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P Liesi

Publications and source records attributed to P Liesi.

9 recordsLinked to original sources

Laminin and its neurite outgrowth-promoting domain in the brain in Alzheimer's disease and Down's syndrome patients.

Immunocytochemistry, radioimmunoassay, immunoblotting, Northern analysis, and polymerase chain reaction (PCR) technique were applied to investigate the distribution of laminin and its neurite outgrowth domain in brains of neuropathologically verified cases of Alzheimer's disease and Down's syndrome. New antibodies against a neurite outgrowth domain of laminin were characterized and were used in localization of this peptide antigen in the human brain. Laminin was found as large punctate deposits in all plaques in the affected brains. Laminin synthesis was increased as assessed by RNA blotting and immunoblotting, and glial cells were heavily immunoreactive with antibodies for a neurite outgrowth-promoting peptide antigen of the B2 chain of laminin. This peptide antigen not only was produced by glial cells but also was deposited in the brain tissue. As this peptide antigen promotes neurite outgrowth at low concentrations, and is specifically neurotoxic at high concentrations, it may play a synergistic role with other molecules in inducing the sprouting and neurodegeneration occurring in brains of patients with either Alzheimer's disease or Down's syndrome.

Adult

Neuronal migration in cerebellar microcultures is inhibited by antibodies against a neurite outgrowth domain of laminin.

The functional role of laminin in neuronal migration was investigated by using polyclonal antibodies or their divalent (Fab')2 fragments to a neurite outgrowth promoting domain of the B2 chain of laminin in a cerebellar microculture system widely recognized as a model for neuronal migration. We show here that these antibodies or their (Fab')2 fragments totally inhibit migration of the mouse cerebellar granule cells along the glial and other neuronal cell processes. Antibodies to native laminin or other control antibodies have no inhibitory effect. Immunocytochemical analysis of the cerebellar microcultures indicates that the functional role of these antibodies may relate to the fact that the punctate deposits of laminin and its neurite outgrowth promoting domain accumulate in between the migrating neurons and the glial cells. These data provide the first direct evidence for the functional role of laminin and its neurite outgrowth domain in neuronal migration in the mammals. They further suggest that a neuronal cell surface contact with the extracellular deposits of a neurite outgrowth domain of the B2 chain of laminin may mediate neuronal-glial interactions.

Animals

The effect of acute distension on vasoactive intestinal polypeptide (VIP), neuropeptide Y (NPY) and substance P (SP) immunoreactive nerves in the female rat urinary bladder.

The effect of acute distension on vasoactive polypeptide (VIP)-, neuropeptide Y (NPY)- and substance P (SP)-immunoreactive nerves in the wall of the urinary bladder was investigated. At the age of 3 months, 25 female albino rats underwent forced diuresis combined with balloon obstruction to achieve maximal distension for 3 h. A modified, indirect immunofluorescence detection method was applied 2 days, 7 days and 21 days after distension. A marked, extensive depletion of VIP, NPY- and SP-immunoreactive nerves was observed after distension. This disturbance was reversible, and increased fluorescence of VIP-, NPY- and SP-immunoreactive nerve fibres compared with control specimens was seen in bladder specimens taken even as soon as 21 days after distension. This transient depletion of peptidergic innervation may partly explain the prolonged voiding problems that often occur after acute urinary retention. The depletion of sensory nerves containing SP shortly after distension may explain the transient benefit obtained from distension therapy in patients with painful bladder disease. It is suggested that the increased SP activity during the recovery phase may be related to neurogenic inflammation.

Animals

Neuronal migration on laminin involves neuronal contact formation followed by nuclear movement inside a preformed process.

