[Mechanisms of long-term synaptic depression in the hippocampus]. / Mekhanizmy dolgovremennoi sinapticheskoi depressii v gippokampe.

Long-term depression (LTD) was studied in hippocampal slices obtained from neonatal rats at the synapses between CA3 and CA1 pyramidal neurons. The induction of the LTD required pairing of Ca2+ influx into the postsynaptic CA1 neuron through voltage-gated Ca2+ channels with activation of metabotropic glutamate receptors. The expression of this form of LTD is at least partly presynaptic, suggesting the need for a retrograde messenger. We present evidence that arachidonic acid might serve such a function. Thus applications of arachidonic acid simulate LTD whereas blockade of arachiidonic acid release inhibits LTD.

[The direct action of high doses of gamma quanta and neutrons of different energies on the sympathetic ganglion neurons in the frog]. / Neposvredstvennoe deistvie vysokikh doz gamma-kvantov i neitronov raznoi énergii na neirony simpaticheskogo gangliia liagushki.

Irradiation of isolated frog sympathetic ganglia IX-X with high doses caused a long-term depolarization of a single ganglion cell and increase of synaptic activation threshold. The radiation effects observed were not accompanied by the transmission failure. The authors suggest that the changes in the synaptic mechanisms play a minor role in the development of the CNS syndrome.

[Comparative research on synaptic transmission in the sympathetic ganglia of rabbits and frogs during acetylcholinesterase inhibition]. / Sravnitel'noe issledovanie sinapticheskoi peredachi v simpaticheskikh gangliiakh krolika i liagushki v usloviiakh ingibirovaniia atsetilkholinésterazy.

Organophosphorus inhibitor of acetylcholinesterase (AChE) armin (1 x 10(-6) M) induced a variety of pre- and postsynaptic effects resulting from the AChE inhibition and subsequent accumulation of acetylcholine (ACh) in the synaptic cleft. The intensity of postsynaptic effects (level of neuron depolarization, degree of action potential depression) was shown to be different in the ganglia of frog and rabbit. This could be explained by differences in the total amount of ACh released in response to nerve stimulation as well as at rest. Both muscarinic and nicotinic cholinoreceptors were involved in the process of sustained depolarization of the neurons in the rabbit superior cervical ganglion after AChE inhibition. In frog ganglion neurons the nicotinic receptors did not participate in depolarization evidently due to their fast desensitization. The activation of presynaptic muscarinic receptors resulted in decrease of ACh released by nerve stimulation seems to weaken depolarization and blockade of synaptic transmission in sympathetic ganglia treated by AChE inhibitors.

[Synaptic effects of nicotinic and muscarinic agonists in the sympathetic ganglia of the frog]. / Sinapticheskie éffekty nikotinovykh i muskarinovykh agonistov v simpaticheskikh gangliiakh liagushki.

Superfusion of isolated frog sympathetic ganglia with nicotinic agonists (suberyldicholine, tetramethylammonium, DMPP), as well as with acetylcholine in the presence of atropine, caused short-term depolarization of a single ganglion cell and blockade of synaptic transmission. Muscarinic agonists (methylfurmethide, methyl dilvasen, acetylcholine) caused sustained depolarization which was not accompanied by transmission failure. Oxotremorine did not change membrane potential at concentrations up to 1.10(-5) mol/l, but at a lower concentration (1.10(-6) mol/l) it produced about a two-fold decrease of EPSP quantum content. This allows the presynaptic muscarinic receptors to be related to M2 type. Inhibition of acetylcholinesterase markedly potentiated postsynaptic effect of methylfurmethide; as a result, there was a shift of the dose-response curve to the lower concentrations of agonist. The postsynaptic muscarinic receptors were found to have high stereoselectivity that was seen in the case of enantiomers of methyl dilvasen (F-2268). The obtained results elucidate changes in the ganglionic transmission, the transmitter being present in the synaptic cleft.