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P Cochard

Publications and source records attributed to P Cochard.

35 records · Page 2Linked to original sources
PubMed1987

In vitro studies on the control of nerve fiber growth by the extracellular matrix of the nervous system.

1. Cultured neurons from embryonic chick sympathetic ganglia or dorsal root ganglia grow nerve fibers extensively on simple substrata containing fibronectin, collagens (types I, III, IV), and especially laminin. 2. The same neurons cultured on substrata containing glycosaminoglycans grow poorly. Glycosaminoglycans (heparin) inhibit nerve fiber growth on fibronectin substrata. 3. Proteolytic fragments of fibronectin support nerve fiber growth only when the cell attachment region is intact. For example, a 105 kD fragment, encompassing the cell attachment region, supports growth when immobilized in a substratum, but a 93 kD subfragment, lacking the cell attachment region, is unable to support fiber growth. When it is added to the culture medium, the 105 kD fragment inhibits fiber growth on substrata containing native fibronectin. 4. In culture medium lacking NGF, DRG neurons extend nerve fibers only on laminin and not on fibronectin, collagen or polylysine. Studies with radioiodinated laminin indicate that laminin binds with a relatively high affinity (kd approximately equal to 10(-9) M) to DRG neurons, and to a variety of other neural cells (NG108 cells, PC12 cells, rat astrocytes, chick optic lobe cells). We have isolated a membrane protein (67 kD) by affinity chromatography on laminin columns and are characterizing this putative laminin receptor. 5. Dissociated DRG neurons or ganglionic explants cultured on complex substrata consisting of tissue sections of CNS or PNS tissues extend nerve fibers onto the PNS (adult rat sciatic nerve) but not CNS (adult rat optic nerve) substrata. Other tissue substrata which support fiber growth in vivo (embryonic rat spinal cord, goldfish optic nerve) support growth in culture. While substrata from adult CNS, which support meager regeneration in vivo (adult rat spinal cord) support little fiber growth in culture. 6. Ganglionic explants cultured in a narrow space between a section of rat sciatic nerve and optic nerve grow preferentially onto the sciatic nerve suggesting that diffusible growth factors are not responsible for the differential growth on the two types of tissues. 7. Dissociated neurons adhere better to sections of sciatic nerve than optic nerve. Laminin, rather than fibronectin or heparan sulfate proteoglycan, is most consistently identifiable by immunocytochemistry in tissues (sciatic nerve, embryonic spinal cord, goldfish optic nerve) which support nerve fiber growth. Taken together, these data suggest that ECM adhesive proteins are important determinants of nerve regeneration.

Animals↗
PubMed1987

Nerve fiber growth in culture on tissue substrata from central and peripheral nervous systems.

In adult mammals, injured neurons regenerate extensively within the PNS but poorly, if at all, within the CNS. We have studied the effect of substrata consisting of tissue sections from various nervous systems on nerve fiber growth in culture and correlated our results with the growth potential of these tissues in vivo. Ganglionic explants from embryonic chicks (9-12 d) fail to extend nerve fibers onto sections of adult rat optic nerve or spinal cord (CNS) but do so on sciatic nerve (PNS). Dissociated DRG neurons behave similarly whether in serum-containing or defined medium. Tissue substrata from nervous systems that support regeneration in vivo--i.e., goldfish optic nerve, embryonic rat spinal cord, degenerating sciatic nerve--also support fiber growth in culture. Within the same culture, neurons will grow onto sciatic nerve rather than neighboring optic nerve sections, suggesting that the responsible agent(s) is not soluble. In addition, neurons adhere more extensively to sciatic nerve substrata than to optic nerve. The occurrence of 3 molecules known to be involved in neuron-substratum adhesion and nerve fiber growth in vitro has been documented immunocytochemically in the tissue sections. One of these, laminin, is demonstrable in all tissues tested that supported nerve fiber growth. Immunoreactivities for fibronectin and heparan sulfate proteoglycan are found in only some of these tissues. None of these 3 molecules can be demonstrated in neural cells of normal adult rat CNS tissue. Our data suggest that these molecules may be important effectors of nerve regeneration in neural tissues.

