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The connections of the middle temporal visual area (MT) and their relationship to a cortical hierarchy in the macaque monkey.

The cortical and subcortical connections of the middle temporal visual area (MT) of the macaque monkey were investigated using combined injections of [3H]proline and horseradish peroxidase within MT. Cortical connections were assigned to specific visual areas on the basis of their relationship to the pattern of interhemispheric connections, revealed by staining for degeneration following callosal transection. MT was shown to be reciprocally connected with many topographically organized cortical visual areas, including V1, V2, V3, and V4. These pathways link regions representing corresponding portions of the visual field in the different areas. In addition, MT has reciprocal connections with two previously unidentified cortical areas, which we have designated the medial superior temporal area (MST) and the ventral intraparietal area (VIP). The laminar distribution of terminals and cell bodies in cortical areas connected with MT follows a consistent pattern. In areas V1, V2, and V3, the projections to MT arise largely or exclusively from cells in supragranular layers, and the reciprocal connections from MT terminate mainly in supragranular and infragranular layers. In contrast, the projections to MST and VIP terminate mainly in layer IV, and the reciprocal pathways originate from cells in both superficial and deep layers. On the basis of this pattern, each connection can be designated as forward or feedback in nature, and a hierarchical arrangement of visual areas can be determined. In this hierarchy, MT is at a higher level than V1, V2, and V3, and at a lower level than MST and VIP. Subcortical projections were seen from MT to the claustrum, the putamen, the caudate nucleus, the inferior and lateral subdivisions of the pulvinar complex, the ventral lateral geniculate nucleus, the reticular nucleus of the thalamus, the superior colliculus, and the pontine nuclei.

Animals↗

[Conditioned reflex changes in the functional connections between adjacent and remote cortical neurons].

A motor conditioned reflex to sound was elaborated in cats with electrodes (nichrome wire dia 50 mcm) chronically implanted in the auditory cortex. Multineuronal activity preceding by 30 s the conditioned signal was analysed. Impulse activity of two to three neurones was isolated from every record by means of an amplitude discriminator. Dependence between impulse series isolated either from one record or from records obtained with two electrodes placed at a distance of up to 200 mcm from one another, was estimated by crossover interval histograms. Consequently functional connections between neurones were defined by the dependence of impulse series. In the process of conditioning dynamic reorganization of interneuronal connections was revealed. With a stable reflex, the number of connections both between neurons in the microregion and between neurones of neighbouring microregions considerably increased due to an increased number of excitatory connections. After extinction of the reflex, the number of connections between adjacent neurons increased still more, though due to enhancement of the inhibitory type connections. Nonetheless, excitatory connections kept dominating. At the same time, the number of connections between neurons of the neighbouring microsystems sharply decreased.

Animals↗

Corticothalamic connections of extrastriate visual areas in rhesus monkeys.

Corticothalamic connections of extrastriate visual areas were studied by using the autoradiographic anterograde tracing technique. The results show that the medial extrastriate region above the calcarine sulcus projects mainly to the lateral pulvinar (PL), medial pulvinar (PM), and lateral posterior (LP) nuclei. In addition, the dorsal portion of the medial region has connections to the lateral dorsal (LD) as well as to intralaminar nuclei. The dorsolateral extrastriate region projects strongly to the PL and LP nuclei, to the PM and inferior pulvinar (PI) nuclei, and to the LD and intralaminar nuclei. The lateral extrastriate region above the inferior occipital sulcus (IOS) has strong connections to both the PL and PI nuclei and has minor projections to the PM and oral pulvinar nuclei. The ventrolateral extrastriate region below the IOS projects mainly to the PI nucleus and to the caudal portion of the PL nucleus and has some projections to the PM nucleus. The ventromedial extrastriate region medial to the occipitotemporal sulcus has strong connections with the ventral and medial sectors of the PI nucleus. This region also projects to the caudal portion of the PL nucleus and has minor connections to the LP nucleus. Finally, the annectant gyrus projects to the PL nucleus and to the rostral portion of the PI nucleus and has minor connections to the PM nucleus. Thus, the medial and dorsolateral extrastriate regions are related mainly to the PL and LP nuclei as well as to intralaminar nuclei. In contrast, the ventrolateral and ventromedial regions are connected strongly with the PI nucleus. This connectional organization appears to reflect functional differentiation at the cortical level.

