Biomedical subjects

W Egido-Villareal

Publications and source records attributed to W Egido-Villareal.

4 recordsLinked to original sources

PubMed1993

[The effect of a decrease in the mobilization of Ca+ and its chemo-controlled intake into the cytoplasm on the modulation of cholinoreceptor neuronal plasticity in Helix lucorum snails by 15-hydroxyeicosatetraenoic acid].

The effects of extracellular solution without Ca2+ and inhibitors of Ca2+ mobilization dependent of Ca2+ (tetracaine) and inositol-1,4,5-trisphosphate (TMB-8) on the modulation of cholinoreceptor (ChR) plasticity of identified Helix lucorum RPa3 and LPa3 neurons by 15(S)-hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid (15-HETE) were investigated. Using the double-electrode voltage-clamp technique, the inward current, induced by local ionophoretic acetylcholine application (ACh-current), was recorded. ChR plasticity was evaluated by extinction of ACh-current developed in a process of rhythmic ACh applications on the soma with an interval 60-240 s. Tetracaine and TMB-8 disturbed long-latent modulatory effect of 15-HETE and did not influence short-latent one. Extraction of Ca2+ from extracellular solution did not affect the modulatory effect of 15-HETE. It was concluded that one of the molecular mechanisms of ChR plasticity deepening due 15-HETE (in long-latent phase) induces potentiation of Ca(2+)- and inositol-1,4,5-trisphosphate-dependent Ca2+ mobilization evoked by 5-lipoxygenase eicosanoids.

Acetylcholine↗

PubMedDate not supplied

The influence of an inhibitor of lipoxygenases on the modulation of the plasticity of cholinoreceptors by 15-HETE.

The role of acyclic eicosanoids in the modulation of the plasticity of somatic cholinoreceptors by 15(S)-hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid (15-HETE) was investigated in identified RPa3 and LPa3 neurons of Helix lucorum using the two-electrode voltage clamping technique. It was demonstrated that the inhibitor of lipoxygenases, nordihydroguaiaretic acid (2-20 microM), completely blocks the short- and long-latency effects of 15-HETE (2-20 microM) on the depth of damping of the inward current induced by rhythmic applications of acetylcholine (ACh) to the soma. It is concluded that the short-latency effect of 15-HETE on the plasticity of cholinoreceptors is determined by its inhibition mainly of 5-lipoxygenase, which leads to a reduction in the level of acyclic eicosanoids that are formed under the influence of this enzyme. The potentiation of the effects of the acyclic eicosanoids, whose synthesis is resumed in the second phase, probably underlies the direct long-latency modulatory effect of 15-HETE.

Acetylcholine↗

PubMedDate not supplied

NO synthase and guanylate cyclase inhibitors block modulation of the plasticity of common snail cholinoreceptors by 15-hydroxy-eicosatetraenoic acid.

The probable role of two second messengers, nitrogen oxide (NO) and cyclic guanosine monophosphate (cGMP) in the short- and long-latency effects of the acyclic eicosanoid 15(S)-hydroxy-5Z,8Z,11Z,13E-eicosatetraenoic acid (15-HETE) on the plasticity of somatic cholinoreceptors of identified RPa3 and LPa3 neurons of Helix lucorum, was investigated using the two-electrode voltage clamp technique on the membrane. It was demonstrated that N omega-methyl-L-arginine (an inhibitor of NO synthase), LY-83,583 [sic], and the dye methylene blue (inhibitors of soluble guanylate cyclase), when applied extracellularly, disrupt the short- and long-latency modulatory influences of 15-HETE on the depression of the inward current induced by acetylcholine during its rhythmic application to the soma. The participation of NO and cGMP in the modulatory effects of 15-HETE on the plasticity of cholinoreceptors is hypothesized.

Acetylcholine↗

PubMedDate not supplied

[The effect of a lipoxygenase inhibitor on the modulation of cholinoreceptor plasticity by 15-HETE].

The role of acyclic eicosanoids in the modulation of the plasticity of somatic cholinoreceptors, due to 15(S)-hydroxy-(5Z,8Z,11Z,13E)-eicosatetraenoic acid (15-HETE), was studied in identified neurons of Helix lucorum. Lipoxygenase inhibitor, nordihydroguaiaretic acid blocks the effects of 15-HETE on the extinction of the inward current, evoked by the rhythmic application of acetylcholine on the neuron. The conclusion was reached that the short-latency effect of 15-HETE, on the plasticity of cholinoreceptors is due to the inhibition it produces on the 5-lipoxygenase. This effect leads to a lowering on the level of acyclic eicosanoids which are formed by the action of this enzyme. The potentiation of the effect of the acyclic eicosanoids, whose synthesis is renewed in the second phase, is a plausible explanation of the long-latency modulatory effect of 15-HETE.

Acetylcholine↗