[Changes of the neuropil ultrastructure in the CA1 hippocampal area of rat pups after hyaluronidase treatment].

Electron microscopical and electrophysiological studies were carried out in cross-sections of the hippocampus of 4-weeks-old male rat pups (n = 35) to detect the ultrastructural changes in CA1 hippocampal area and the peculiarities of excitatory postsynaptic potential formation in this brain area after the incubation of the sections in the solution of hyaluronidase (10 U/ml), the enzyme which specifically degrades the extracellular matrix glycosaminoglycan--the hyaluronic acid. The reduction of the width of synaptic cleft by 15-25% in the axo-dendritic contacts of the stratum radiatum of CA1 hippocampal area was detected 1.5 min following the application of enzyme, coinciding with the increase of the excitatory postsynaptic potential amplitude. The width of synaptic cleft was further reduced by 45-55% after 4.5 min of incubation; during this period the blockade of signal transmission along the Schaffer's collaterals to CA1 hippocampal area was observed. Thus, the structural and functional state of glycosaminoglycans is one of the factors controlling the efficiency of synaptic transmission in the brain.

[Nitrogen monoxide and nociceptive processes]. / Monooksid azota i notsitseptivnye protsessy.

Experiments on conscious rats studied the effects of systemic or central application of a nitric oxide (NO) donor or NO-synthase inhibitor on the pain sensitivity threshold. Injection of SNAP in doses of 0.2, 2.0, and 20.0 micrograms into the subarachnoidal space of the ventral medulla through a preimplanted steel cannula was accompanied by a dose-dependent change in tail-flick latency. Intraperitoneal injection of 30 mg L-NAME also increased pain sensitivity threshold levels. The findings suggest that the decrease in pain sensitivity after systemic NO-synthase inhibitor administration is due to the modulation of NO-dependent processes at both the central and peripheral levels.

[Ultrastructure of neurons and glial cells in the solitary tract nucleus and in the ventrolateral sections of the rat medulla oblongata after subdiaphragmatic vagotomy]. / Ul'trastruktura neironov i glial'nykh kletok v iadre solitarnogo trakta i v ventrolateral'nykh otdelakh prodolgovatogo mozga krys posle poddiafragmal'noi vagotomii.

Using electron microscopy, complex remodelling of neuronal and glial cell ultrastructure was demonstrated in the solitary tract nucleus and ventrolateral medulla at different time intervals following bilateral subdiaphragmatic truncal vagotomy. Four weeks after vagotomy phagocytizing microgliocytes were demonstrated in the vicinity of nuclei of degenerating neurons within the rostral, but not the caudal, areas of solitary tract nucleus and ventrolateral medulla. It is suggested that the ultrastructural changes observed in the medulla after vagotomy depend on the distribution pattern of vagal projections to the caudal brainstem.

[Changes in the ultrastructure of the rat bulbar nuclei caused by kainic acid administration]. / Izmeneniia ul'trastruktury kletok bul'barnykh iader krysy pri vozdeistvii kainovoi kisloty.

The effect of kainic acid (KA) injection into the commissural area of nucleus tractus solitarii (NTS) of rats was studied to evaluate its influence on the ultrastructure of neurons and gliocytes at the site of injection and in the ventrolateral medulla (VM). 30 min after KA injection, in the perikarya of neurons in rostral and caudal NTS and VM the increased number of ribosomes, lysosomes, lipofuscin granules and edema of mitochondria were noted. Giant mitochondria were found in terminals and axons of myelin fibers. 14 days after KA injection, the increased volume of Golgi complex cisterns was found in single neurons in NTS rostral parts, while the neurons of caudal NTS demonstrated pronounced degenerative and destructive changes. During this period, the volume of mitochondria and of vacuoles was increased in dendrites within caudal NTS and VM, where degenerating processes of the nervous cells were found. In gliocytes of caudal NTS, the hypertrophy of cytoplasm was noted with the accumulation of dilated cisterns of endoplasmic reticulum and redistribution of nuclear chromatin. In the same areas of NTS the reaction of endotheliocytes and pericytes, perivascular edema and accumulation of microgliocytes were found. The results obtained indicate the reactive changes in VM in response to intracentral injection of neurotoxin.

Changes in neuropil ultrastructure in hippocampal field CA1 in rat pups after application of hyaluronidase.

Electron microscopy and electrophysiological studies were performed on cross-sectional slices of the hippocampus of four-week-old male rat pups (n = 35) to detect ultrastructural changes in hippocampal field CA1 and the characteristics of the formation of excitatory postsynaptic potentials in this area of the brain after incubation of slices in hyaluronidase solution (10 U/ml), whose specific substrate is the extracellular matrix glycosaminoglycan hyaluronic acid. At 1.5 min after enzyme application, there were reductions in synaptic cleft widths in axodendritic contacts of the striatum radiatum of hippocampal field CA1 by 15-25%, which were consistent with increases seen in the amplitudes of excitatory postsynaptic potentials. At 4.5 min of incubation, the lumens of synaptic clefts decreased by 45-55%: during this time there was blockade of signal transmission via Schäffer collaterals to hippocampal field CA1. Thus, the structural-functional state of glycosaminoglycans is among the factors determining the efficiency of synaptic transmission in the brain.

[Long-term potentiation of AMPA- and NMDA-components of minimal postsynaptic currents in CA1 area of the rat hippocampus]. / Dolgovremennaia potentsiatsiia AMPA- i NMDA-komponent minimal'nykh postsinapticheskikh tokov v oblasti CA1 gippokampa krys.

Excitatory postsynaptic currents (EPSC) were recorded from pyramidal neurons of the rat hippocampal slices as well as the AMPA and NMDA components. A strong enough correlation between the amplitudes of the components provided a reliable evidence of their generation by the same synapse. Both components revealed similar LTP following afferent tetanisation. The data obtained do not support postsynaptic mechanisms of the LTP maintenance but suggest that increased presynaptic release represents a basic mechanism of the early LTP maintenance.