Animals↗

Inductive action of epithelium on differentiation of intestinal connective tissue of Xenopus laevis tadpoles during metamorphosis in vitro.

The action of the epithelium on differentiation of connective tissue cells of Xenopus small intestine during metamorphosis was investigated by using culture and morphological techniques. Connective tissue fragments isolated from the small intestine at stage 57 were cultivated in the presence or absence of homologous epithelium. In the presence of the epithelium, metamorphic changes in the connective tissue were fully induced by hormones including thyroid hormone (T3), as during spontaneous metamorphosis, whereas they were partially induced in the absence of the epithelium. Macrophage-like cells showing non-specific esterase activity in the connective tissue were much fewer in the absence of the epithelium than in the presence of it, and aggregates of fibroblasts possessing well-developed rough endoplasmic reticulum developed only in the presence of the epithelium. Just before the aggregation of the fibroblasts, the connective tissue close to the epithelium became intensely stained with concanavalin A (ConA) and wheat germ agglutinin (WGA). The present results indicate that the epithelium plays important roles in the differentiation of intestinal connective tissue cells, which in turn affect the epithelial transformation from larval to adult form during anuran metamorphosis. Thus, the tissue interaction between the epithelium and the connective tissue in the anuran small intestine is truly bidirectional.

Animals↗

Genetic analysis of familial connective tissue alterations associated with cervical artery dissections suggests locus heterogeneity.

BACKGROUND AND PURPOSE: Cervical artery dissections (CAD) can be associated with connective tissue aberrations in skin biopsies. The analysis of healthy relatives of patients suggested that the connective tissue phenotype is familial with an autosomal dominant inheritance. METHODS: We performed genetic linkage studies in 3 families of patients with CAD. Connective tissue phenotypes for the patients and all family members were assessed by electron microscopic study of skin biopsies. A genome-wide linkage analysis of 1 family (1 patient with 8 healthy relatives) indicated 2 candidate loci. Three genes were subsequently studied by sequence analysis. Part of the genome was also studied by linkage analysis in 2 further families. RESULTS: The genome-wide scan in a single family suggested linkage between the hypothetical mutation causing the connective tissue phenotype and informative genetic markers on chromosome 15q24 (logarithm of the odds score: Z= +2.1). A second possible candidate locus (Z=+1.9) was found on chromosome 10q26. Sequence analysis of 3 candidate genes in the suggestive locus (chondroitin sulfate proteoglycan4 [CSPG4], lysyl oxidase-like1 [LOXL1] and fibroblast growth factor receptor2 [FGFR2]) did not lead to the identification of a mutation responsible for connective tissue alterations. In 2 additional smaller families the loci on chromosome 15q24 and 10q26 were excluded by linkage analysis. CONCLUSIONS: Linkage analysis of a large family with CAD-associated connective tissue alterations suggested the presence of a candidate locus on chromosome 15q2 or on chromosome 10q26. Sequence analysis did not lead to the identification of a mutated candidate gene in 1 of these loci. The study of 2 additional pedigrees indicated locus heterogeneity for the connective tissue phenotype of CAD patients.

Adult↗

Immune response to connective tissue components of the basement membrane.

