Biomedical subjects

T Tsintsadze

Publications and source records attributed to T Tsintsadze.

6 recordsLinked to original sources

PubMed2005

[Employment of the laser apparatus SL-30 in complex treatment of chronic recurrent herpetic stomatitis].

The purpose of the study was the estimation of complex treatment effectiveness of chronic recurrent herpetic stomatitis using portable laser device "Beurer" (Germany). Fifty patients 17 till 55 years of age were investigated. Among them 28 were women and 22 were men. They were divided into two groups. All patients were treated by standard algorithm according to the severity of the disease. In the patients from the second group laser therapy by means of SL-30, 15-30 min per day was administered. After the completion of the course of treatment positive therapeutic effect has been achieved in all patients from the second group. Disappearance of the subjective symptoms and the initiation of the reparative-regenerative processes has occurred much faster in this group which gave us an opportunity to reduce the number of sessions by 5-6 in comparison with the first group. Thus, it was shown that the use of apparatus SL-30 in complex treatment of the chronic recurrent herpetic stomatitis increases the efficiency of the treatment.

Adolescent↗

PubMed2001

New channel blocker BIIA388CL blocks delayed rectifier, but not A-type potassium current in central neurons.

A new substance (R,S)-(3,4-dihydro-6,7-dimethoxyisoquinoline-1-yl)-2-cyclohexyl-N-(3,3-diphenylpropyl)-acetamide hydrochloride (BIIA388Cl), which demonstrates neuroprotective properties in animal models, was examined for its action on K(+) currents in acutely isolated rat hippocampal neurons using the patch-clamp/concentration clamp techniques in the whole-cell configuration. The delayed rectifier K(+)-current (I(DR)) was strongly inhibited by externally applied BIIA388Cl, while the transient A-current (I(A)) remained virtually unaffected. Block of I(DR) by the pre-applied BIIA388Cl was revealed as a rapid decay of the current indicating direct interaction of the drug with the open state of the channel. The removal of the block upon repolarization was also rapid (tau=22 ms). The dose-response relationship for the blocking action of BIIA388Cl revealed an IC(50) value of 300 nM for the peak I(DR), whereas the IC(50) value for I(DR) measured 300 ms after the onset of depolarization was 120 nM. The blocking action of BIIA388Cl on I(A) was at least 200 times less potent. These data allow us to conclude that BIIA388Cl is an effective and selective blocker of I(DR). This current is the main pathway for the loss of intracellular potassium by depolarized neurons. Selective obstruction of this pathway could be useful for neuroprotection.

Animals↗

PubMed2001

Modulation of ion channels in rat neurons by the constituents of Hypericum perforatum.

Despite almost forty years of widespread use of antidepressant drugs, their mode of action is still unknown. Hyperforin, a phloroglucinol derivative, is a major pharmacologically and therapeutically active constituent of Hypericum perforatum extract that is widely used as an herbal antidepressant drug. However, the mechanism or mechanisms of action of these naturally abundant, non-toxic extracts remain unclear. Enzymatically isolated patch-clamped rat central and peripheral neurons exposed to rapid changes in the composition of external medium (concentration clamp) were used in our experiments to investigate the modulation of the various voltage- and ligand-gated channels by hyperforin, as well as by other constituents of Hypericum perforatum. At nanomolar concentrations, hyperforin induced significant inhibition of various ion channels. In the case of P-type Ca2+ channels, we established that hyperforin acts via interaction with calmodulin or through calmodulin-activated pathways involving at least one second messenger. The results presented here indicate that multiple mechanisms and extract constituents may be involved in the antidepressant action of Hypericum extracts, and that they could also possess neuroprotective and analgesic effects.

Animals↗

PubMed2000

Hyperforin modulates gating of P-type Ca2+ current in cerebellar Purkinje neurons.