Neuronal migration was investigated in rodent cerebellum in vitro and in vivo. Time-lapse video recording showed that cultured neurons migrated on laminin by first extending neurites that formed contacts with other neurons. This was followed by movement of the cell nucleus inside the preformed process. No guidance cues other than laminin were required. When the rodent premigratory (E18-P0) cerebellum was examined by immunocytochemistry, the radial glial cells were found to have extracellular punctate deposits of laminin along their fibers. Such punctate deposits of laminin were more numerous in the premigratory cerebellum than during the peak of neuronal migration (e.g., at 7-10 days postnatally). At the same time (E18-P0) L1 antigen- and neurofilament-positive, presumably granule cell processes extend radially from the external granule cell layer (EGL). These results imply that neuronal migration on laminin in vitro involves neuronal contact formation followed by nuclear movement inside a preformed process. That this mode of neuronal migration may occur in vivo is indicated by the fact that L1 antigen- and neurofilament-positive "pioneer neurites" colocalize with the punctate deposits of laminin deposited along the radial glial processes in the premigratory EGL. Taken together these results imply that the established glial dependency of the granule cell migration may in fact be dependency of the granule cells and their pioneer neurites on the punctate deposits of laminin produced and laid down by the glial cells.

Animals

Immunoreactive neuropeptides in nerves in ligamentous tissue. An experimental neuroimmunohistochemical study.

A search for neuropeptide nerves in the healing of the experimentally ruptured medial collateral ligament (MCL) of the rabbit knee used specific antisera to the neuropeptides Substance P, calcitonin gene-related peptide (CGRP), and galanin. Sutured and unsutured MCLs were studied four and 14 weeks postoperatively. Both fluorescent thin nerve strands and small dotlike nerve terminals were regularly seen in the healing zone and in the adjacent normal ligamentous tissue, suggesting innervation of such structures by neuropeptide nerves. All three neuropeptides were more abundant in sutured ligaments than in unsutured ligaments, which may suggest beneficial effects of the apposition of the torn ligament ends on local nerve regeneration. Active involvement of the neural elements in the healing process was also suggested by kinetic studies showing a decrease in Substance P and CGRP staining as well as an increase in galanin staining during the study period. These changes in the periphery parallel the reactive changes earlier described in the dorsal root ganglion and dorsal horn cells occurring after a peripheral nerve injury. This may depend on the antidromic transport to the periphery of neuropeptides synthesized in the central nervous system. This experimental neuroimmunohistochemical mapping study and the known effects of neuropeptides on blood vessels, macrophages, and fibroblasts should stimulate further work on the role of innervation in ligamentous healing.

Animals

Extracellular matrix and neuronal movement.

During brain development, both neuronal migration and axon guidance are influenced by extracellular matrix molecules present in the environment of the migrating neuronal cell bodies and nerve fibers. Glial laminin is an extracellular matrix protein which these early brain cells preferentially attach to. Extracellular glycosaminoglycans are suggested to function in restricting neuronal cell bodies and axons from certain brain areas. Since laminin is deposited along the radial glial fibers and along the developing nerve pathways in punctate form, the punctate assemblies may be one of the key factors in routing the developing neurons in vivo. This review discusses the role of laminin in neuronal movement given the present concept of the extracellular matrix molecules and their proposed interactions.

Animals

Immunohistochemical demonstration of nociceptors in the ligamentous structures of the lumbar spine.

Substance P, a physiologically potent neuropeptide is known to participate in the sensory, and especially nociceptive, transmission of neural impulses. On histologic grounds, the nerve terminals of the sinuvertebral nerve formerly have been suggested to be sensory in character and to mediate the low-back pain syndrome. Samples of paramedullary ligamentous structures were collected on disc operations. A positive immunoreaction as an indicator of substance P was confirmed in some nerve terminals of the posterior longitudinal ligament. Neither the yellow ligament nor the intervertebral disc showed such nociceptive-type nerves.

Humans

Innervation of synovial membrane and meniscus.

Substance P-immunofluorescent nerves, which are closely connected to pain transmission, were shown in human knee synovial membrane and menisci. Both tissues also contained enkephalin-immunofluorescent nerves, which are probably involved in the modulation of pain transmission. Previous suggestions on the presence of nociceptive receptors in these non-cartilaginous joint structures, made on a histological basis, are thus confirmed by a specific immunohistochemical method.

Enkephalins