The immune response to connective tissue components of basement membrane (type IV collagen and laminin) and to interstitial collagen (type I) has been examined in human and murine systems. We also examined the role that immunologic sensitization to autologous connective tissue components might play in inducing an inflammatory response resulting in pathologic sequelae. Mice receiving a single subcutaneous injection of 5 micrograms type IV or type I murine collagens, or murine laminin in complete Freund's adjuvant mount a delayed-type hypersensitivity response characterized by a mononuclear cell infiltrate when challenged in the footpad with the sensitizing antigen. Cell-mediated immunity to these connective tissue antigens can be transferred to normal syngeneic mice with sensitized T-lymphocytes. In addition, repeated immunizations with these homologous connective tissue components elicit antibody responses in mice. Our data demonstrate the immunogenic nature of types IV and I collagen, and of laminin in a syngeneic murine model. We have demonstrated autoantibodies to the basement membrane and interstitial collagens in the sera of patients with scleroderma (systemic sclerosis); ELISA ratios correlate directly with the extent of pulmonary fibrosis in these patients. Anti-type IV collagen autoantibodies were found to be primarily IgM and anti-type I collagen antibodies, primarily IgG. An antibody response to autologous connective tissue antigens could lead to complement activation, immune complex formation, and deposition of the complexes along vascular endothelium with recruitment of blood monocytes in situ, mirroring the early scleroderma lesion (perivascular mononuclear cell filtrates). In vitro we examined the role of human peripheral blood mononuclear cells in the activation of fibroblasts. Adherent human blood monocytes release mediators which stimulate fibroblast proliferation and collagen deposition. A model is presented for the induction of immunity to autologous connective tissue components, leading to mononuclear cell inflammation, fibroblast activation and fibrosis. Selective immunity to basement membrane collagens may influence the clinical expression of diffuse connective tissue syndromes such as scleroderma (systemic sclerosis).

Animals↗

Discovery of a connective tissue dysplasia in the Martin-Bell syndrome.

The fact that a connective tissue dysplasia is a component of the Martin-Bell syndrome was a fortuitous discovery. A 26-month-old developmentally delayed boy had many signs of a connective tissue dysplasia for which he was referred to a University center where he was found to be fragile (X)-positive without confirmation of a connective tissue problem. Sensitized by these events and observations, we were able to predict at a glance in an unrelated family the fragile (X)-positive status of 2 subsequently referred brothers with mental retardation and prominent manifestations of connective tissue dysplasia. Thus, the Martin-Bell syndrome is an incompletely recessive, pleiotropic trait involving CNS, testes and connective tissues. The characteristic facial appearance of affected males largely represents interaction of mental retardation, congenital CNS based muscle hypotonia and connective tissue dysplasia. At the 1983 NIH workshop on XLMR there was a general consensus that a connective tissue dysplasia is a component of the Martin-Bell syndrome, a fact since confirmed by others on the basis of objective measurements of finger joint hypermobility and frequent presence of mitral valve prolapse.

Abnormalities, Multiple↗

Longitudinal functional network connectivity changes across the clinical stages of C9orf72 hexanucleotide repeat expansion carriers.

INTRODUCTION: Intrinsic functional connectivity network abnormalities in C9orf72 hexanucleotide repeat expansion carriers emerge during the asymptomatic phase, yet longitudinal studies remain limited. We examined cross-sectional abnormalities and longitudinal connectivity changes across clinical stages. METHODS: We analyzed task-free functional magnetic resonance imaging (fMRI) and structural MRI data in 36 asymptomatic (aSxC9), 17 prodromal (proC9), and 29 symptomatic (SxC9) carriers, and 107 healthy controls (HCs). Functional networks previously found altered in C9orf72, including salience, sensorimotor, default mode, and medial pulvinar thalamic networks, were examined. Associations between longitudinal connectivity and gray matter decline with baseline neurofilament light chain (NfL) concentrations and symptom severity were assessed. RESULTS: aSxC9 and SxC9 showed longitudinal connectivity changes within specific networks. In aSxC9, connectivity changes correlated with baseline NfL. In proC9 and SxC9, changes in connectivity and gray matter were associated with baseline NfL and symptom severity. DISCUSSION: C9orf72 expansion carriers demonstrate stage-specific network connectivity changes.

