PubMed Health⌕ Search

Biomedical subjects

B Sultanov

Publications and source records attributed to B Sultanov.

5 recordsLinked to original sources
PubMed2005

[Blood serum of patients with secondary progressive multiple sclerosis changes neuron electric activity].

An effect of 20% blood serum estimated by the changes of background and excited spike activity of Retzius' neuron by Hirudo medicinalis, which does not contain myelin, has been studied in 2 groups of patients. The first group comprised patients with serum, containing antibodies to gangliosides, and the second one--patients without such antibodies. Incubation of Reitzius neurons in the serum with GM1-antibodies within 40 min resulted in the change of spike form, increase of cell stimulation threshold by average 20%, reduction of the frequency of spontaneous impulse activity by average 28%, decrease of the spikes number in response to the lower frequency (0.5 Hz) synaptic stimulation and inhibition of adaptation to the high frequency (10 Hz) stimulation. The use of the serum without GM1-antibodies caused a different change of the spike form and increased the stimulation threshold by 8% and sparser background impulse activity of the neuron by 40%. During low frequency synaptic activation of the neuron (0.5%), there was sensitivity disturbance and inhibition of the electric response to the high frequency stimulation. The results suggest that neuron injuries in multiple sclerosis may develop before morphological appearances of myelin lesions.

Adult↗
PubMed2002

[Axonal reaction precedes demyelination in experimental models of multiple sclerosis].

Taking into consideration that myelin phospholipids may be partially synthesized in neuronal bodies, while neurilemma readily reacts with antibodies against gangliosides by changing the properties of membrane ionic channels, the attempt was made to test the proposed assumption of the early axonal reaction in demyelinating processes in experimental models of multiple sclerosis. The models of chronic allergic encephalomyelitis in Lewis rats injected with homogenate of highly purified myelin or total brain gangliosides were used. First signs of demyelination (the destruction of intermediate dense lines) were demonstrated in the inner layers of myelin close to axon and were shown to develop synchronously with the aggregation of filamentous-tubular material in the neuroplasm. These changes are associated with significant shift of the ratio of myelin sheath thickness to axonal diameter (from 1:7-1:3 to 2:1-3:1). This swelling of myelin seems to be caused by neuroplasmic proteins aggregation, that must be accompanied by the drop in oncotic pressure and the separation of loosely-bound water fraction that may be assimilated by myelin. At light microscopic level the increase of myelin thickness is clearly observed that is in exact correspondence with the decrease in axonal diameter. The process starts with the exfoliation and swelling of the nodes of Ranvier and the incisures of myelin, which fuse after elongation, that corresponds to the total disintegration of myelin with the preservation of continuity of axon which appears to be harshly shrunken.

Animals↗
PubMed2001

Serum ganglioside patterns in multiple sclerosis.

The relative distribution of gangliosides was determined in the serum of 37 patients with multiple sclerosis (MS) and of 30 healthy subjects. There was a significant increase of GM1 and GD1a, and a decrease of GM3 proportion in the serum of relapsing-remitting MS patients (RRMS) during their first MS attack. The RRMS patients in relapse with a long duration of the disease had a significant decrease of GM1 and an increase of GD1a portion in the serum. An increase of GD1a, one of the major brain neuron ganglioside fraction, suggested the neuron injury in the early and with a long duration RRMS. The finding of an increase of GM1, the main human myelin ganglioside, during the first MS attack in RRMS patients confirms previous evidence for the possible involvement of gangliosides in the early pathological course of demyelination in MS.

G(M1) Ganglioside↗