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PubMed2005

Visualization of localized store-operated calcium entry in mouse astrocytes. Close proximity to the endoplasmic reticulum.

Unloading of endoplasmic reticulum (ER) Ca(2+) stores activates influx of extracellular Ca(2+) through 'store-operated' Ca(2+) channels (SOCs) in the plasma membrane (PM) of most cells, including astrocytes. A key unresolved issue concerning SOC function is their spatial relationship to ER Ca(2+) stores. Here, using high resolution imaging with the membrane-associated Ca(2+) indicator, FFP-18, it is shown that store-operated Ca(2+) entry (SOCE) in primary cultured mouse cortical astrocytes occurs at plasma membrane-ER junctions. In the absence of extracellular Ca(2+), depletion of ER Ca(2+) stores using cyclopiazonic acid, an ER Ca(2+)-ATPase inhibitor, and caffeine transiently increases the sub-plasma-membrane Ca(2+) concentration ([Ca(2+)](SPM)) within a restricted space between the plasma membrane and adjacent ER. Restoration of extracellular Ca(2+) causes localized Ca(2+) influx that first increases [Ca(2+)](SPM) in the same restricted regions and then, with a delay, in ER-free regions. Antisense knockdown of the TRPC1 gene, proposed to encode endogenous SOCs, markedly reduces SOCE measured with Fura-2. High resolution immunocytochemistry with anti-TRPC1 antibody reveals that these TRPC-encoded SOCs are confined to the PM microdomains adjacent to the underlying 'junctional' ER. Thus, Ca(2+) entry through TRPC-encoded SOCs is closely linked, not only functionally, but also structurally, to the ER Ca(2+) stores.

Animals↗

PubMed1988

Cerebrovascular and cerebral effects of nimodipine--an update.

A survey is given on the vascular and neuronal effects of calcium antagonists under physiological and pathological conditions. Special emphasis is put on vasospasm caused by subarachnoid haemorrhage and on postischaemic cerebral hypoperfusion following different forms of cerebral ischaemia, and on the attempts to influence these phenomena pharmacologically. Regarding its neuronal effects it seems likely that nimodipine potently blocks calcium entry during pathological conditions like cerebral ischaemia and spreading cortical depression. Positive effects also have been seen during epileptic seizures and withdrawal syndromes, whereas calcium entry under normal physiological conditions does not appear to be affected. Possible clinical consequences are discussed.

Animals↗

PubMed2006

Migratory response of interneurons to different regions of the developing neocortex.

The interactions between migrating interneurons and their environment that lead to stereotypic migration pathways remain largely undefined. We have used time-lapse imaging to record the migratory responses of labeled interneurons to different regions of the migratory pathway in organotypic slice cultures. We tested the hypothesis that the length of the migratory pathway is not equally permissive for interneuron migration, with separate zones of inhibition and attraction. Three different experimental approaches were used to address this issue, including explant cocultures, cortical overlay cultures, and rotation of cortical slices. The results clearly identify the lateral region to be an attractive substrate for interneuron entry at embryonic day 12.5, whereas the medial region at this stage contains a zone of inhibition. This property of the medial neocortex is temporally regulated with switching from inhibition to attraction within 24 h. We suggest that this temporal regulation may provide a mechanism for gating the entry of interneurons into the hippocampus while ensuring that cortical interneurons are properly confined within the neocortical wall. In this manner, interneurons arising from common precursors and sharing common migratory pathways are able to populate different pallial structures.

Aging↗

PubMed1994

Passive mechanical behavior of human neutrophils: effect of cytochalasin B.