Humans↗

Proliferative responses of endothelial cell populations to experimentally induced inflammatory lesions of gingival connective tissues in the cynomolgus monkey (Macaca fascicularis).

BACKGROUND: Endothelial cells exhibit heterogeneous and tissue-selective responses to injury and inflammation. The regulation of the size of endothelial populations in specific tissue sites is poorly characterized, particularly in soft connective tissues adjacent to bone. To investigate the effect of a primarily lymphocytic infiltrate on endothelial cell proliferation and growth of blood vessels, a primate model was used that reliably exhibits localized, distinct inflammatory, and destructive lesions in isolated sites of mucosal connective tissues adjacent to bone and epithelium around teeth. METHODS: Three Cynomolgus monkeys with healthy periodontium and two with spontaneously occurring inflammation or induced connective tissue destruction were pulse labeled with 3H-thymidine. Morphometric analyses of radioautographs from mid-sagittal supra-alveolar gingival connective tissues of incisor teeth were performed in sites subjacent to junctional, sulcular, and oral epithelium, in the body of the lamina propria and just superior to the alveolar bone crest. RESULTS: Subjacent to the sulcular epithelium there was a statistically significant (P < 0.01) increase in lymphocyte density between health and inflammation. The percentage of endothelial cells incorporating 3H-thymidine label (LI) and the number of blood vessels per unit area were significantly increased in this same site in inflamed samples (P < 0.02) but were not elevated further in lesions in which there was destruction of soft connective tissues. However, there was no increase of the numbers or the cross-sectional areas of blood vessels between samples of inflamed and destroyed tissues. CONCLUSIONS: 1) Experimentally induced inflammation and connective tissue destruction in the gingival connective tissues of Cynomolgus monkeys is associated with site-specific perturbations in the turnover of endothelial cells that is closely linked to lymphocytic infiltration; 2) the vascular response is a generalized increase in endothelial cell proliferation and blood vessel numbers but not lumen size or number of endothelial cells, suggesting the existence of homeostatic controls for preservation of the whole population in a steady state.

Animals↗

A critical assessment of the relationship between silicone breast implants and connective tissue diseases.

Concerns regarding the possible role of breast implants (particularly silicone breast implants) in the development of connective tissue diseases were raised by case reports of connective tissue diseases in women with breast implants. Case reports, however, are not appropriate for causation assessment. Within the past few years, epidemiologic studies have begun to appear. Based on a comprehensive literature search, 15 epidemiologic studies on breast implants and connective tissue diseases, which satisfied certain basic epidemiologic requirements, were included in the critical assessment. These studies utilized either the case-control or the cohort study design. Although each individual study was relatively small, and the statistical power to detect a modest risk increase in specific categories of connective tissue diseases was limited, the results of these studies, however, were strikingly consistent, particularly those reported in case-control studies. To increase statistical power and to take the consistency of results into consideration, meta-analyses were used to summarize results from individual studies quantitatively. Based on data from case-control studies, meta-analyses of rheumatoid arthritis, systemic sclerosis (scleroderma), and systemic lupus erythematosus were performed. These case-control studies represented a combined database of approximately 4000 cases of connective tissue diseases, and the power was sufficient to detect a relatively small increase in risk. Based on the meta-analyses, the relative risks (95% confidence intervals) were 0.85 (0.48-1.51) for rheumatoid arthritis, 0.82 (0. 50-1.35) for systemic sclerosis, and 0.33 (0.06-2.03) for systemic lupus erythematosus, indicating that there was no increased risk of connective tissue diseases associated with breast implants. The findings derived from the meta-analyses of case-control studies were supported by results from cohort or prospective studies. It was concluded that epidemiologic data did not provide any evidence for a causal relationship between silicone breast implants and connective tissue diseases.

Arthritis, Rheumatoid↗

The influence of subepithelial connective tissues on epithelial proliferation in the adult mouse.

