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Activation by GABAb, reduction of the intracellular concentration of Ca++ and inhibition of protein kinases are possible mechanisms of the long-term aosttetanic modification of the efficiency of inhibitory transmission in the new cortex

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Abstract

A hypothetical mechanism is proposed for the induction of long-term posttetanic potentiation of the efficiency of inhibitory synaptic transmission (LTPi). The data we have previously obtained have made it possible to hypothesize that modifiable inhibitory synapses are situated on the dendritic spines on which there are metabotropic GABAb receptors. It is hypothesized that modification of inhibitory transmission is determined precisely by these receptors, the activation of which leads to inactivation of protein kinases C and A (PKC and PKA) as a result of a decrease in the intracellular concentration of Ca++ and the inhibition of cAMP. The hypothesis is confirmed by experiments in which it was demonstrated that an effect similar to LTPi took place as a result of the inactivation of PKC and PKA. It is hypothesized that eicanoid [sic] acids may be retrograde messengers during LTPi. A new hypothetical mechanism underlying long-term depression of excitatory transmission (LTDe) is proposed, according to which tetanized afferent fibers must simultaneously monosynaptically excite and disynaptically inhibit one and the same postsynaptic cell. LTDe may be induced only in those pathways which activate [are activated by — unclear from Russian text — Trans.] GABAb receptors. The proposed hypotheses make it possible to explain the results of certain experiments.

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References

  1. N. V. Veber, S. Sh. Rapoport, and I. G. Sil'kis, “The long-term changes in the excitability of pyramidal tract neurons in the cat”,Zh. Vyssh. Nerv. Deyat.,34, 572 (1984).

    CAS  Google Scholar 

  2. I. G. Sil'kis, S. Sh. Rapoport, N. V. Veber, and A. M. Gushchin, “Long-term homosynaptic depression of impulse reactions of neurons of the motor cortex of the cat”,Zh. Vyssh. Nerv. Deyat.,43, No. 5, 925 (1993).

    Google Scholar 

  3. I. G. Sil'kis, “Long-term posttetanic changes in the efficiency of inhibitory connections in thalamocortical neuronal networks”Doklady Akad. Nauk RFSFR,337, 413 (1994).

    Google Scholar 

  4. I. G. Sil'kis, “Inhibitory interactions in neuronal networks including cells of the auditory cortex and medial geniculate body”,Zh. Vyssh. Nerv. Deyat.,44, 1046 (1994).

    Google Scholar 

  5. A. Baranyi, M. B. Szente, and C. D. Woody, “Activation of protein kinase C induces long-term changes of postsynaptic currents in neocortical neurons”,Brain Res.,440, 341 (1988).

    Article  PubMed  CAS  Google Scholar 

  6. L. J. Bindman, K. P. S. Murphy, and S. Pockett, “Postsynaptic control of the induction of long-term changes in efficacy of transmission at neocortical synapses in slices of rat brain”,J. Neurophysiol.,60, 1053 (1988).

    PubMed  CAS  Google Scholar 

  7. T. V. P. Bliss and G. L. Collingridge, “A synaptic model of memory: long-term potentiation in the hippocampus”,Nature,361, 31 (1993).

    Article  PubMed  CAS  Google Scholar 

  8. P. M. Bradley, B. D. Burns, J. Titmuss, and A. C. Webb, “Morphological correlates of protein kinase C induced potentiation in the chick brain slice”,Neuroreport.,3, 223 (1992).

    Article  PubMed  CAS  Google Scholar 

  9. S. Brocher, A. Artola, and W. Singer, “Intracellular injection of Ca++ chelators blocks induction of long-term depression in rat visual cortex”,Proc. Natl. Acad. Sci.,89, 123 (1992).

    PubMed  CAS  Google Scholar 

  10. J. P. Burke and J. J. Hablitz, “Presynaptic depression of synaptic transmission mediated by activating of metabotropic glutamate receptors in rat neocortex”,J. Neurosci.,14, 5120 (1994).

    PubMed  CAS  Google Scholar 

  11. U. Campbell, N. Berrow, and A. C. Dolphin, “GABAb receptor modification of Ca++ currents in rat sensory neurons by the G-protein G(0) anticence [sic] oligonucleotide studies”,J. Physiol. (London),470, 1 (1993).