Actin is a ubiquitous protein in eukaryotic cells. It plays a major role in cell motility and in the maintenance and control of cell shape. In this article, we intend to address the contribution of actin to the passive mechanical properties of human neutrophils. As a framework for assessing this contribution, the neutrophil is modeled as a simple viscous fluid drop with a constant cortical ("surface") tension. The reagent cytochalasin B (CTB) was used to disrupt the F-actin structure, and the neutrophil cortical tension and cytoplasmic viscosity were evaluated by single-cell micropipette aspiration. The cortical tension was calculated by simple force balance, and the viscosity was calculated according to a numerical analysis of the cell entry into the micropipette. CTB reduced the cell cortical tension in a dose-dependent fashion: by 19% at a concentration of 3 microM and by 49% at 30 microM. CTB also reduced the cytoplasmic viscosity by approximately -25% at a concentration of 3 microM and by approximately 65% at a concentration of 30 microM when compared at the same aspiration pressures. All three groups of neutrophils, normal cells, and cells treated with either 3 or 30 microM CTB, exhibited non-Newtonian behavior, in that the apparent viscosity decreased with increasing shear rate. The dependence of the cytoplasmic viscosity on deformation rate can be described empirically by mu = mu c(gamma m/gamma c)-b, where mu is cytoplasmic viscosity, gamma m is mean shear rate, mu c is the characteristic viscosity at the characteristic shear rate gamma c, and b is a material coefficient. The shear rate dependence of the cytoplasmic viscosity was reduced by CTB treatment. This is reflected by the changes in the material coefficients. When gamma c was set to 1 s-1, pc = 130 +/- 23 Pa.s and b = 0.52 +/- 0.09 for normal neutrophils and pc = 54 +/- 15 Pa.S and b = 0.26 +/- 0.05 for cells treated with 30 micro M CTB. These results provide the first quantitative assessment of the role that Pa-s-actin structure plays in the passive mechanical properties of human neutrophils.

Actins↗

PubMed2005

Expression of various scinderin domains in chromaffin cells indicates that this protein acts as a molecular switch in the control of actin filament dynamics and exocytosis.

Stimulation-induced chromaffin cell cortical F-actin disassembly allows the movement of vesicles towards exocytotic sites. Scinderin (Sc), a Ca2+-dependent protein, controls actin dynamics. Sc six domains have three actin, two PIP2 and two Ca2+-binding sites. F-actin severing activity of Sc is Ca2+-dependent, whereas Sc-evoked actin nucleation is Ca2+-independent. Sc domain role in secretion was studied by co-transfection of human growth hormone (hGH) reporter gene and green fluorescent protein (GFP)-fusion Sc constructs. Cells over-expressing actin severing Sc1-6 or Sc1-2 (first and second actin binding sites) constructs, increased F-actin disassembly and hGH release upon depolarization. Over-expression of nucleating Sc5-6, Sc5 or ScABP3 (third actin site) constructs decreased F-actin disassembly and hGH release upon stimulation. Over-expression of ScL5-6 or ScL5 (lack of third actin site) produced no changes. During secretion, actin sites 1 and 2 are involved in F-actin severing, whereas site 3 is responsible for nucleation (polymerization). Sc functions as a molecular switch in the control of actin (disassembly left arrow over right arrow assembly) and release (facilitation left arrow over right arrow inhibition). The position of the switch (severing left arrow over right arrow nucleation) may be controlled by [Ca2+]i. Thus, increase in [Ca2+]i produced by stimulation-induced Ca2+ entry would increase Sc-evoked cortical F-actin disassembly. Decrease in [Ca2+]i by either organelle sequestration or cell extrusion would favor Sc-evoked actin nucleation.

Actin Cytoskeleton↗

PubMed1993

Glutamate receptor antagonists in experimental focal cerebral ischaemia.

Excessive activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor has been implicated in the sequence of neurochemical events in cerebral ischaemia that results in irreversible neuronal damage. The effects of the NMDA antagonist MK-801 upon the amount of ischaemic brain damage has been assessed quantitatively in a cat and in a rat model of focal cerebral ischaemia. In chloralose-anaesthetised cats, focal cerebral ischaemia was produced by permanent occlusion of one middle cerebral artery (MCA) and the animal sacrificed 6 hours later. Pretreatment with the non-competitive NMDA antagonist, MK-801 (5 mg/kg, i.v.) reduced significantly the volume of ischaemic damage in the cerebral cortex by 57% compared to vehicle-treated cats. A similar degree of neuroprotection could be demonstrated in the cat MCA occlusion model if treatment with MK-801 was initiated 2 hours after the induction of ischaemia. In halothane-anaesthetised rats, focal cerebral ischaemia was produced by permanent MCA occlusion and the animals sacrificed 3 hours later. Pretreatment with MK-801 (0.5 mg/kg, i.v.) reduced the volume of ischaemic damage in the cerebral cortex by 38%; treatment with MK-801 initiated 30 minutes after MCA occlusion was equally effective in reducing cortical damage. In contrast to calcium entry blockers such as nimodipine in the rat MCA occlusion model, the improved histopathological outcome with MK-801 is not associated with improvement in cerebral tissue perfusion to the ischaemic tissue. The increasing evidence that NMDA receptor antagonists are beneficial in experimental focal cerebral ischaemia is reviewed.