Subepithelial connective tissue is capable of modulating the pattern of histodifferentiation of stratified epithelia from adult animals, but it is not known whether the supporting connective tissue also influences epithelial proliferative activity. Epithelial and connective tissues of murine skin and oral mucosa, differing in their morphology and proliferative activity, were separated and heterotypically recombined prior to grafting to histocompatible hosts. After 3 or 8 weeks in situ, mitotic activity was determined following the administration of vinblastine sulfate. Although the mitotic activity in each of the epithelia could be modulated by some connective tissues, there was no distinct pattern of behavior. In combination with connective tissues from tongue or palate, the ear epidermis acquired a significantly increased mitotic activity. In contrast, when oral epithelia with high mitotic activity were recombined with dermal connective tissue, there was usually a significant reduction in proliferative activity. As there was no apparent association between mitotic activity and the induced changes in either organization or histodifferentiation, it is suggested that subepithelial connective tissue is capable of directly influencing the mitotic activity in the overlying epithelium.

Animals↗

Alteration of tumour cell arrangement related to connective tissue stroma in metastatic brain tumours. Histological and immunohistochemical studies of 68 autopsy cases.

Tumour cell arrangements of a variety of 68 tumours metastatic to brain parenchyma and leptomeninges were compared histologically and immunohistochemically with those of the primary tumours in regard to their connective tissue stroma. In the brain parenchyma, more than 90% of 31 metastatic differentiated adenocarcinomas from various organs changed in cell arrangement from a tubular to a papillary pattern, in which tumour cells lined the increased perivascular connective tissue, rich in both type III collagen and fibronectin, the typical constituents of interstitial type extracellular matrices. Twelve (39%) and 3 of 31 cases were rearranged in a partially or completely tubular pattern respectively, within the metastatic nodules. Most of these neoplastic tubules were surrounded by diffusely proliferating connective tissue. Metastatic growth of carcinoma cells in the absence of supporting connective tissue in the nervous tissue was rare. A similar result was obtained for differentiated squamous cell carcinoma. In contrast, metastatic undifferentiated carcinoma and tumours with some neuro-ectodermal characteristics showed a sheet-like arrangement without pronounced connective tissue proliferation, similar to that of the primary tumours. In the leptomeninges, differentiated carcinoma cells were arranged in a tubular or a squamoid pattern and were frequently accompanied by marked stromal response. These results indicate that differentiated carcinomas require connective tissue stroma for metastatic growth, and that tumour cell arrangement in the brain varies depending upon the amount and distribution of proliferating connective tissue stroma. In undifferentiated carcinomas and tumours with neuro-ectodermal characteristics lacking stromal dependency, the tumor cell arrangement remains unchanged. The degree of stromal response to metastatic tumours in the brain parenchyma is related to the degree of epithelial differentiation.

Adenocarcinoma↗

Demonstration of thyrotropin binding sites in orbital connective tissue: possible role in the pathogenesis of thyroid-associated ophthalmopathy.

The thyrotropin (TSH) receptor is implicated in the pathogenesis of thyroid-associated ophthalmopathy, but its presence has not been demonstrated in orbital tissues. Binding of 125I-TSH to porcine orbital connective tissue and thyroid membranes was studied. At pH 7.4 125I-TSH bound to thyroid membranes with high affinity, but not to orbital connective tissue membranes. At pH 5.2, binding of 125I-TSH was evident on thyroid and orbital connective tissue membranes, although of low affinity. Low affinity binding at pH 5.2, could also be demonstrated on orbital fibroblasts; binding to membranes prepared from extraocular muscle, or from abdominal adipose tissue was not detected. Immunoglobulin G from healthy subjects (n = 17) and patients with ophthalmopathy (n = 19) were tested for inhibition of 125I-TSH binding to membranes. As anticipated patients' IgG exhibited greater inhibition than normal controls with thyroid membranes at pH 7.4 (p < 0.001). Similar results were obtained with thyroid membranes (p < 0.05), and orbital connective tissue membranes at pH 5.2 (p < 0.001). Significant correlations were found when percentage inhibition by IgG was compared between: thyroid membranes at pH 7.4 and thyroid membranes at pH 5.2, orbital connective tissue membranes at pH 5.2 and thyroid membranes at pH 7.4, and orbital connective tissue membranes at pH 5.2 and thyroid membranes at pH 5.2. A low affinity TSH-binding site is present in orbital connective tissue, and is recognized by IgG's from patients with ophthalmopathy which suggests that TSH receptor antibodies may target the orbit.