    CAS  Google Scholar 

  12. V. Crepel, C. Roviru, and Y. Ben-Ari, “The K+ channel opener diazoxide enhances glutamatergic currents and reduces GABAergic currents in hippocampal neurons”,J. Neurophysiol.,69, 494 (1993).

    PubMed  CAS  Google Scholar 

  13. C. Dehay, R. J. Douglas, K. A. C. Martin, and C. Nelson, “Excitation by geniculocortical synapses is not “vetoed” at the level of dendritic spines in cat visual cortex”,J. Physiol. (London),440, 723 (1991).

    CAS  Google Scholar 

  14. C. Drapeou, L. Pellerin, L. S. Wolfe, and M. Pivoli, “Long-term changes of synaptic transmission induced by arachidonic acid in the CA1 subfield of the rat hippocampus”,Neurosci. Lett.,115, 286 (1990).

    Article  Google Scholar 

  15. E. Fifkova, H. Eason, and P. Schaner, “Inhibitory contacts on dendrite spines of the dentate fascia”,Brain Res. 577, 331 (1992).

    Article  PubMed  CAS  Google Scholar 

  16. A. Fucuda, I. Mody, and D. A. Prince, “Differential ontogenesis of presynaptic and postsynaptic GABAb inhibition in rat somatosensory cortex”,J. Neurophysiol.,70, 448 (1993).

    Google Scholar 

  17. E. D. Kanter and L. B. Haberly, “Associative long-term potentiation, of piriform cortex slices requires GABAa blockade”,J. Neurosci.,13, 2477 (1993).

    PubMed  CAS  Google Scholar 

  18. C. Koch and A. Zador, “The function of dendritic spines: devices subserving biochemical rather than electrical compartmentalization”,J. Neurosci.,13, 413 (1993).

    PubMed  CAS  Google Scholar 

  19. Y. Komatsu and M. Iwakiri, “Long-term modification of inhibitory synaptic transmission in developing visual cortex”,Neuroreport.,4, 907 (1993).

    PubMed  CAS  Google Scholar 

  20. S. V. Kombian and R. Malenka, “Simultaneous LTP of non-NMDA and LTD of NMDA-receptor mediated responses in the nucleus accumbens”,Nature,368, 242 (1994).

    Article  PubMed  CAS  Google Scholar 

  21. B. J. Krishek X. Xie C. Blackstone, et al., “Regulation of GABAa receptor function by protein kinase C phosphorylation”,Neuron. 12, 1081 (1994).

    Article  PubMed  CAS  Google Scholar 

  22. K. Kuriyama, M. Hirouchi, and H. Nakayasu, “Structure and function of cerebral GABAa and GABAb receptors”,Neurosci. Res.,17, 91 (1993).

    Article  PubMed  CAS  Google Scholar 

  23. N. A. Lambert and W. A. Wilson, “Discrimination of post-and presynaptic GABAb receptor mediated responses by tetrahydro aminoacridine in area CA3 of the rat hippocampus”,J. Neurophysiol.,69, 630 (1993).

    PubMed  CAS  Google Scholar 

  24. D. J. Linden, “Long-term synaptic depression of the mammalian brain”,Neuron.,12, 457 (1994).

    Article  PubMed  CAS  Google Scholar 

  25. Y. B. Liu, J. E. Disterhoft, and N. T. Slater, “Activation of metabotropic glutamate receptors induces long-term depression of GABAergic inhibition in hippocampus”,J. Neurophysiol.,69, 1000 (1993).

    PubMed  CAS  Google Scholar 

  26. D. M. Lovinger, E. Tayler, S. Fidler, and A. Merrit, “Properties of a presynaptic metabotropic glutamate receptor in rat neostriatal slices”,J. Neurophysiol.,69, 1236 (1993).

    PubMed  CAS  Google Scholar 

  27. R. Malinow, M. Schulman, and R. W. Tsiln, “Inhibition of postsynaptic PKC or CaMK11 blocks induction but not expression of LTP”,Science,245, 862 (1989).