Animals↗
PubMed1986

Development of the monoaminergic innervation of the avian gut: transient and permanent expression of phenotypic markers.

Specific cellular accumulation of [3H]5-hydroxytryptamine ([3H]5-HT) occurs during development of the avian gut. This accumulation is transient in extraganglionic mesenchymal cells (TES cells) but is a permanent characteristic of enteric serotonergic neurons (ESN). Species-specific differences were found in the location of TES cells and ESN. In chicks TES cells surrounded myenteric ganglia and ESN were restricted to the myenteric plexus. In quails TES cells surrounded submucosal ganglia and [3H]5-HT-labeled submucosal as well as myenteric neurons. [3H]Norepinephrine accumulated only in noradrenergic terminals and not in TES cells or ESN. The origins of TES cells and ESN were studied in chimeras, in which neuraxis from appropriate or inappropriate axial levels was grafted from quail to chick. Both types of chimeric bowel contained TES cells and ESN. Most TES cells in chimeras were chick in origin and distributed as in chicks (around myenteric ganglia); however, some TES cells and all ESN were quail cells. To test whether crest cells are required for development of TES cells and ESN, aneuronal chick hindgut was explanted and grown alone, or with quail neuraxis, as chorioallantoic membrane (CAM) grafts. TES cells appeared in CAM grafts whether or not crest cells were present; however ESN only appeared in explants when quail neuraxis was included. In addition, an ectopic [3H]5-HT-labeled chromaffin-like cell, also of quail origin, was found in enteric plexuses in these combined explants of crest and gut. Most TES cells, therefore, are neither derived from nor dependent on the presence of crest cells in the gut wall. Since even an inappropriate axial level of crest was found to produce ESN when it was experimentally induced to colonize the bowel the enteric microenvironment probably plays a critical role in serotonergic neural development. The species-specific location of TES cells and ESN is consistent with the hypothesis that TES cells constitute an important component of this microenvironment.

Animals↗
PubMed1984

Reserpine induction of tyrosine hydroxylase in paraplegia.

Reserpine induction of tyrosine hydroxylase (TH) activity reflects the biochemical adaptability of sympathetic neurons. Midthoracic spinal cord transection in adult animals precludes TH induction in the sixth lumbar (L6) ganglion, a ganglion innervated by spinal segments caudal to the lesion. However, in animals receiving lesions as neonates, an elevation in L6 ganglion TH activity occurred after reserpine. This retained biochemical adaptability indicates an increased recuperative capacity of developing neurons.

Animals↗
PubMed1984

[The cells with a transient adrenergic phenotype in the embryonic intestines of rodents are neuronal in nature].

In the gut of Rat and Mouse embryos, a cell population transiently expresses tyrosine hydroxylase (TOH), as well as other adrenergic phenotypic characters, during the initial stages of the formation of the intrinsic innervation. The nature of these cells has been determined by immunohistochemical methods, using anti-neurofilament (NF) protein antibodies. NF first appear at 10.5 days of gestation and are detectable in most TOH-containing cells between 10.5 and 12.5 days of gestation. Consequently, the transient adrenergic gut cells are neurons. In turn, this indicates their neural crest origin. They form a large proportion of the initial cell population of enteric neurons.

Animals↗
PubMed1984

Initial expression of neurofilaments and vimentin in the central and peripheral nervous system of the mouse embryo in vivo.

The appearance of neurofilaments (NFs) and vimentin (Vim) in the nervous system of the mouse embryo was documented using immunohistochemical techniques. The three NF protein subunits appear early and simultaneously in central and peripheral neurons at 9 to 10 days of gestation. The onset of NF expression is concomitant with axon elongation and correlates extremely well with neurofibrillar differentiation and, in the case of autonomic ganglia, with the expression of adrenergic neurotransmitter properties. In the central and peripheral nervous system, NF expression is preceded by that of Vim, and both types of intermediate filaments coexist within the same cell for a short period of time.

Animals↗
PubMed1983

Long-term effects of spinal transection on the development and function of sympathetic ganglia.