Adolescent↗

Connective tissue: a body-wide signaling network?

Unspecialized "loose" connective tissue forms an anatomical network throughout the body. This paper presents the hypothesis that, in addition, connective tissue functions as a body-wide mechanosensitive signaling network. Three categories of signals are discussed: electrical, cellular and tissue remodeling, each potentially responsive to mechanical forces over different time scales. It is proposed that these types of signals generate dynamic, evolving patterns that interact with one another. Such connective tissue signaling would be affected by changes in movement and posture, and may be altered in pathological conditions (e.g. local decreased mobility due to injury or pain). Connective tissue thus may function as a previously unrecognized whole body communication system. Since connective tissue is intimately associated with all other tissues (e.g. lung, intestine), connective tissue signaling may coherently influence (and be influenced by) the normal or pathological function of a wide variety of organ systems. Demonstrating the existence of a connective signaling network therefore may profoundly influence our understanding of health and disease.

Animals↗

Causal relationship between white matter structural connectivity and epilepsy.

White matter structural connectivity has recently been linked to epilepsy pathogenesis, yet its causal role remains unclear. This study used Mendelian randomization (MR) to investigate the causal relationship between white matter structural connectivity and epilepsy. GWAS summary statistics for white matter structural connectivity were sourced from the UK Biobank, while epilepsy data were obtained from FinnGen R10 and the International League Against Epilepsy (ILAE). Our MR analysis revealed significant causal links between white matter structural connectivity and epilepsy risk. Increased connectivity between the right hemisphere visual and salience/ventral attention networks (RH Vis to RH Sal/VentAttn WMSC) was associated with higher epilepsy risk in FinnGen_R10_FE_STRICT (OR&#xa0;=&#xa0;2.25, 95&#xa0;% CI&#xa0;=&#xa0;1.43-3.56, p&#xa0;<&#xa0;0.01, FDR P&#xa0;=&#xa0;0.019). Conversely, increased connectivity between left and right hemisphere salience/ventral attention networks (LH Sal/VentAttn to RH Sal/VentAttn WMSC) was linked to reduced epilepsy risk in FinnGen_R10_GE_STRICT (OR&#xa0;=&#xa0;0.17, 95&#xa0;% CI&#xa0;=&#xa0;0.07-0.46, p&#xa0;<&#xa0;0.01, FDR P&#xa0;=&#xa0;0.033). A total of 15 nominally significant associations were identified across datasets. These findings suggest a causal relationship between white matter structural connectivity and epilepsy, offering insights into disease mechanisms and potential therapeutic targets.

Humans↗

Keratinocytes inhibit expression of connective tissue growth factor in fibroblasts in vitro by an interleukin-1alpha-dependent mechanism.

