PubMed Health⌕ Search

Biomedical subjects

N A Lavidis

Publications and source records attributed to N A Lavidis.

43 records · Page 3Linked to original sources

The dependence of excitatory junction potential amplitude on the external calcium concentration in narcotic tolerant mouse vas deferens.

The dependence of neurotransmitter secretion on external calcium ions during development of opiate tolerance in the mouse vas deferens was studied. The writhing response of mice to an i.p. injection of acetylcholine was inhibited by morphine. Reversal of this antinociceptive effect of morphine during chronic treatment signalled the development of tolerance. Tolerance to morphine at the neuromuscular junction was shown as a reversal of the initial shift of the size of the excitatory junction potential (e.j.p.) vs extracellular calcium concentration relationship back towards the control without any change in the power of 2.4. Facilitation in the amplitude of the e.j.p. occurs with low frequency (2 Hz) stimulation. The initial increase in facilitation induced by morphine was reversed by chronic morphine treatment without any change in the plateau e.j.p. amplitude achieved after a long low frequency train of impulses. At high frequencies (10 Hz) the initial increase in e.j.p. amplitude was followed by a depression. Acute morphine administration decreased the size of the e.j.p., this was followed by an increase in facilitation and a decrease in depression. These effects were reversed after chronic morphine treatment. Tolerance to morphine involves a counteradaptive process which restores the normal entry of calcium ions or its actions within the release sites in promoting transmitter release.

Acetylcholine↗

The dependence of excitatory junction potential amplitude on the external calcium concentration in mouse vas deferens during narcotic withdrawal.

The dependence of neurotransmitter release on calcium was evaluated in adrenergic terminals from mice that were acutely withdrawn from chronic morphine treatment (CMT). A two fold increase in the number of writhes in response to an i.p. injection of acetylcholine was induced in mice by CMT and subsequent withdrawal. A shift to the left in the relationship between the excitatory junction potential (e.j.p.) amplitude and extracellular calcium concentration ([Ca]o) was induced in vasa deferentia from CMT-withdrawn mice. A reduction in the degree of facilitation of transmitter release during a short low-frequency train of impulses and an increase in the amount of transmitter release during a high-frequency train of impulses was induced in vasa deferentia from CMT-withdrawn mice. The adaptive mechanism of the terminals to the sustained presence of morphine may involve an increase in the probability that the release sites will release transmitter either via increase in calcium influx or an increase in the affinity of calcium to the hypothetical X-receptor.

Acetylcholine↗

Development of the topographical projection of motor neurons to a rat muscle accompanies loss of polyneuronal innervation.

The rat lateral gastrocnemius muscle receives a topographical projection from lumbar segmental nerves L4 and L5. A study has been made of the development of this projection during the period when polyneuronal innervation is eliminated. The tetanic contraction due to stimulation of each nerve was compared with that due to stimulation of both nerves simultaneously. This percentage of contraction declined from about 90% to 70% for L4 from birth to 2 postnatal weeks; it declined from about 90% to 30% for L5 over the same period. The innervation of about 60% of the cells by both L4 and L5 is therefore eliminated during 2 postnatal weeks. Tetanic and twitch contraction due to stimulation of ventral rootlets of segmental level L4 and L5 was compared to stimulation of the whole muscle directly. There was a general reduction in the size of the motor units from both L4 and L5. A selective reduction in the number of L5 motor units was observed during the first 5 postnatal days. The distribution of L4 and L5 terminals on the dorsal surface of the muscle was determined by intracellular impalement of muscle cells and was determined by recording endplate potentials (EPPs) due to stimulation of L4 and L5. Polyneuronal innervation of the lateral gastrocnemius is eliminated by about 2 postnatal weeks. The percentage of muscle cells innervated by L4 or L5 in each of six equal-size muscle sectors was ascertained during this period. This percentage of innervation of muscle cells by L5 declined in all sectors between 3 days and 2 weeks postnatal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Variation in quantal secretion at different release sites along developing and mature motor terminal branches.

