic apparatus was found, with a shift to a strategic position in the vicinity of the synaptic cleft. This redistribution evidently makes it possible to increase the supply of neurotransmitter needed for hyperfunction of the synaptic apparatus in kindling.

Animals↗
PubMed1992

Opioid inhibition of GABA release from presynaptic terminals of rat hippocampal interneurons.

Opiates and the opioid peptide enkephalin can cause indirect excitation of principal cortical neurons by reducing inhibitory synaptic transmission mediated by GABAergic interneurons. The mechanism by which opioids mediate these effects on interneurons is unknown, but enkephalin hyperpolarizes the somatic membrane potential of a variety of neurons in the brain, including hippocampal interneurons. We now report a new, more direct mechanism for the opioid-mediated reduction in synaptic inhibition. The enkephalin analog D-Ala2-Met5-enkephalinamide (DALA) decreases the frequency of miniature, action potential-independent, spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) without causing a change in their amplitude. Thus, we conclude that DALA inhibits the action potential-independent release of GABA through a direct action on interneuronal synaptic terminals. In contrast, DALA reduces the amplitude of action potential-evoked, GABA-mediated IPSCs, as well as decreases their frequency. This suggests that the opioid-mediated inhibition of non-action potential-dependent GABA release reveals a mechanism that contributes to reducing action potential-evoked GABA release, thereby decreasing synaptic inhibition.

Action Potentials↗
PubMed2003

Glutamate-dependent stabilization of presynaptic terminals.

Dissecting the mechanisms underlying synapse formation and elimination is fundamental to understand how the nervous system is constructed and subsequently modified. Two studies by Tashiro et al. and by Hashimoto and Kano in this issue of Neuron provide new insights into the roles of neurotransmitter glutamate release in regulating the motility of hippocampal mossy fiber filopodia and synaptic competition among climbing fibers.

Animals↗
PubMed1991

Induction of formation of presynaptic terminals in neuroblastoma cells by synapsin IIb.

The synapsins are a family of closely related phosphoproteins (termed synapsins Ia, Ib, IIa and IIb) associated with synaptic vesicles and implicated in the short-term regulation of neurotransmitter release from nerve endings. During development, expression of the synapsins correlates temporally with synapse formation, but there has been no direct evidence that they are involved in synaptogenesis. Here we report that overexpression of synapsin IIb in the neuroblastoma x glioma hybrid clonal cell line NG108-15 leads, during cell differentiation, to marked increases in the number of neuritic varicosities and in the numbers of small clear vesicles and large dense core vesicles per varicosity, as well as to the appearance of synapse-like cell-cell contacts. Thus, synapsin IIb may be involved in the regulation of synapse formation and, as a result, in long-term neuronal signalling.

Animals↗
PubMed1992

[Quantitative fluorescence-immunohistochemistry of presynaptic terminals using a monoclonal antibody against a synaptic vesicle-specific protein (SVP-38) in paraffin sections].

We developed a method for investigating impairment of synaptogenesis quantitatively involving measurement of the fluorescence intensity emitted by immunohistochemically stained paraffin sections of rat brain using a monoclonal antibody (Mab 171B5) against a synaptic vesicle protein (SVP-38). We applied this method to congenitally hydrocephalic and non-hydrocephalic brains of HTX-rats, and compared the postnatal changes in the fluorescence intensity in the molecular layer of the cerebral cortex. In non-hydrocephalic HTX-rats, the fluorescence intensity remained nearly unchanged from the 1st to 7th postnatal day and then increased at an almost linear rate until the 21st postnatal day, when it reached 4.5 times the value on the 7th postnatal day. The increase thereafter was gradual until the 28th postnatal day. In hydrocephalic HTX-rats, the fluorescence intensity showed a marked reduction on the 28th postnatal day (p < 0.01). This finding indicated impairment of synaptogenesis. We believe that this method provides useful information for evaluating the impairment of synaptogenesis in various pathological conditions in mammarian brains. The basic aspects of this method which support its validity are also discussed.

Animals↗