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G La Spada

Publications and source records attributed to G La Spada.

10 recordsLinked to original sources
PubMed2001

Morphological characteristics by SEM observations and regulatory volume decrease (RVD) of tentacular nematocytes isolated by heat dissociation from Aiptasia diaphana (Cnidaria: Anthozoa).

This paper examines the morphological characteristics and response to hyposmotic shock of nematocytes isolated by heat dissociation at 45 degrees C for 20 min from the tentacles of Aiptasia diaphana, an anthozoan living in the brackish water of Lake Faro (Messina, Italy). Morphological characteristics were evaluated by scanning electron microscopy (SEM) observations and cytological test, functional characteristics by exposure to 35% hyposmotic stress. 81% of the population of isolated nematocytes had ciliary protrusions. Microbasic-mastigophore and amastigophore nematocytes had a hair bundle at the crown shaped apex composed of ciliary protrusions of different heights and diameters. In basitrichs, instead, a single ciliary protrusion was observed. Following exposure to 35% hyposmotic shock, nematocytes isolated by heat dissociation did not show RVD, while, following treatment with 1 microM and 2 microM gramicidin-S, activation of volume regulation in conditions of hyposmoticity was observed. The effect of gramicidin was concentration-dependent and confirmed the relevant role of conductance to K+ in volume regulation, as previously described (17) on nematocytes isolated by chemical methods.

Animals↗
PubMed1999

Regulatory volume decrease in nematocytes isolated from acontia of Aiptasia diaphana.

Regulatory volume decrease (RVD) and the mechanisms of its regulation were investigated in microbasic mastigophore nematocytes isolated from the acontia of Aiptasia diaphana (Coelenterates, Cnidaria), a marine species that can be exposed to considerable changes in osmotic pressure. Exposure of isolated cells to a 35% hypoosmotic shock lead to the expected osmotic swelling followed by a rapid RVD. RVD was blocked if Ca2+ influx was prevented either by applying a Ca2+-free medium or by treating the cells with Gd3+. Furthermore, the calmodulin action inhibitor trifluoperazine (TFP), prevented RVD and also caused a larger swelling than that induced by preventing Ca2+ influx. Treatment of nematocytes with quinine completely blocked the RVD. Such an effect was prevented by gramicidine. A partial inhibition of RVD was caused by treatment with 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). It is concluded that: i) the nematocytes regulate volume under hypoosmotic shock; ii) the regulatory mechanisms consist mainly in increased conductance to K+, and consequently, of Cl-, and, to a lesser extent, in H+/K+-Cl-/HCO3- exchange, and iii) the ionic fluxes are triggered by increased [Ca2+]i with the possible involvement of calmodulin.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

Gadolinium is a powerful blocker of the activation of nematocytes of Pelagia noctiluca.

The activation properties of in situ nematocytes of Pelagia noctiluca (Scyphozoa) were investigated by physical contact with a gelatin probe that, besides stimulating the nematocyte battery, retains the discharged nematocysts, thereby allowing a quantitative evaluation of the response. In oral arms previously treated with 2 mmol l-1 La3+ the discharge was inhibited. This result confirms the Ca(2+)-dependence of nematocyte activation. A similar inhibitory effect was induced by treatment with 20 mumol l-1 Gd3+, a powerful blocker of mechanosensitive ion channels. It is therefore proposed that Ca(2+)-permeable mechanosensitive channels are involved in the activation of nematocytes. 50 mumol l-1 Gd3+ added to the gelatin probe was effective in otherwise untreated oral arms. This result suggests that Gd3+ could be useful in preventing stings from harmful Cnidaria.

Animals↗
PubMed1983

Response of satellite cells and muscle fibers to long-term compensatory hypertrophy.

The ultrastructural changes of the plantaris muscle of the rat have been investigated during long-term compensatory hypertrophy. The latter was induced by the removal of the synergistic gastrocnemius muscle. Transmission electron microscope (TEM) observations were performed on the 20th, 40th and 60th days after surgery on overloaded and control muscles. The plantaris muscle had hypertrophied 54.8% after 20 days, 74.4% after 40 days and 79.8% after 60 days. It was observed that activation of the satellite cell developed as shown by an increase in cytoplasmic volume, together with diffuse presence of polyribosomes and a rough endoplasmic reticulum. On the 40th day masses of swollen mitochondria grouped at the edge of muscle fibers were observed. On the 60th day structures completely covered with basal lamina, whose cytoplasm was filled with mitochondria and polyribosomes, were partially detached from the fibers. The above ultrastructural changes were absent in control contralateral muscles. These findings suggest that surgically induced overload produces a relevant ultrastructural re-arrangement in muscle tissue.

Animals↗
PubMed1980

New muscle fiber production during compensatory hypertrophy.

Morphological changes exhibited by satellite cells during compensatory hypertrophy have been observed through a scanning electron microscope on m. plantaris of young, adult rats. Compensatory hypertrophy was induced by ablation of the synergistic m. gastrocnemius. Muscles were observed 15, 30, and 60 days post-operative. A consistent increase in wet-weight of m. plantaris (60.3,77.2, and 93.7% more than the contralateral control muscle) indicated the degree of developing hypertrophy. The satellite cells exhibited the following successive changes: (1) cells enlarged and became freed of connective network sheath, (2) cell distance from the associated fibers increased though still attached to the latter, (3) subsequent cell division, giving rise to rows of cells, that with time-lapse formed elongated structures with a common sheath, (4) elongated structures developed into new muscle fibers.

Animals↗
PubMed1979

Activation of satellite cells induced by chronic neostigmine administration in the rat.

Muscle fibrillation has been suggested as a possible trigger for activation of satellite cells, a well known phenomenon associated with denervation. In order to test such a hypothesis fibrillation has been induced in normally innervated muscles by chronic administration of neostigmine and the response of satellite cells has been observed with a scanning electron microscope. The results show that satellite cells protrude from the profile of the muscle fiber, become partially separated from the latter, and align in rows. Elongated structures and presumable new muscle fibers are observed after 14 days of treatment. It is concluded that the overactivity of muscle fibers which is induced during fibrillation causes activation and differentiation of satellite cells. This result is consistent with that of a previous experiment showing that satellite cells are activated during acute increase in workload.

Animals↗