Whole-cell, patch-clamp recordings from acutely isolated cerebellar Purkinje neurons demonstrate a two-stage modulation of P-type high-voltage-activated (HVA) Ca2+ current by a constituent of St. John's wort, hyperforin (0.04-0.8 microM). The first stage of modulation was voltage dependent and reversible. It comprised slow-down of the activation kinetics and a shift in the voltage dependence of P-current to more negative voltages. Hyperforin (0.8 microM) shifted the maximum of the current/voltage (I/V) relationship by -8+/-2 mV. The second, voltage-independent stage of modulation was manifested as a slowly developing inhibition of P-current that could not be reversed within the period of study. Neither form of modulation was abolished by intracellular guanosine 5'-O-(2-thiodiphosphate) (GDPPS) or guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS) or by strong depolarising pre-pulses, indicating that modulation via guanine nucleotide-binding proteins (G proteins) is not involved in the observed phenomenon. Calmidazolium (0.5 microM), an antagonist of the intracellular Ca2+-binding protein calmodulin significantly inhibited the hyperforin-induced shift of the IIV curve maximum and the slow-down of the activation kinetics. It did not, however, affect the delayed inhibition of P-current, indicating that the two stages of modulation are mediated by separate mechanisms.

Animals↗

PubMed1996

NMDA receptor-mediated synapses between CA1 neurones: activation by ischaemia.

Using an in situ patch clamp in hippocampal CA1 mini-slices, we measured excitatory postsynaptic currents (EPSC) by varying the strength of the stimulus applied to the axons of CA3 neurones. The kinetics of the EPSC was initially independent of the stimulus strength. Post-ischaemic potentiation of the EPSC was observed 60-80 min after brief periods (10 min) of anoxia/aglycaemia. The decay of the EPSC slowed significantly in most of the examined neurones. In 11 of 17 cells the EPSC kinetics became dependent on stimulus strength: a slower decay corresponded to a stronger stimulus. This effect was not abolished by N-methyl-D-aspartate (NMDA) or a non-NMDA receptor blocker (D-2-amino-5-phosphonovaleric acid or 6-cyano-7-nitroquinoxaline-2,3-dione respectively) indicating the polysynaptic nature of the modified EPSC: transient ischaemia led to the long-term recruitment of previously inactive, possibly latent NMDA synapses between CA1 neurones.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1995

Latent N-methyl-D-aspartate receptors in the recurrent excitatory pathway between hippocampal CA1 pyramidal neurons: Ca(2+)-dependent activation by blocking A1 adenosine receptors.

When performed at increased external [Ca2+]/[Mg2+] ratio (2.5 mM/0.5 mM), temporary block of A1 adenosine receptors in hippocampus [by 8-cyclopentyltheophylline (CPT)] leads to a dramatic and irreversible change in the excitatory postsynaptic current (EPSC) evoked by Schaffer collateral/commissural (SCC) stimulation and recorded by in situ patch clamp in CA1 pyramidal neurons. The duration of the EPSC becomes stimulus dependent, increasing with increase in stimulus strength. The later occurring component of the EPSC is carried through N-methyl-D-aspartate (NMDA) receptor-operated channels but disappears under either the NMDA antagonist 2-amino-5-phosphonovaleric acid (APV) or the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). These findings indicate that the late component of the SCC-evoked EPSC is polysynaptic: predominantly non-NMDA receptor-mediated SCC inputs excite CA1 neurons that recurrently excite each other by predominantly NDMA receptor-mediated synapses. These recurrent connections are normally silent but become active after CPT treatment, leading to enhancement of the late component of the EPSC. The activity of these connections is maintained for at least 2 hr after CPT removal. When all functional NMDA receptors are blocked by dizocilpine maleate (MK-801), subsequent application of CPT leads to a partial reappearance of NMDA receptor-mediated EPSCs evoked by SCC stimulation, indicating that latent NMDA receptors are recruited. Altogether, these findings indicate the existence of a powerful system of NMDA receptor-mediated synaptic contacts in SCC input to hippocampal CA1 pyramidal neurons and probably also in reciprocal connections between these neurons, which in the usual preparation are kept latent by activity of A1 receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