Animals↗

PubMed1986

Kinematics of gray crescent formation in Xenopus eggs: the displacement of subcortical cytoplasm relative to the egg surface.

Specification of the amphibian dorso-ventral axis takes place in the period between fertilization and first cleavage when the gray crescent forms. In the course of gray crescent formation, the egg reorganizes its periphery by a movement for which two descriptions have been given. According to the "rotation hypothesis," which was originated and supported for Rana eggs, the entire egg cortex rotates by an arc of 30 degrees relative to the stationary subcortical cytoplasm, leaving the crescent as a zone of altered coloration. The "contraction hypothesis" on the other hand, which was proposed for Xenopus and Rana eggs, asserts that there is a cortical contraction focused at the sperm entry point that leads to stretching of the opposite equatorial zone at which the crescent appears. We have reinvestigated the case of Xenopus eggs by imprinting one kind of fluorescent dye pattern (Nile blue) onto the subcortical cytoplasm and another kind (fluorescein-lectin) onto the egg surface. When the egg surface is held fixed by embedding the egg in gelatin, two major movements of the subcortical cytoplasm are observable. First, starting at time 0.3 (30% of the time between fertilization and first cleavage), the animal hemisphere subcortical cytoplasm converges toward a point, while the vegetal hemisphere is quiescent. This convergence continues with decreasing strength until approximately 0.8 of the first cell cycle. Second, at 0.45, an overall rotation of the animal and vegetal subcortical cytoplasm commences, superimposed on the animal hemisphere convergence. By 0.8-0.9 the rotation is complete, having accomplished a 30 degrees displacement of the subcortical cytoplasm relative to the surface. This rotation reliably locates the future dorsal midline of the embryo at the meridian on which the displacement of the subcortical cytoplasm is greatest in a vegetal direction. In normal unembedded eggs, when the egg surface is free to move, it rotates 30 degrees relative to the subcortical cytoplasm, which remains stationary in a position of gravitational equilibrium. Although both a convergence and rotation occur in the Xenopus egg, we give evidence that the rotation, not the convergence (perhaps equated with contraction), specifies the embryo's prospective axis. Even though the Xenopus egg does not form a classical gray crescent, due to its particular pigment distribution, the reorganization process which specifies the future embryonic axis resembles that of the Rana egg.

Animals↗

PubMed1996

Motor recovery after stroke. Morphological and functional brain alterations.

The aim of this study was to evaluate the relationships of morphological and CBF patterns with both the severity and the evolution of the motor deficit in the late phase of stroke and, in particular, to identify morphological and/or functional brain alterations associated with a persistent severe motor deficit or a poor, delayed motor recovery. We analysed CT/MRI and single photon emission tomography (SPET) findings from 37 patients studied in the chronic phase of stroke (mean duration +/- SD = 3.6 +/- 1.6 months), whom we were able to follow clinically for a period of 3 months. The eventual degree of motor recovery correlated significantly (negatively) with the time since stroke at entry, but not with the severity of neurological impairment at entry. The volume, side and location (cortical or subcortical) of the infarct did not correlate with either the severity or the evolution of the motor deficit. Patients with a CT/MRI lesion of the parietal lobe (n = 8) showed a more severe motor deficit than those with other cortical locations. The severity of the motor deficit correlated significantly (negatively) with CBF values in the supplementary motor area (SMA) and parietal areas of the damaged hemisphere, and in the contralateral undamaged primary motor cortex. The degree of motor improvement correlated significantly (positively) with CBF values in the contralateral undamaged thalamus, lentiform and caudate nuclei, and premotor cortex. In the late phase of stroke, the severity of the motor deficit may be positively associated with the functional impairment of associative parietal and frontal areas of the damaged hemisphere. The functional impairment of the basal ganglia-frontal network in the undamaged hemisphere seems to be related to a poor, delayed motor recovery.

Aged↗

PubMed1992

Danger zone of the acetabulum.

