Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl
Preferences help
enabled [disable] Abstract
Number of results

Results found: 4

Number of results on page
first rewind previous Page / 1 next fast forward last

Search results

help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
EN
The electrophysiological studies indicate that peripheral autonomic and primary sensory neurones display a wide variety of ionic currents. The experiments aimed at biophysical and pharmacological analysis of ionic currents are frequently performed on isolated neurones devoid of axones and dendrites. Consequently the ionic currents recordings are limited to the cell soma. The function of somatic ionic channels is largely unknown. We suggest that the functional meaning of the somatic ionic currents can be facilitated by analysis currents properties in functionally identified neurones. Examples are given of different biophysical and pharmacological currents properties in cardiac, glandular, cutaneous and muscular sympathetic neurones. It is concluded that the resting and reflex activity in different categories of sympathetic neurones may be profoundly affected by the biophysical properties of ionic channels expressed in their soma.
EN
The experiments were performed on 9 cat and 18 rat isolated stellate ganglia. Rats and cats were anesthetized with alpha glucochloralose or urethane, respectively. The ganglia, isolated with their branches, were transferred to a recording chamber and constantly superfused with artificial extracellular fluid bubbled with 95% O2 and 5% CO2. Branches of the ganglion were one by one placed in suction electrodes and stimulated. Antidromic evoked potentials were systematically recorded from numerous points on the ganglion surface. The area under the curve of the negative wave of each recorded potential was considered proportional to the number of neurons located in the vicinity of the recording electrode, projecting to the stimulated nerve. We have found that: (1) cardiac sympathetic neurons are located in the lower, caudal half of the ganglia; (2) vertebral sympathetic neurons occupy the cranial, upper half of the ganglia; (3) neurons with axons in the ansae are positioned near the point of exit of the respective ansa from the ganglion; (4) localization of neurons projecting to the same branches is very similar on both sides right and left; (5) this localization is also similar in rats compared to cats.
EN
Pain is generated by activation of specific dorsal root ganglion (DRG) neurons termed the nociceptive neurons. The nociceptive DRG neurons express 3 categories of ionic channels a. Channels gated by pain stimuli, b. Channels responsible for the transmission of information from sensory receptors to the spinal cord, c. Channels resposible for the release of neurotransmitters in the spinal cord. There is evidency that kinetic properties, molecular structure and functional significance of the ionic channels expressed in nociceptive DRG neurons are different compared to the other types of DRG neurons. The ionic channels are strictly controlled by receptors for neurotransmitters expressed in the plasma membrane of nociceptive DRG neurons.
EN
Our work assesses the effects of ? opioid receptor activation on high-threshold Ca2+/Ba2+ currents in freshly dispersed pyramidal neurons of the medial prefrontal cortex in rats. Application of the specific ? receptor agonist (D-Ala2, N-Me-Phe4, Gly5-ol)-enkephalin (DAMGO) at 1 muM decreased Ca2+ current amplitudes from 0.72 to 0.49 nA. The effect was abolished by naloxone and ?-Conotoxin GVIA. Inhibition was not abolished by strong depolarisation of the cell membrane. In addition, a macroscopic Ba2+ current recorded in cell-attached configuration was inhibited when DAMGO was applied outside the patch pipette. An adenylyl cyclase inhibitor (SQ 22536) and a protein kinase A inhibitor (H-89) decreased Ca2+ current amplitude. Moreover, the inhibitory effect of mu opioid receptors on Ca2+ currents required the activation of protein kinase A. We conclude that activation of mu opioid receptors in medial prefrontal cortex pyramidal neurons inhibits N type Ca2+ channel currents, and that protein kinase A is involved in this transduction pathway.
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.