The long-term effect of interruption of descending central pathways on the biochemical development and function of sympathetic neurons was examined in the sixth lumbar (L6) sympathetic ganglia of the rat. Previous investigations had defined the normal maturation of presynaptic choline acetyltransferase (CAT) activity, postsynaptic tyrosine hydroxylase (T-OH) activity and total protein in L6 ganglia. Neonatal spinal cord transection prevented the normal ontogeny of CAT activity: enzyme activity was 40% of control one week and one year after surgery. Similarly, T-OH activity failed to develop normally after transection and was 22% of control one year postoperatively. Spinal transection at 30 days of age did not alter baseline CAT or T-OH activities in L6 ganglia when examined up to 6 months after surgery. Apparently during the first month of life descending central pathways exert critical facilitatory influences on sympathetic ganglia maturation; interruption of these influences results in long-lasting biochemical deficits. We also examined the role of central mechanisms in adult sympathetic function. Stressful stimuli, including reserpine treatment, normally induce adult T-OH through reflex sympathetic activation. This biochemical adaptability was studied by treating rats with reserpine after spinal transection. After motor and autonomic spinal reflexes returned in paraplegic animals, reserpine treatment was initiated. Spinal animals did not exhibit T-OH induction. These observations indicate that central rather than spinal mechanisms govern this biochemical adaptability of mature sympathetic neurons.

Aging↗
PubMed1983

Cholinergic traits in the neural crest: acetylcholinesterase in crest cells of the chick embryo.

Previous work by our group has demonstrated that mesencephalic neural crest cells at an early stage of migration are able to synthesize acetylcholine (ACh). Acetylcholinesterase (AChE), the enzyme responsible for ACh degradation, was examined in neural crest cells of the chick embryo, using cytochemical and biochemical methods. Observations at the light microscope level showed that cholinesterase activity, identified as true AChE, was present at all axial levels in presumptive crest cells of the neural folds, soon after closure of the neural tube. Subsequently, AChE activity was found in cells of the individualized neural crest and in crest cells migrating at cephalic and trunk levels. Cell counts revealed that 88-94% of the total crest population was AChE-positive. Electron microscope observations indicated that the enzyme was confined to perinuclear and endoplasmic reticulum cisternae. The AChE of migrating mesencephalic neural crest cells was identified as the dimeric form (sedimentation coefficient 6.9 S) of the catalytic subunit. These results indicate that the specific AChE is present in the majority of neural crest cells all along the neural axis. Thus the ability to synthesize and degrade ACh is expressed at least in some neural crest cells at an early stage of development.

Acetylcholinesterase↗
PubMed1981

Effects of spinal cord transection on synapse numbers and biochemical maturation in rat lumbar sympathetic ganglia.

The effects of interruption of descending central pathways on the morphological and biochemical ontogeny of peripheral sympathetic ganglia were examined in the sixth lumbar (L6) sympathetic rat ganglia. Previous studies defined the normal maturation of presynaptic choline acetyltransferase (CAT) activity, postsynaptic tyrosine hydroxylase (T-OH) activity, and total protein in the L6 ganglion. In the present investigations ganglion synapse numbers and adrenergic neuron numbers were examined in transected and sham-operated littermate controls 6 weeks after surgery at 10 days of age and correlative biochemical studies were performed. Spinal transection resulted in a reduction in synapse number on ganglion cell bodies (53.5% reduction) and neuronal processes (55.8% reduction). This abnormality in synapse number was associated with a reduction of CAT activity to 56% of control. Although T-OH activity also failed to develop normally and was 25% of control, there was no associated alteration in adrenergic neuron number. These studies suggest that descending central pathways regulate the maturation of presynaptic cholinergic terminals (and hence synapse number) in sympathetic ganglion and that CAT activity serves as an accurate marker for these terminals. Additionally, the ontogeny of ganglion T-OH activity is altered by central lesions and this effect is not secondary to a decrease in adrenergic neuron number.

Animals↗
PubMed1979

Selective loss of noradrenergic phenotypic characters in neuroblasts of the rat embryo.

