Biomedical subjects

Aidas Alaburda

Publications and source records attributed to Aidas Alaburda.

6 recordsLinked to original sources

PubMed2006

Identification of partially presented meaningless patterns: effect of completeness and distinctiveness.

The role of parts versus that of wholes in a visual perception has been debated for a century as two opposite approaches, namely, an analytic and holistic. In two psychophysical experiments we investigated whether the stimulus completeness or distinctiveness is essential for identification of the partially presented patterns under brief presentation conditions. For this purpose, a special class of stimuli was constructed in such a way that the patterns could be divided into informative and redundant parts. The first experiment clearly demonstrated the importance of the redundant part for effective pattern identification for the majority of subjects. The second experiment revealed the direct dependence of identification accuracy of the patterns on their completeness (2, 3, 4, 5, or 6 elements). Familiarisation of subjects with the test stimuli influenced the strength of this dependence.

Adult↗

PubMed2003

Metabotropic modulation of motoneurons by scratch-like spinal network activity.

Glutamate is the main excitatory transmitter in the spinal motor network. The excitation is to a large extent mediated by ionotropic receptors, but glutamate also activates metabotropic receptors. In motoneurons in spinal cord slices the activation of group I metabotropic glutamate (mGlu1) receptors leads to facilitation of CaV1.3 L-type calcium channels. Here we investigate whether this pathway is activated by motor network activity induced by natural sensory stimuli. The lumbar carapace and spinal cord were isolated from adult turtles. In this preparation, mechanical stimulation in the receptive field for the scratch reflex induced episodes of rhythmic motor network activity. During an episode the excitability of coactivated motoneurons increased. This increase was associated with an increased persistent inward current and was abolished by local blockade of either mGlu1 receptors or CaV1.3 L-type calcium channels near the recording site. We conclude that glutamate released during spinal motor network activity excites motoneurons by parallel activation of ionotropic and mGlu1 receptors. The metabotropic facilitation of L-type calcium channels contributes significantly to this excitation. Our findings establish intrinsic modulation as an active component in the spinal motor network for limb movements.

Animals↗

PubMed2003

5-HT1A receptors increase excitability of spinal motoneurons by inhibiting a TASK-1-like K+ current in the adult turtle.

The modulatory effects of serotonin mediated by 5-HT1A receptors in adult spinal motoneurons were investigated by intracellular recordings in a slice preparation from the turtle. In current-clamp mode, activation of 5-HT1A receptors by 8-OH-DPAT led to depolarization and an increase in input resistance in most motoneurons but caused hyperpolarization and a decrease in input resistance in the remaining smaller fraction of cells. When slices were preincubated in medium containing the 5-HT1A receptor antagonist WAY-100635, 8-OH-DPAT had no effect. In voltage-clamp mode, with 1 mM CsCl in the bathing medium, 8-OH-DPAT consistently inhibited a leak current that was sensitive to extracellular acidification and anandamide, a TASK-1 channel blocker. In medium with a low pH, as in the presence of anandamide, 8-OH-DPAT had no effect. Our results show that activation of 5-HT1A receptors contributes to the excitatory effect of serotonin on spinal motoneurons by inhibition of a TASK-1 potassium channel leading to depolarization and increased input resistance.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2002

An M-like outward current regulates the excitability of spinal motoneurones in the adult turtle.

The excitatory action of muscarine on spinal motoneurones was investigated with intracellular recordings in a slice preparation from adult turtles. In these cells muscarine is known to facilitate a persistent inward current mediated by L-type Ca(2+) channels. When this effect was blocked by nifedipine, muscarine still increased the excitability. In voltage clamp, a slowly activating outward current, generated during depolarizing voltage commands and deactivating as a tail current on return to the holding voltage, was reduced by muscarine. This outward current was activated when the voltage was stepped to potentials positive to -60 mV, was voltage sensitive and had a deactivation time constant of approximately 80 ms. These findings are compatible with an M-current. This possibility was also supported by the finding that the current was reduced by XE-991 - a selective blocker of the KCNQ potassium channels underlying M-currents in other cell types. Our findings suggest that an M-like current, mediated by a KCNQ channel, contributes to the intrinsic response properties of motoneurones in the adult spinal cord by increasing adaptation of repetitive firing and decreasing the slope of the frequency-current relation.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2002

Mechanisms causing plateau potentials in spinal motoneurones.

Plateau potentials are generated by a voltage sensitive persistent inward current. In spinal motoneurones this current is predominantly mediated by influx of Ca2+ through L-type Ca2+ channels of the Ca(v)1.3 subtype. Depolarisation-induced facilitation of L-type Ca2+ channels is thought to be the mechanism for delayed activation (wind-up and warm-up) of the plateau potential and for the hysteresis in firing frequency and I-V relation during triangular depolarisation. L-type Ca2+ channels and plateau potentials in spinal motoneurones are facilitated by activation of metabotropic receptors for glutamate, acetylcholine, noradrenaline and serotonin and down regulated by activation of GABA(B) receptors. The facilitation has been shown to depend on activated calmodulin.

Animals↗

PubMed2002

Spinal plasticity mediated by postsynaptic L-type Ca2+ channels.

In the spinal cord, motoneurons and specific subgroups of interneurons express L-type Ca(2+) channels. As elsewhere, these dihydropyridine-sensitive channels mediate a slowly activating inward current in response to depolarisation and show little or no inactivation. The slow kinetics for activation and deactivation provide voltage-sensitive properties in a time range from hundreds of milliseconds to tens of seconds and lead to plateau potentials, bistability and wind-up in neurons in both sensory and motor networks. This slow dynamics is in part due to facilitation of L-type Ca(2+) channels by depolarisation. The voltage sensitivity of L-type Ca(2+) channels is also regulated by a range of metabotropic transmitter receptors. Up-regulation is mediated by receptors for glutamate, acetylcholine, noradrenaline and serotonin in motoneurons and by receptors for glutamate and substance P in plateau-generating dorsal horn interneurons. In both cell types, L-type Ca(2+) channels are down-regulated by activation of GABA(B) receptors. In this way, metabotropic regulation in cells expressing L-type Ca(2+) channels provides mechanisms for flexible adjustment of excitability and of the contribution of plateau currents to the intrinsic properties. This type of regulation also steers the magnitude and compartmental distribution of Ca(2+) influx during depolarisation, thus providing a signal for local synaptic plasticity.

Animals↗