    PubMed  CAS  Google Scholar 

  28. S. M. Marchenko, “Mechanism of modulation of GABA-activated current by internal calcium in rat central neurons”,Brain Res.,546, 355 (1991).

    Article  PubMed  CAS  Google Scholar 

  29. L. R. Merline and R. K. S. Wong, “Synaptic modifications accompanying epileptogenesisin vitro-long-term depression of GABA mediated inhibition”,Brain Res.,627, 330 (1993).

    Article  Google Scholar 

  30. M. A. Musgrave, B. A. Ballyk, and J. W. Goh, “Coactivation of metabotropic and NMDA receptors is required for LTP induction”Neuroreport.,4, 171 (1993).

    PubMed  CAS  Google Scholar 

  31. H. R. Olpe, W. Worner, and T. Ferrat, “Stimulation parameters determine role of GABA (B) receptors in long-term potentiation”,Experimentia,49, 542 (1993).

    Article  CAS  Google Scholar 

  32. T. S. Otis and I. Mody, “Differential activation of GABAa and GABAb receptors by spontaneously released transmission”,J. Neurophysiol.,67, 227 (1992).

    PubMed  CAS  Google Scholar 

  33. M. Pende, M. Lanza, G. Bonanno, and M. Raiteri, “Release of endogenous glutamatic [sic] and aspartate [sic] acids from cerebrocortex synaptosomes and its modulation through activation of gamma-aminobutyric acid b (GABAb) receptor subtype”,Brain Res.,604, 325 (1993).

    Article  PubMed  CAS  Google Scholar 

  34. N. M. Porter, R. E. Twyman, M. D. Uhler, and R. L. Macdonald [sic] “Cyclic AMP-dependent protein kinase decreases GABAa receptor current in mouse spinal neurons”,Neuron.,5, 789 (1990).

    Article  PubMed  CAS  Google Scholar 

  35. W.-X. Shi and S. Rayport, “GABA synapses formedin vitro by local axon collaterals of nucleus accumbens neurons”,J. Neurosci.,14, 4548 (1994).

    PubMed  CAS  Google Scholar 

  36. P. C. Schwindt, W. J. Spair, and W. E. Crill, “Calcium-dependent potassium current in neurons from cat sensorimotor cortex”,J. Neurophysiol.,67, 216 (1992).

    PubMed  CAS  Google Scholar 

  37. A. Stelser, N. T. Slater, and G. Bruggencate, “Activation of NMDA receptors blocks GABAergic inhibition in anin vitro model of epilepsy”,Nature Lond.,326, 698 (1987).

    Article  Google Scholar 

  38. M. V. Szente, A. Baranyi, and C. D. Woody, “Effects of, protein kinase C inhibitor H-7 on membrane properties and synaptic responses of neocortical neurons of awake cats”,Brain Res.,506, 281 (1990).

    Article  PubMed  CAS  Google Scholar 

  39. T. Tsumoto, “Long-term potentiation and long-term depression in the neocortex”,Progress in Neurobiol.,39, 209 (1992).

    Article  CAS  Google Scholar 

  40. J. H. Williams, and T. V. P. Bliss, “Induction but not maintenance of calcium-induced long-term potentiation in dentate gyrus and area CA1 of the hippocampal slice is blocked by norhydroguaiaretic acid”,Neurosci. Lett.,88, 81 (1988).

    Article  PubMed  CAS  Google Scholar 

  41. X. Xie T. W. Berger, and G. Barranuevo, “Isolated NMDA-receptor-mediated synaptic, responses express both LTP and LTD”,J. Neurophysiol.,67, 1009 (1992).

    PubMed  CAS  Google Scholar 

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  1. I. G. Sil'kis
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Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow. Translated from Zhurnal Vysshei Nervnoi Deyatel'nosti imeni I.P. Pavlova, Vol. 45, No. 1, pp. 18–28, January–February, 1995.

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Sil'kis, I.G. Activation by GABAb, reduction of the intracellular concentration of Ca++ and inhibition of protein kinases are possible mechanisms of the long-term aosttetanic modification of the efficiency of inhibitory transmission in the new cortex. Neurosci Behav Physiol 26, 88–97 (1996). https://doi.org/10.1007/BF02391160

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  • DOI: https://doi.org/10.1007/BF02391160

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