To define the fate of embryonic neuroblasts in rat gut, which transiently express several noradrenergic traits, we investigated the high-affinity uptake of norepinephrine. At 12.5 days of gestation, these cells exhibited immunoreactivity to tyrosine hydroxylase [tyrosine 3-monoxygenase; L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] and endogenous catecholamine fluorescence. However, by 13.5 days these noradrenergic neurotransmitter phenotypic characters essentially disappeared. In contrast, norepinephrine uptake, which was also apparent at 12.5 days, persisted at least through 17.5 days. These observations indicate that norepinephrine uptake develops as an additional noradrenergic characteristic in these cells and persists after the disappearance of other noradrenergic traits. Consequently, neurotransmitter phenotypic characters may be transiently displayed during normal development in vivo.

Adrenergic Fibers↗
PubMed1978

Ontogenetic appearance and disappearance of tyrosine hydroxylase and catecholamines in the rat embryo.

The ontogenetic pattern of noradrenergic differentiation in rat embryonic autonomic neuroblasts was defined in vivo. Noradrenergic specialization was examined by documenting the immunohistochemical appearance of tyrosine hydroxylase [Tyr-OH; tyrosine 3-monooxygenase; L-tyrosine,-tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] and the development of histofluorescence due to catecholamine (CA). Tyr-OH and CA were undetectable in the dorsal neural crest or the ventrally migrating crest cells and first appeared at 12.5 days of gestation (36--37 somite stage) in sympathoblasts that had formed sympathetic ganglion primordia. Fluorescence intensity and the number of fluorescent cells increased progressively thereafter. In addition, Tyr-OH and CA transiently appeared in scattered presumptive neuroblasts in the gut. The enzyme and transmitter were first detectable at 11.5 days of gestation and thereafter decreased progressively so that, by 14.5 days, only rare cells were encountered. There was remarkable synchrony in the appearance and disappearance of Tyr-OH and CA. These observations suggest that a number of noradrenergic transmitter mechanisms develop simultaneously in the differentiating neuroblast. The relevance of these results to the elucidation of developmental regulatory mechanisms is discussed.

Animals↗
PubMed1977

Development of choline acetyltransferase and cholinesterase activities in enteric ganglia derives from presumptive adrenergic and cholinergic levels of the neural crest.

The cholinergic differentiation of enteric ganglia in embryos of chick and quail was studied with particular reference to cholinesterase and choline acetyltransferase activities. Differentiation during normal development was compared with that obtained after culture of the neural primordium or neural crest in direct association with aneural hindgut. Biochemically differentiated cholinergic ganglia developed in explants containing cells from either the 'vagal' (presumptive cholinergic) or 'truncal' (presumptive adrenergic) levels of the neural crest. Neither extra-intestinal migration of neural crest cell nor the presence of central preganglionic fibres is a prerequisite for enteric ganglion differentiation.

Animals↗
PubMedDate not supplied

Critical analysis of the supraspinatus outlet view: rationale for a standard scapular Y-view.

The supraspinatus outlet view has been standardized under fluoroscopic control to become reproducible and comparable; it is the normalized scapular Y-view. Four hundred four healthy shoulders from patients 20 to 80 years old and 63 shoulders with rotator cuff tears underwent x-ray evaluation and were compared. A qualitative study was carried out on the shape of the acromion in relation to Bigliani's types (I, II, III and on the presence or absence of a bony spur on the anterior part of the acromion. Quantitative measurements were determined; the subacromial peak and the spinoacromial angle were assessed for a statistical comparison among the various populations. The acromions of healthy shoulders varied with age (8% type III in patients younger than 60 years, 27% in those older than 60 years), although not significantly. The dominant side and sex of the subjects had no effect. With 29% type III acromions the shoulders with cuff tears differed from those of the healthy shoulders (14% type III). No close correlation was seen between type III acromions and cuff ruptures. The quantitative values of the acromions had no predictive value for cuff rupture. Acromion typology failed to confirm that a type III acromion was responsible for rotator cuff rupture. Spurs are found in increasing incidence with age and in the presence of cuff rupture; whether they are caused by subacromial impingement or by natural aging of the acromion is uncertain.

Acromion↗