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Biomedical subjects

M R Bennett

Publications and source records attributed to M R Bennett.

At least 253 records · Page 14Linked to original sources
PubMed1982

Loss of axons from the optic nerve of the rat during early postnatal development.

The number of axons in the optic nerve of the newborn rat has been compared with the number present in the adult animal. Nerves taken from animals on the day of birth contain 242,000 +/- 29,000 (S.D.) fibres (n = 5). By the sixth postnatal day, the number of axons has fallen to the stable values of adults (99,000 +/- 3700, n = 8). Thus development of the rat's visual system during the first 5 days of life is associated with a loss of 60% of the axons present in the optic nerve at birth. Counts made on the remaining nerve after enucleation of one eye suggest that the presence of retino-retinal axons during the first 5 postnatal days cannot account for all of this reduction.

Age Factors↗
PubMed1982

Variation in the size of synaptic contacts along developing and mature motor terminal branches.

The secretion of a quantum from groups of release sites (me) declines along the length of terminal branches at the amphibian neuromuscular junction. The morphological basis of this decline in me has been studied at neuromuscular junctions in juvenile muscles (fibre length 4 mm) and adult muscles (fibre length 22 mm). Serial sections cut through the length of the junctions have been examined with both light and electron microscopy. Juvenile junctions consist of two short (less than 50 micron) terminal branches; adult junctions often consist of 4 long (100-500 micron) terminal branches. Synaptic contacts are largest near the origins of terminal branches and decline in size towards the end of branches. The number of horseradish peroxidase-labelled synaptic vesicles at release sites, following stimulation in the presence of the enzyme, is largest for sites closest to the origin of the terminal branches. The results suggest that the decline in me along the length of terminal branches is due to decline in the size of release sites.

Animals↗
PubMed1982

The growth of segmental nerves from the spinal cord to the hind limb-bud in the axolotl.

It has been concluded from previous experiments involving the growth of segmental nerves from the amphibian spinal cord to the limb-bud that axons are attracted to the limb-bud region by their target tissue (Hamburger, 1929; Hughes and Tschumi, 1958). In the present study this hypothesis has been tested by obstructing the pathways over which the nerves normally grow. It was found that for those nerves which marginally obstructed far fewer axons were able to reach their target. The spinal ganglia associated with these nerves contained up to 50% fewer cells than the adjacent unobstructed segmental level. These results suggest that nerves are not attracted from the spinal cord by the target tissue, but rather that the pathways provided by the axial segmental nerves are essential if a normal number of axons are to reach their target.

Ambystoma mexicanum↗
PubMed1981

Embryonic chick retinal ganglion cells identified "in vitro". Their survival is dependent on a factor from the optic tectum.

When HRP is injected into the optic tecta of embryonic or newly hatched chicks, the ganglion cells in the contralateral retina can be successfully dissociated into culture and identified at any time by appropriate histochemical staining. Histological examination of whole mounts of retinae both ipsilateral and contralateral to an injection site indicated that no HRP diffused out of an injected tectum, and that the only reaction product that could be visualized was restricted to the ganglion cell layer of the contralateral eye. Because retinal ganglion cells are the only retinal neurons to project to the optic tectum, the intraxonal retrograde transport of HRP to these cells allows their unequivocal identification from amongst the heterogeneous population of retinal neurons present after dispersal into single cells in monolayer culture. The presence of HRP in the cell bodies did not appear to impair their ability to survive, grow or express neurites. Counts of labeled cells from progressively aged birds confirmed that the peak number of generated ganglion cells occurs on embryonic day 10,and that is a 40% decline in the number these neurons over the following 3 days. However, when labelled ganglion cells from 10 day embryos were grown in culture with optic tectum, all the ganglion cells survived over the following 4 days, including those destined to die in vivo. This trophic effect cannot be induced by cerebellum, but is partly induced by media first conditioned over tectal cells. The trophic effect exerted by optic tectum appears therefore to be specific and chemically mediated. We suggest that the death of retinal ganglion cells in vivo may be a consequence of the inability of some cells to establish adequate supplies of a growth factor from the optic tectum.

Animals↗
PubMed1981

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↗
PubMed1980

The growth of segmental nerves from the brachial myotomes into the proximal muscles of the chick forelimb during development.

A study has been made of the growth of segmental nerves 13 to 16 (SN13 to SN16) into the chick limb bud, from the time when they have just reached the ends to the brachial myotomes (stage 21: Hamburger and Hamilton, '51), until they enter the newly formed ventral (stage 24) and dorsal (stage 25) pre-muscle cell masses in the limb bud. At stage 22 axon bundles of SN13 to SN16 have grown off the ends of their respective myotomes, and converge towards the most densely packed mesenchyme in the limb bud at segmental level 15. As a consequence, the first axon bundles of SN14 and SN16 have almost joined those of SN15, whereas the further removed SN13 axon bundles have not yet reached the level of SN15. By stage 23 the first axon bundles from SN14 to SN16 have joined at segmental level 15 to form a nerve which grows toward the ventral pre-muscle cell mass. At stage 24 axon bundles from SN13 have joined those from SN14 to SN16 to form the brachialis longus inferior nerve, which enters the densest region of the ventral pre-muscle. Other axons from SN13 to SN15 grow along the pathways provided by the early arriving axon bundles towards the ventral pre-muscle, but diverge from those at segmental level 14 to grow to the dorsal pre-muscle. By stage 25 axon bundles from SN13 to SN15 have joined to form the brachialis longus superior nerve which enters the densest region of the dorsal pre-muscle. At stage 26 a plexus has formed due to this pattern of growth of the segmental nerves between stages 22 and 25. It is suggested that pre-muscle cells synthesize a nerve growth factor which directs the growth of axons into the limb bud.

