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Biomedical subjects

W B Levy

Publications and source records attributed to W B Levy.

17 recordsLinked to original sources
PubMed1992

Longevity of synaptic depression in the hippocampal dentate gyrus.

This study used urethane-anesthetized rats to investigate the longevity of heterosynaptically evoked depression of the monosynaptic response generated by synapses between entorhinal cortical (EC) afferents and the cells of the dentate gyrus (DG). Brief, high-frequency activation of the converging ipsilateral EC-DG input depressed the synaptic response of the contralateral EC-DG synapses without prior experimentally induced potentiation. This depression lasted for hours. Such observations are consistent with a role for heterosynaptically induced long-term depression in the encoding functions of synapses.

Animals↗
PubMed1979

Functional effects of lesion-induced plasticity: long term potentiation in formal and lesion-induced temporodentate connections.

The crossed temporodentate pathway from the entorhinal cortex of one hemisphere which proliferates in response to a contralateral entorhinal lesion in adult rats was analyzed for its ability to exhibit long term potentiation of synaptic efficacy similar to that which occurs in the normal ipsilateral temporodentate pathway. It was found that while the small synaptic response evoked by contralateral entorhinal cortical stimulation in normal rats does not undergo long term potentiation, after unilateral entorhinal lesions and proliferation of the crossed temporodentate pathway, the crossed pathway acquires a capacity for potentiation of synaptic action which qualitatively resembles that of the normal ipsilateral temporodentate circuit. However, despite the potentiation of synaptic drive, no long term enhancement of cell discharge was observed in the re-innervated dentate gyrus even through potentiation of this parameter was very prominent in the ipsilateral pathway. Mechanisms are discussed by which a previously non-potentiating pathway may acquire, as a consequence of lesion-induced sprouting, an ability to undergo long term potentiation of synaptic efficacy in a fasion similar to the ablated pathway. Reasons for the failure to observe potentiation of cell firing are also considered.

Acetylcholinesterase↗
PubMed1979

Synapses as associative memory elements in the hippocampal formation.

This report analyzes long term potentiation (LTP) and associative interactions between synapses of the ipsilateral and crossed entorhinal cortical (EC) pathways to the dentate gyrus (DG). In the anesthetized rat, conditioning stimulation to one EC-DG pathway reliably elicits LTP at the ipsilateral synapses, while the synapses of the collateral, crossed pathway to the contralateral DG do not exhibit LTP. Furthermore, in the DG ipsilateral to the conditioning stimulation the convergent crossed pathway from the contralateral side, which had not been itself conditioned, failed to exhibit heterosynaptic LTP. These results are consistent with a specific 'synaptic' localization of the changes responsible for LTP, and suggest that some critical number of synapses must be activated in order to observe LTP. While the crossed EC-DG projection never exhibited LTP when conditioned alone, the crossed input could be potentiated under certain circumstances. Specifically, paired conditioning of ipsi- and contralateral inputs by nearly simultaneous conditioning stimulation of the EC bilaterally results in LTP in the crossed system. Furthermore, this associatively induced LTP of the crossed system can be reversed by subsequent conditioning of the ipsilateral system alone. Successive potentiating and depotentiating sequences are possible using paired and non-paired stimulation procedures even after lesions which prevent neural loops through the EC. The results are interpreted as evidence for a 'Hebb' type synapse which has the capability for erasure. This synaptic type is not appropriate for classical conditioning without appendant circuitry, but is suited for other forms of associative learning.

Animals↗
PubMed1978

A study of the localization of high mobility group proteins in chromatin.

High mobility group (HMG) proteins from fetal calf thymus and mouse brain chromatin were purified and compared electrophoretically. The four major HMG proteins characteristic of fetal calf thymus chromatin (HMG's 1, 2, 14, and 17) were also found to be present in mouse brain chromatin. Nuclei from these two eucaryotic tissues were digested with DNase I and micrococcal nuclease and the acid-soluble proteins solubilized by the two nucleases in both tissues were analyzed on starch gels. Limited digestion of fetal calf thymus nuclei with DNase I led to the solubilization of a substantial fraction of proteins HMG-1 and HMG-2 together with smaller amounts of H1. In addition, limited digestion with micrococcal nuclease released approximately 70% of HMG's 1 and 2 and variable amount of H1 into the soluble fraction. The observation that HMG proteins 1 and 2 are selectively solubilized under conditions in which active genes have been shown to be preferentially digested in various other cell types suggests their selective association with chromatin regions which are transcriptionally competent.

Animals↗
PubMed1977

Reiteration frequency of the protamine genes in rainbow trout (Salmo gairdnerii).

Protamine mRNA was isolated in a very pure form from trout testis and used as a template for the synthesis of a complementary DNA of high specific activity. The cDNA represented a full copy of the mRNA template and was used in hybridization reactions with purified trout DNA to determine the number of genes for protamines in trout testis. Our results indicate that there are less than four genes for each protamine polypeptide per the content of DNA in the male gamete and that the control of protamine synthesis in trout testis cells does not involve specific amplification of the protamine genes.

Animals↗
PubMed1976

Stimulation-dependent depression of readily releasable neurotransmitter pools in brain.

Previously accumulated GABA was released from isolated forebrain synaptosomes with repeated calcium stimulation in elevated-potassium medium. Fractional release (calcium-dependent) in response to a second calcium pulse (90-120 sec later) was depressed to approximately 60% of initial release. Neither initial GABA release nor the subsequent depression of release was affected by variations in the labelling duration. Stimulation-dependent depression of labelled GABA and norepinephrine release was demonstrated from both cerebral cortex and cerebellum synaptosomal preparations. In addition, depression resulted from prior stimulation in the presence of veratridine, A23187 or elevated-potassium. Although release of previously accumulated GABA was depressed by calcium stimulation, the release of GABA accumulated between stimulations was not. Release of this recently accumulated GABA was indistinguishable from the initial release of previously accumulated GABA and larger than the subsequently depressed release from the previously accumulated pools. These data imply (1) that the depressed release resulted from a decrease of available transmitter in pools that support secretion processes, (2) that depressed release did not result from a depression of stimulus-secretion coupling processes, and (3) that transmitter accumulated subsequent to release events is released preferentially to transmitter accumulated prior to the intervening stimulation.

Aminobutyrates↗
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↗