The danger zone of the acetabulum is defined by Marvin Tile as that part of the posterior wall and column at the mid-acetabulum lying above the ischial spine. Screws inserted in the danger zone are at risk of violating the hip joint. Unfortunately, this zone is frequently used in the fixation of posterior wall and column fractures. Cadaveric studies were performed analyzing 1-cm cross-sections through the acetabulum for the purpose of studying the anatomical configuration of the danger zone. The plane of the cross-section was perpendicular to the posterior column. Each cross-section had the medial boundary of the acetabulum projected onto the posterior column. The cross-sections were then assembled to form the original acetabulum. By analyzing the projections on the posterior column, the exact configuration of the danger zone was determined. Screws placed at the margin of the danger zone and directed perpendicular to the posterior column violated the hip joint. Through analysis of the cross-sections, safe anatomic pathways were developed for screw placement. Cortical screws (4.5 mm), placed at entry points of 2 cm and 3 cm medial to the lateral acetabular margin and angled medially 45 degrees and 15 degrees, respectively, did not violate the hip joint. The angulation was respective to the perpendicular to the posterior column. In this study, the average width of the posterior column at the mid-acetabular level was 4.8 cm. Computed tomography scan of the acetabulum yielded valuable information regarding screw placement in the posterior column.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetabulum↗

PubMed1995

Distribution of a brain-specific proteoglycan, neurocan, and the corresponding mRNA during the formation of barrels in the rat somatosensory cortex.

Neurocan is a developmentally regulated chondroitin sulphate proteoglycan in the rat brain. In the present study, spatiotemporal patterns of expression of neurocan and the corresponding mRNA were examined in the developing cortical barrel field of the rat brain by using a monoclonal antibody that was highly specific to neurocan and a riboprobe for a portion of the mRNA. Immunohistochemical analysis revealed that neurocan was distributed throughout the cerebral cortex during early postnatal development but was excluded from the centres of cortical barrels at the time of entry and arborization of thalamocortical axons. At this developmental stage, expression of neurocan mRNA was shown by in situ hybridization to be down-regulated in the barrel centres. When a row of whisker follicles was laser-cauterized on postnatal day 1, the pattern of expression of neurocan was disturbed in the row of barrels that corresponded to the lesioned whisker follicles in the contralateral somatosensory cortex. From these observations, it appears that neuronal stimuli through early thalamocortical fibres from the sensory periphery cause reduced expression of neurocan mRNA in neurocan-producing cells in the presumptive barrel centres. Our findings also suggest that the pattern of distribution of neurocan in early postnatal barrel fields may be due mainly to the down-regulation of expression of neurocan mRNA.

Animals↗

PubMed2005

Genetic ablation of Rhbg in the mouse does not impair renal ammonium excretion.

NH(4)(+) transport by the distal nephron and NH(4)(+) detoxification by the liver are critical for achieving regulation of acid-base balance and to avoid hyperammonemic hepatic encephalopathy, respectively. Therefore, it has been proposed that rhesus type B glycoprotein (Rhbg), a member of the Mep/Amt/Rh NH(3) channel superfamily, may be involved in some forms of distal tubular acidosis and congenital hyperammonemia. We have tested this hypothesis by inactivating the RHbg gene in the mouse by insertional mutagenesis. Histochemical studies analyses confirmed that RHbg knockout (KO) mice did not express Rhbg protein. Under basal conditions, the KO mice did not exhibit encephalopathy and survived well. They did not exhibit hallmarks of distal tubular acidosis because neither acid-base status, serum potassium concentration, nor bone mineral density was altered by RHbg disruption. They did not have hyperammonemia or disturbed hepatic NH(3) metabolism. Moreover, the KO mice adapted to a chronic acid-loading challenge by increasing urinary NH(4)(+) excretion as well as their wild-type controls. Finally, transepithelial NH(3) diffusive permeability, or NH(3) and NH(4)(+) entry across the basolateral membrane of cortical collecting duct cells, measured by in vitro microperfusion of collecting duct from KO and wild-type mice, was identical with no apparent effect of the absence of Rhbg protein. We conclude that Rhbg is not a critical determinant of NH(4)(+) excretion by the kidney and of NH(4)(+) detoxification by the liver in vivo.

Acidosis, Renal Tubular↗

PubMed1989

Apparent viscosity and cortical tension of blood granulocytes determined by micropipet aspiration.

