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M T Duffy

Publications and source records attributed to M T Duffy.

5 recordsLinked to original sources
PubMed1992

Axonal sprouting and frank regeneration in the lizard tail spinal cord: correlation between changes in synaptic circuitry and axonal growth.

In our previous studies, we found that the number of supraspinal neurons projecting to the level of tail spinal cord increases by 74% during tail regeneration and that the number of local spinal neurons with descending projections increases 233%. However, only a small fraction of the supraspinal axons (less than 4%) and half of the local spinal axons actually enter the regenerated spinal cord. We suggested that this may be the result of "synaptic capture" in which regrowing axons make synapses on denervated targets rostral to the transection, aborting further regeneration. To examine this hypothesis, morphometric analysis of electron microscope (EM) photomontages was used to test for changes in synaptic distribution on ventral horn neurons rostral to regenerating tail spinal cord. In addition, 3H-thymidine and retrograde markers were used to determine whether the regenerate axons arose from cut axons, neurogenesis, or sprouting from uninjured neurons. 3H-thymidine injections during regeneration, combined with retrograde HRP pathway tracing, did not reveal the production of new neurons in the tail spinal cord. To test whether cut axons regenerate, fluorescein isothiocyanate conjugated latex beads were applied to the exposed end of the tail spinal cord. After tail regeneration, HRP was applied to the new spinal cord in the regenerated tail. Examination of local spinal neurons (the primary source of axons that enter the regenerated tail spinal cord) revealed that 28% of the neurons contained both labels. This indicated that cut axons successfully regrew into the new tail spinal cord. The regenerated axons that fail to enter the new tail spinal cord can be found in the normal spinal cord immediately rostral to the regenerated tail. To determine whether these axons were making synaptic contacts, lamina IX ventral horn neurons were examined. EM photomontages of the spinal cord rostral to the regenerate tail revealed the following properties: (1) neurons rostral to regenerated tails are larger in area compare to non-regenerates (mean increase = 112%); (2) axosomatic contacts cover a greater percentage of the neuronal soma following regeneration compared to normal (mean increase = 23%); and (3) this increased innervation is the result of an increase in the number of synaptic boutons rather than larger boutons. The number of synaptic contacts in regenerated lizards returned to normal following lumbar transection, indicating that supraspinal and/or long descending propriospinal afferents were the major source of the increased synaptic contacts.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Bulbospinal and intraspinal connections in normal and regenerated salamander spinal cord.

The salamander is the only limbed adult vertebrate which can regenerate portions of cervical, thoracic, or lumbar spinal cord. While the salamander has been a popular model for regeneration of the spinal cord, it is still not known what portions of the nervous system participate in the regeneration process. In the experiments reported here we examine the bulbospinal and intraspinal projections to the lumbar spinal cord in normal and regenerated salamanders (Notophthalmus viridescens). HRP application to the lumbar enlargement of normal salamanders labeled cells in the ventral thalamus, the rostral tegmentum in the proposed homolog of the red nucleus, the reticular neurons of the rhombencephalon, and the midline regions of the rhombencephalon which are possibly equivalent to raphe nuclei of other vertebrates. In the brachial spinal cord HRP-labeled cells were located in dorsal, intermediate, and ventral regions of the spinal gray matter and tended to be located at the periphery of the gray matter. To examine the spinal circuitry of regenerated salamanders, animals received complete spinal transections at the junction of the thoracic and lumbar spinal cord, abolishing all spontaneous coordinated hindlimb and tail movements. Animals exhibited walking and swimming within 60 days at which time a pledget of HRP was inserted into a gap in the spinal cord made by a transection 10.0 mm (six animals) or 5.0 mm (one animal) caudal to the first lesion. On average, the number of HRP labeled brain stem neurons in regenerated animals was 40% of that found in normal animals. The number of labeled cells in the brachial spinal cord was within the range of normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Amputation, Surgical↗
PubMed1989

Reconstruction of the mandibular condyle using ramus osteotomies: a preliminary report.

Reconstruction is required for a number of conditions in which condylar bone is lost resulting in dental and skeletal change. Ramus osteotomies are described as an alternative to the currently used methods. Four cases are described to illustrate the use of this technique. These osteotomies have several advantages over other methods and have the potential for better functional results.

Adult↗
PubMed1988

Simultaneous measurement of luteinizing hormone (LH)-releasing hormone, LH, and follicle-stimulating hormone release in intact and short-term castrate rats.

The temporal relationship between LHRH release and gonadotropin secretion as well as the effects of castration on LHRH release were investigated in conscious, freely moving male rats. LHRH release was measured in hypothalamic/median eminence perfusates, while levels of pituitary gonadotropins (LH, FSH) were determined in sequential blood samples obtained via atrial catheters. Twenty-four to 26 h before experiments, rats underwent sham surgery or castration. LHRH release in push-pull perfusates from both groups was pulsatile, and nearly all identified LH pulses (83.3%) were temporally associated with LHRH pulses. Of the fewer irregular FSH pulses that were observed, only 43.7% were temporally associated with LHRH pulses. Mean LHRH pulse amplitude and mean LHRH levels were not different in intact and castrate animals. The frequency of LHRH pulses was moderately increased in castrate rats (1.30 pulses/h) compared to that in intact animals (0.83 pulses/h), and this acceleration was accompanied by a significant increase in LH pulse frequency, pulse amplitude, and mean level. It was also noted that the number of silent LHRH pulses (those not associated with LH pulses) was dramatically reduced in castrate animals. Characteristics of gonadotropin release (pulse frequency, pulse amplitude, and mean level) were not significantly different in animals undergoing push-pull perfusion/bleeding procedures from those in rats not receiving push-pull cannula implants. We conclude from these studies that 1) LH pulses show a high concordance with LHRH pulses, providing evidence that the LHRH pulse generator operates as the neural determinant of LH pulses in male rats, 2) FSH secretion is not associated with LHRH release in an obvious and consistent manner, suggesting that LHRH/FSH relationships are not easily discerned in these animals or that a FSH-releasing factor distinct from the LHRH decapeptide may regulate FSH secretion, 3) a modest increase in LHRH pulse frequency occurs 24-30 h after castration, and 4) silent LHRH pulses occur with much greater regularity in intact than in castrate rats. The latter two observations suggest that both hypothalamic and intrapituitary sequelae of castration may be critically important in the development of postcastration increases in LH secretion and the negative feedback of gonadal steroids.

Animals↗