The wound healing process concludes with downregulation of fibroblast activity. Clinical observations suggest that the regenerating epidermis suppresses this activity. An important regulator of fibroblast activity is the fibrogenic cytokine connective tissue growth factor. We hypothesized that epidermal keratinocytes may affect fibroblast activity via this cytokine. We demonstrate keratinocyte-mediated suppression of connective tissue growth factor at both the mRNA and protein levels by around 50% or more when fibroblasts were cultured in multiwell plates with keratinocyte cultures in accompanying semipermeable cell culture inserts, or stimulated by keratinocyte-conditioned media. Both basal and transforming-growth-factor-beta1-stimulated levels of connective tissue growth factor were inhibited. A 3 h coculture period with keratinocytes was sufficient to suppress connective tissue growth factor expression by fibroblasts, but the inhibition developed over a time period of around 16 h. The putative keratinocyte-derived factor(s) responsible for these effects was found to be soluble and stable. By analyzing cytokines secreted by keratinocytes we identified interleukin-1alpha as a potent inhibitor of connective tissue growth factor mRNA expression in fibroblasts. Involvement of this cytokine in keratinocyte-mediated connective tissue growth factor suppression was confirmed by using anti-interleukin-1alpha antibodies. Tumor necrosis factor alpha or prostaglandins did not appear to be involved. In conclusion, our results indicate that interleukin-1alpha secretion by keratinocytes provides a mechanism for the downregulation of connective tissue activity during the end-stage of wound healing, when epithelia coverage has developed over the wound area.

Coculture Techniques↗

The association between connective tissue laxity and the risk of an abdominal aortic aneurysm.

AIMS: to investigate whether connective tissue laxity is associated with abdominal aortic aneurysms (AAA). METHODS: a nested case control study in a population-based screening programme. The presence of pes planus, scoliosis, pectus deformities, flexible auricular cartilages and Gorling's sign were combined with the Beighton joint mobility score to form a connective tissue laxity score. The association between connective tissue laxity and the risk of AAA was investigated through a logistic regression model. Type III collagen turnover was assessed using a serum radio-immunoassay for type III procollagen (PIIINP). RESULTS: data from 231 controls (aortic diameter <2.5 cm) and 190 cases (AAA >2.9 cm) were analysed. Odds ratios (OR), adjusted for known confounders were 3.1 (95% CI: 1. 1-8.6) for the highest group of connective tissue scores and 2.4 (95% CI: 1.0-5.4) for the middle group, compared with those with no signs of abnormal connective tissue function. There was no difference in mean collagen turnover between cases and controls, nor between those with a stable AAA >4 cm and those with an expanding AAA. CONCLUSION: connective tissue laxity is associated with a higher risk of having an AAA. The collagen turnover is similar in subjects with an AAA and controls. Aneurysms may be associated with abnormal connective tissue rather than an increased breakdown of normal collagen.

Aortic Aneurysm, Abdominal↗

An ultrastructural study of connective tissue in mollusc integument: I. Bivalvia.

The ultrastructure of the subepidermal connective tissue (SEC) in different areas of the integument of the bivalves Callista chione, Pecten jacobaeus, Mytilus galloprovincialis and Ostrea edulis was studied by transmission electron microscopy. The main organisation of the SEC was broadly similar in all species: the SEC was connected to the epidermis by a basement membrane and merged directly with the deeper connective tissue surrounding muscles. The SEC was not differentiated into layers like the papillary and reticular dermis of mammals, however, the architecture, thickness and shape of the basement membrane varied from species to species, as well as within species (in the foot, central or marginal zones of the mantle). The ultrastructure of the lamina densa was broadly similar to that in mammals: although basotubules and double pegs were absent, proteoglycans and rod-like units homologous to 'double tracks' were always abundant. A zone similar to the lamina lucida was irregularly present and was shot thorough with small protrusions of the lamina densa that connected with the epithelial hemidesmosomes or focal adhesions. Nevertheless zones were observed where the lamina densa fuse directly to the epithelial plasmamembrane. This variability of connection may be related to the various types of epidermal cell. A lamina fibroreticularis was not recognized since anchoring fibrils and microfibrils were not present; lamina densa protrusions into the extracellular matrix (ECM) of SEC characterize the connection between basement membrane and SEC. Collagen fibrils were small and of constant diameter and were never organised into fibres. Anchoring devices - similar to the anchoring plaques of mammalian dermis - were abundant and scattered between SEC collagen fibrils. The orange-pink pigmentation of C. chione seems due to electron-dense granules embedded within the connective ECM.

Animals↗