Continuous deformation and entry flow of single blood granulocytes into small caliber micropipets at various suction pressures have been studied to determine an apparent viscosity for the cell contents and to estimate the extent that dissipation in a cortical layer adjacent to the cell surface contributes to the total viscous flow resistance. Experiments were carried out with a wide range of pipet sizes (2.0-7.5 microns) and suction pressures (10(2)-10(4) dyn/cm2) to examine the details of the entry flow. The results show that the outer cortex of the cell maintains a small persistent tension of approximately 0.035 dyn/cm. The tension creates a threshold pressure below which the cell will not enter the pipet. The superficial plasma membrane of these cells appears to establish an upper limit to surface dilation which is reached after microscopic "ruffles" and "folds" have been pulled smooth. With aspiration of cells by small pipets (less than 2.7 microns), the limit to surface expansion was derived from the maximal extension of the cell into the pipet; final areas were measured to be 2.1 to 2.2 times the area of the initial spherical shape. For suctions in excess of a threshold, the response to constant pressure was continuous flow in proportion to excess pressure above the threshold with only a small nonlinearity over time until the cell completely entered the pipet (for pipet calibers greater than 2.7 microns). With a theoretical model introduced in a companion paper, (Yeung, A., and E. Evans., 1989, Biophys. J. 56:139-149) the entry flow response versus pipet size and suction pressure was analyzed to estimate the apparent viscosity of the cell interior and the ratio of cortical flow resistance to flow resistance from the cell interior. The apparent viscosity was found to depend strongly on temperature with values on the order of 2 x 10(3) poise at 23 degrees C, lower values of 1 x 10(3) poise at 37 degrees C, but extremely large values in excess of 10(4) poise below 10 degrees C. Because of scatter in cell response, it was not possible to accurately establish the characteristic ratio for flow resistance in the cortex to that inside the cell; however, the data showed that the cortex does not contribute significantly to the total flow resistance.

Granulocytes↗

PubMed1998

In vitro culture retards spontaneous activation of cell cycle progression and cortical granule exocytosis that normally occur in in vivo unfertilized mouse eggs.

We have previously demonstrated that metaphase II-arrested eggs recovered from oviducts at increasing times after hCG administration display a time-dependent spontaneous entry into anaphase, as well as release of cortical granules (CGs) and the associated modifications of the zona pellucida (ZP), a decrease in histone H1 and mitogen-activated protein kinase activities, and the recruitment of maternal mRNAs [Xu et al., Biol Reprod 1997; 57:743-750). These changes are correlated with the time-dependent increase in susceptibility of these eggs to undergo parthenogenetic activation. We report here the effect of culture of ovulated eggs, retrieved 13 or 16 h post-hCG administration and cultured in vitro for various periods of time, on the aforementioned parameters of egg activation and cell cycle resumption. In contrast to extended residence of the eggs in the oviduct, culture in vitro retarded cell cycle events associated with completion of the second meiotic reduction and inhibited CG release and the associated modifications of the ZP, as well as the recruitment of maternal mRNAs. The retardation or inhibition of these changes during in vitro culture resulted in eggs that were less susceptible to parthenogenetic activation than eggs that resided in the oviduct for comparable time periods. Results of these experiments indicate that egg culture in vitro (which likely occurs under suboptimal conditions) inhibits, rather than accelerates, the progression into the interphase-like state as compared to that seen in eggs residing in the oviduct for increasing periods of time. These results also suggest that, for studies focused on in vitro fertilization or egg activation, the ovulated eggs should be placed under appropriate in vitro conditions as soon as possible.

Animals↗

PubMed2004

Cortical flows powered by asymmetrical contraction transport PAR proteins to establish and maintain anterior-posterior polarity in the early C. elegans embryo.

The C. elegans PAR proteins PAR-3, PAR-6, and PKC-3 are asymmetrically localized and have essential roles in cell polarity. We show that the one-cell C. elegans embryo contains a dynamic and contractile actomyosin network that appears to be destabilized near the point of sperm entry. This asymmetry initiates a flow of cortical nonmuscle myosin (NMY-2) and F-actin toward the opposite, future anterior, pole. PAR-3, PAR-6, and PKC-3, as well as non-PAR proteins that associate with the cytoskeleton, appear to be transported to the anterior by this cortical flow. In turn, PAR-3, PAR-6, and PKC-3 modulate cortical actomyosin dynamics and promote cortical flow. PAR-2, which localizes to the posterior cortex, inhibits NMY-2 from accumulating at the posterior cortex during flow, thus maintaining asymmetry by preventing inappropriate, posterior-directed flows. Similar actomyosin flows accompany the establishment of PAR asymmetries that form after the one-cell stage, suggesting that actomyosin-mediated cortical flows have a general role in PAR asymmetry.

Actins↗

PubMed2002

Pathways that control cortical F-actin dynamics during secretion.