Animals↗
PubMed1980

Segmental innervation of rotated and supernumerary axolotl hindlimbs.

The segmental nerve supply to axolotl limbs was misrouted by severing the limbs at the level of the femur, rotating them 180 degrees around their long axis, and then suturing them to the intact proximal stump. Following return of the blood supply to the rotated limb by the cross-anastomosing of blood vessels, a blastema often formed to the side of the rotation site giving rise to a supernumerary limb. The muscles of both rotated and supernumerary limbs were innervated by the segmental nerves. The percentage of cells innervated by segmental nerves 16 and 17 in each muscle was determined with intracellular electrodes at 14 weeks after the operation. Despite histological evidence that nerves had been misrouted in the rotated limb, the percentage innervation of each muscle by nerves 16 and 17 was similar to that in the unoperated contralateral controls. The same results were obtained for the supernumerary limbs. In some muscles a few synaptic sites were found innervated by segmental nerves which did not innervate that muscle in the contralateral controls. These had synaptic potentials with very low quantal contents if immediately adjacent sites were innervated by the segmental nerve, which did innervate that muscle in the contralateral controls. The results suggest that the selective properties of synaptic sites are alone sufficient to determine the entire segmental innervation pattern of the muscles in a limb.

Ambystoma↗
PubMed1980

The radioimmunoassay of buprenorphine.

Antisera to buprenorphine were obtained in rabbits immunised with 3-0-carboxymethylbuprenorphine and N-hemisuccinyl-norbuprenorphine conjugated to bovine serum albumin. Using the latter antiserum and tritium labelled buprenorphine a radioimmunoassay have good accuracy and precision was developed for concentrations as low as 50 picograms in 1 ml of plasma. The N-hemisuccinyl antiserum crossreacted with norbuprenorphine, and the 3-0-glucuronide conjugate with the 3-0-carboxymethyl antiserum. Cross-reactivity of both antisera to other pharmacologically related compounds was negligible. The assay was employed to determine plasma buprenorphine concentration following its parenteral administration to dog and man.

Animals↗
PubMed1980

Buprenorphine kinetics.

Buprenorphine kinetics was determined in surgical patients using radioimmunoassay. Buprenorphine was measured in the plasma of 24 patients who had received 0.3 mg buprenorphine intraoperatively. After 3 hr 10 of these patients then received a further 0.3 mg buprenorphine intravenously for postoperative pain relief, and 11 patients were given 0.3 mg intramuscularly; again, plasma levels were measured for 3 hr. The data fitted closely to a triexponential decay curve. There was a very fast initial phase, with a half-life (t1/2) of 2 min. The terminal t1/2 was slow, approximately 3 hr. Comparison of the kinetics of the same patient, awake and anesthetized, showed that the clearance was significantly lower in the anesthetized state. A notable feature of the drug given intramuscularly is rapid systemic availability, so that peaks are obtained in 2 to 5 min, and in 10 min the resulting levels are the same as for the intravenous and intramuscular routes.

Anesthesia↗
PubMed1980

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↗
PubMed1979

The regression of synapses formed by a foreign nerve in a mature axolotl striated muscle.

A study has been made of the factors which determine that the terminals of a foreign flexor nerve at synaptic sites in a unrodele extensor muscle regress on return of the original extensor nerve. The quantal content (m) of the endplate potential (EPP) at flexor nerve terminal synapses, during innervation of a previously denervated extensor muscle, increased in about 8 weeks to reach the same size as at normal extensor nerve terminals; the same time was taken for m to reach normal size at extensor nerve terminals when these reinnervated their own muscle. At flexor nerve terminals, m decreased eventually to zero if the extensor nerve terminals returned within about 6 weeks of synapse formation by the flexor nerve terminals to the same or an immediately adjacent synaptic site to that occupied by these terminals. During this decrease in m at flexor nerve terminals, stimulation of the flexor nerves in the presence of horseradish peroxidase (HRP) showed HRP-labelled flexor nerve terminals present only in those regions of the extensor muscle in which the electrical signs of flexor nerve terminals were observed, indicating that the decrease in m at regressing flexor terminals was accompanied by their vacating synaptic sites. However, flexor nerve terminals failed to regress from the extensor muscle on return of the original nerve supply if the flexor nerve allowed to form synapses for more than about 10 weeks before the return of the extensor nerve.

Ambystoma↗