The secretion of a quantum by groups of release sites (me) along the length of nerve terminal branches has been studied with extracellular electrodes at mature and juvenile toad neuromuscular junctions. The position of the recording sites with respect to the terminal branches was determined following zinc-iodide staining of terminals. me declined with distance from the last myelin segment along individual terminal branches: in a [Ca]o of 0.35 mM, me declined by 80% over a distance of 60 micron along mature terminal branches. Simultaneous recording of secretion from adjacent groups of release sites with two extracellular electrodes confirmed that secretion of a quantum at release sites declines with the distance of the sites from the last myelin segment. The secretion of a quantum by groups of release sites along juvenile terminal branches also declines with distance from the last myelin segment: me is always largest for the first release sites to be laid down. The facilitated secretion of quanta at sites with low me is larger than those with high me; as a consequence, all sites secrete similar numbers of quanta at the end of a short high-frequency train.

Animals↗

Development of the topographical projection of motor neurons to amphibian muscle accompanies motor neuron death.

The topographical projection of segmental nerves 8 and 9 to the glutaeus muscle of developing frogs was determined during the motor neuron death period (stages 54 to 59). Electrophysiological techniques showed that at stage 54 the entire glutaeus muscle received an innervation from both nerves 8 and 9. By stage 59 the muscle received an innervation from nerve 8 only on one side and by nerve 9 only on the opposite side. The emergence of this mature innervation pattern is accompanied by motor neuron death, with which it may be causally related.

Amphibians↗

An electrophysiological analysis of the effects of morphine on the calcium dependence of neuromuscular transmission in the mouse vas deferens.

1 The effects of morphine on the Ca-dependence of the synaptic potential amplitude in the mouse vas deferens have been determined. 2 The synaptic potential increased with a power factor of 2.4 for [Ca]o between 0.7 mM and 1.8 mM. Morphine (40 nM) decreased the synaptic potential, without altering the second power relationship between the synaptic potential and [Ca]o. 3 Morphine reversed the depression in the synaptic potential which develops during a short high-frequency (10 Hz) train of impulses to facilitation. Consequently the synaptic potential beyond the tenth impulse was unaffected by morphine. 4 Morphine did not alter the facilitation of the synaptic potential which develops during a short low-frequency (less than or equal to 2 Hz) train of impulses in normal [Ca]o. Consequently morphine decreased the synaptic potential for each impulse by about the same percentage amount. 5 Morphine increased the small facilitation in the synaptic potential which occurs during a short low-frequency (less than or equal to 2 Hz) train of impulses in high [Ca]o. This facilitation approximated the predictions based on the assumption that each impulse leaves residual Ca ions bound to receptors involved in transmitter release from the nerve terminal.

Action Potentials↗

The effect of calcium ions on the secretion of quanta evoked by an impulse at nerve terminal release sites.

A study has been made of the effects of calcium ions on the number of quanta secreted from all the release sites at an amphibian motor nerve terminal recorded with an intracellular microelectrode (m) compared with the number secreted simultaneously from a small number of release sites recorded with an extracellular microelectrode (me). If the endplate potential was made subthreshold by lowering the external calcium concentration ([Ca]o less than or equal to 0.4 mM), it was possible to find small groups of release sites for which me was comparable to m, indicating considerable nonuniformity in the probability of release of a quantum at different groups of release sites (Pe) in a given [Ca]o. Increasing [Ca]o in the range from 0.25 to 0.4 mM increased the probability of release of a quantum at groups of release sites (Pe), independent of the initial value of Pe, and the dependence of Pe on [Ca]o followed a fourth power relationship. A conditioning impulse enhanced the probability of release of a quantum by a subsequent test impulse at release sites, if Pe was less than 1.0 during the conditioning impulse. It is shown that the present observations regarding the dependence of Pe on [Ca]o and on conditioning impulses can be quantitatively predicted from previous observations regarding the dependence of the binomial parameters m, p, and n on [Ca]o and on conditioning impulses determined with intracellular electrodes, if the probability of secretion of a quantum at a release site (Pj) is different for different release sites and Pj is distributed as a beta random variable.

Action Potentials↗