Chromaffin cells possess a mesh of filamentous actin underneath the plasma membrane which acts as a barrier to the chromaffin vesicles access to exocytotic sites. Disassembly of cortical F-actin in response to stimulation allows the movement of vesicles from the reserve pool to the release-ready vesicle pool and, therefore, to exocytotic sites. The dynamics of cortical F-actin is controlled by two mechanisms: a) stimulation-induced Ca2+ entry and scinderin activation and b) protein kinase C (PKC) activation and MARCKS phosphorylation as demonstrated here by experiments with recombinant proteins, antisense olygodeoxynucleotides and vector mediated transient expressions. Under physiological conditions (i.e., cholinergic receptor stimulation followed by Ca2+ entry), mechanism (a) is the most important for the control of cortical F-actin network whereas when Ca2+ is released from intracellular stores (i.e., histamine stimulation) cortical F-actin is regulated mainly by mechanism b.

Actins↗

PubMed2006

Unraveling the relationship between macula densa cell volume and luminal solute concentration/osmolality.

At the macula densa, flow-dependent changes in luminal composition lead to tubuloglomerular feedback and renin release. Apical entry of sodium chloride in both macula densa and cortical thick ascending limb (cTAL) cells occurs via furosemide-sensitive sodium-chloride-potassium cotransport. In macula densa, apical entry of sodium chloride leads to changes in cell volume, although there are conflicting data regarding the directional change in macula densa cell volume with increases in luminal sodium chloride concentration. To further assess volume changes in macula densa cells, cTAL-glomerular preparations were isolated and perfused from rabbits, and macula densa cells were loaded with fluorescent dyes calcein and 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene p-toluenesulfonate. Cell volume was determined with wide-field and multiphoton fluorescence microscopy. Increases in luminal sodium chloride concentration from 0 to 80 mmol/l at constant osmolality led to cell swelling in macula densa and cTAL cells, an effect that was blocked by luminal application of furosemide. However, increases in luminal sodium chloride concentration from 0 to 80 mmol/l with concomitant increases in osmolality caused sustained decreases in macula densa cell volume but transient increases in cTAL cell volume. Increases in luminal osmolality with urea also resulted in macula densa cell shrinkage. These studies suggest that, under physiologically relevant conditions of concurrent increases in luminal sodium chloride concentration and osmolality, there is macula densa cell shrinkage, which may play a role in the macula densa cell signaling process.

Animals↗

PubMed1999

Store-operated Ca2+ entry: evidence for a secretion-like coupling model.

The elusive coupling between endoplasmic reticulum (ER) Ca2+ stores and plasma membrane (PM) "store-operated" Ca2+ entry channels was probed through a novel combination of cytoskeletal modifications. Whereas coupling was unaffected by disassembly of the actin cytoskeleton, in situ redistribution of F-actin into a tight cortical layer subjacent to the PM displaced cortical ER and prevented coupling between ER and PM Ca2+ entry channels, while not affecting inositol 1,4,5-trisphosphate-mediated store release. Importantly, disassembly of the induced cortical actin layer allowed ER to regain access to the PM and reestablish coupling of Ca2+ entry channels to Ca2+ store depletion. Coupling is concluded to be mediated by a physical "secretion-like" mechanism involving close but reversible interactions between the ER and the PM.

Actins↗

PubMed1986

Urodele egg jelly and fertilization.

Fertilization of urodele amphibians is physiologically polyspermic. These amphibians lack sperm entry blocking mechanisms at the egg surface, such as a cortical reaction or a membrane depolarization. Although, egg jelly is necessary for sperm capacitation, a late block to sperm entry does occur about 30 min after fertilization at a precise interface between jelly layers. The jelly is secreted by oviductal cells. In order to investigate its role in fertilization, we studied some biochemical properties of the oviductal secretions of eight species. In double diffusion experiments on agarose plates, some components secreted by the anterior and the middle parts of the oviduct interacted together and formed precipitin lines. This reaction might be responsible for the formation of the dense zone that delimits the capsular chamber. A hemagglutinating activity was found in the anterior or in the posterior part of the oviduct depending on the species. A 18K or 26K lectin was purified respectively from the oviduct of Ambystoma mexicanum and Pleurodeles waltl. In both species, the site where the late block to sperm entry is operative was spatially related to the location of the lectin in the jelly. However, sperm in contact with the purified lectins did not undergo any visible morphological change.

Animals↗