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W B Levy

Publications and source records attributed to W B Levy.

79 records · Page 5Linked to original sources
PubMed1976

On the functional coupling of neurotransmitter uptake and release in brain.

1 Isolated synaptosomal fractions from mouse forebrains were incubated [14C]-gamma-aminobutyric acid ([14C]-GABA). Release of the accumulated label in high potassium solution was measured. 2 The fractional release dependent upon calcium was decreased by raising the concentration of [14C]-GABA during labeling but was not affected by altering the time allowed for labelling or the time between labelling and stimulation. 3 These data suggest that extracellular GABA gains rapid access to available intraterminal pools. The relative distribution of the accumulated GABA in differerent pools can be influenced by the concentration of GABA in the incubation medium but, once (stored", there is no net redistribution of accumulated GABA in the absence of stimulation.

Animals↗
PubMed1973

Stimulus-coupled secretion of gamma-aminobutyric acid from rat brain synaptosomes.

Synaptosomes treated with radioactive gamma-aminobutyric acid can be stimulated to release this substance. The release is maximal within 40 seconds after stimulation and is dependent on calcium. Magnesium and manganese ions, known to block stimulus-secretion coupling processes, depress calcium-dependent release. This release is specific to synaptosomes because microsomal or myelin fractions do not release accumulated gamma-aminobutyric acid. The data illustrate a simple in vitro system suitable for analysis of secretion of gamma-aminobutyric acid in brain and in addition describe several new aspects of uptake and secretion of this compound at brain nerve endings.

Aminobutyrates↗
PubMedDate not supplied

Long-term potentiation and evidence for novel synaptic association in CA1 stratum oriens of rat hippocampus.

In CA1 stratum oriens of hippocampal slices, a robust long-term potentiation (LTP) induced by tetanic stimulation (20 pulses at 100 Hz, 10 trains delivered at 0.1 Hz) was accompanied by a slowly developing potentiation in a second, untetanized pathway. N-methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-5-phosphonovaleric acid (D-APV, 50 or 100 microM) reduced the homosynaptic LTP by 80% but failed to affect heterosynaptic LTP. The metabotropic receptor antagonist DL-2-amino-3-phosphonopropionic acid DL-AP3, 300 microM) or (+)-alpha-methyl-4-carboxyphenylglycine (MCPG, 500 microM), applied with DL-APV, further reduced homosynaptic LTP and blocked heterosynaptic LTP. The inhibitor of Ca(2+)-induced Ca2+ release dantrolene (20 microM), also applied with DL-APV, blocked both components of LTP. Importantly, when low-frequency test stimulation (0.017 Hz) to the untetanized, heterosynaptic pathway was interrupted for 30 min after homosynaptic tetanization, heterosynaptic LTP did not develop. These results demonstrate homosynaptic and heterosynaptic LTP inductions in stratum oriens of the area CA1 and suggest that the heterosynaptic LTP is induced by NMDA-independent, novel associative processes between tetanized and untetanized pathways.

Animals↗
PubMedDate not supplied

Perforant path activation modulates the induction of long-term potentiation of the schaffer collateral--hippocampal CA1 response: theoretical and experimental analyses.

In one computational model of hippocampal function, the entorhinal cortical input to CA1 is hypothesized to play a key role in the ability of CA1 to decode CA3 recodings. Here, we develop a modification of this CA1 decoder hypothesis that is applicable to several computational theories of hippocampal function, and then we electrophysiologically investigate one assumption of this new hypothesis. First, using biologically realistic estimates, we calculate that CA3-induced CA1 excitation is too high and that inhibition plausibly plays a role in this CA1 decoder model. Thus motivated, we turn to a physiological demonstration to substantiate the plausibility of the proposed mechanism. Using the rat hippocampal slice, we examine an interlaminar interaction between the distal perforant path input to hippocampal CA1 stratum moleculare and the more proximal Schaffer collateral input to stratum radiatum. Perforant path activation provides sufficient inhibition to block homosynaptic long-term potentiation elicited by a suitably strong stratum radiatum input. For this interlaminar interaction to be most effective, perforant path activation must both precede and follow Schaffer collateral activation. Perforant path-evoked inhibition in CA1 can thus serve as a viable mechanism in the learned decoder theory of hippocampal CA1.

Animals↗