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PubMed1985

Critical neuromonitoring at spinal and brainstem levels by somatosensory evoked potentials.

Electronic averaging makes it possible to analyze somatosensory evoked potentials (SEP) recorded noninvasively from the body surface in man. With noncephalic reference recording, the SEP discloses a series of components that are volume-conducted from distinct open-field generators with a geometry adequate to produce external potential gradients over the head. Farfields are brief positive dips with widespread distribution that present stationary onset and peak latencies all over. They reflect the propagated afferent volley in axons bundles, thus in brachial plexus (P9), dorsal column (P11), and medial lemniscus (P14). Somehow unexpectedly, SEP traces also disclose a widespread prolonged farfield N18 of negative polarity that reflects neural generators in the brainstem below thalamus. Nearfields can be positive or negative, and they reflect neural generators located less than about 50 mm from the electrode. They are influenced to a greater extent by the position of the recording electrodes. For example, neck electrodes can follow the upward propagation of the dorsal column volley (N11), whereas scalp electrodes can map out the distinct contralateral parietal (N20, P27) or frontal (P22, N30) cortical generators. Electrodes around the neck also disclose the posterior N13 and anterior P13 responses that reflect the two sides of the same dorsal horn generator with a horizontal axis. Bit-mapped topographic color imaging of potential fields provides detailed data on time and spatial features of the different SEP neural generators. SEP neuromonitoring can use these results to titrate input to spinal cord (nerve potentials or P9 farfield), spinal generators (N11 nearfield or N13-P13 nearfield in posterior-to-anterior neck montages), brainstem generators (P14 farfield and N18 response), or cortical generators (parietal N20-P27 or frontal P22-N30). The central somatosensory conduction time can be titrated from the spinal entry and cortical arrival times measured in neck and scalp recordings.

Adult↗

PubMed2001

Nicotinic receptors mediate the release of amino acid neurotransmitters in cultured cortical neurons.

Nicotine stimulation of cortical neurons obtained from gestation day 19 rats provoked a dose-dependent release of aspartate, glutamate, glycine and GABA, indicating a functional role for the nicotinic receptor in this model. This release was exclusively Ca2+-dependent (vesicular release) in the case of aspartate and dual Ca2+-dependent and Ca2+-independent) for glutamate, glycine and GABA. Nicotine also raised the membrane potential and the intracellular calcium concentration. These effects were specific, since they were reversed by hexamethonium, an antagonist of the nicotinic receptor. It was shown that L, N, and P/Q type Ca2+ channels are involved in nicotine-mediated Ca2+ entry into cortical neurons. Evaluation of the effects of nicotine on Ca2+ entry in isolated cells showed that 100% of the cells responded to nicotine, although the intensity of the response was variable: 63% of the neurons showed an increase in intracellular Ca(2+) of 152 +/- 5 grey levels, 25% of 88 +/- 12 grey levels and 12% of 48 +/- 1 grey levels. Tetrodotoxin, which blocks voltage-dependent Na(+) channels, completely reversed nicotine-induced Ca2+ entry into single cells. This suggests that the Ca2+ increment is mediated by opening of Ca2+ channels and not by the nicotinic receptor.

Animals↗

PubMed1990

The kappa-opiate agonist U50488H decreases the entry of 45Ca into rat cortical synaptosomes by inhibiting N- but not L-type calcium channels.

The selective kappa-opiate agonist U50488H (1-100 microM) significantly reduced the uptake of 45Ca into cortical synaptosomes from the brain of the rat, in a time- and dose-dependent manner. In physiological medium, the maximum inhibition occurred after 2 min; this was approximately 55% (at 100 microM) and the IC50 was 80 nM. Nifedipine (1 microM) had no significant effect on the influx of Ca2+ in physiological medium (containing 5 mM K+), though, in fact, there was an approximately 20% decrease in the presence of 100 microM of drug. Nifedipine, however, did cause a significant blockade of the entry of 45Ca in medium containing 10 or 15 mM K+, demonstrating that L-type channels on synaptosomes were operational under depolarising conditions. Under these depolarising conditions, there was an additive inhibitory effect on entry of 45Ca into synaptosomes when U50488H (1 microM) and nifedipine (1 microM) were incubated together. Treatment of synaptosomes with omega-conotoxin (omega-CgTx, 0.5 microM) resulted in a 35% reduction in the uptake of 45Ca. omega-Conotoxin (0.5 microM) or naloxone (20 microM) abolished the inhibitory effect of U50488H on the uptake of 45Ca, but naloxone did not alter the blockade of L-type Ca2+ channels, caused by nifedipine. In conclusion, the data demonstrate that under depolarising conditions, there are functional L-type calcium channels on nerve endings in the CNS.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed2001

N-methyl-D-aspartate channel and consciousness: from signal coincidence detection to quantum computing.

Research on Blindsight, Neglect/Extinction and Phantom limb syndromes, as well as electrical measurements of mammalian brain activity, have suggested the dependence of vivid perception on both incoming sensory information at primary sensory cortex and reentrant information from associative cortex. Coherence between incoming and reentrant signals seems to be a necessary condition for (conscious) perception. General reticular activating system and local electrical synchronization are some of the tools used by the brain to establish coarse coherence at the sensory cortex, upon which biochemical processes are coordinated. Besides electrical synchrony and chemical modulation at the synapse, a central mechanism supporting such a coherence is the N-methyl-D-aspartate channel, working as a 'coincidence detector' for an incoming signal causing the depolarization necessary to remove Mg(2+), and reentrant information releasing the glutamate that finally prompts Ca(2+) entry. We propose that a signal transduction pathway activated by Ca(2+) entry into cortical neurons is in charge of triggering a quantum computational process that accelerates inter-neuronal communication, thus solving systemic conflict and supporting the unity of consciousness.

Animals↗

PubMed2001

Zn(2+) induces permeability transition pore opening and release of pro-apoptotic peptides from neuronal mitochondria.

Rapid entry of Ca(2+) or Zn(2+) kills neurons. Mitochondria are major sites of Ca(2+)-dependent toxicity. This study examines Zn(2+)-initiated mitochondrial cell death signaling. 10 nm Zn(2+) induced acute swelling of isolated mitochondria, which was much greater than that induced by higher Ca(2+) levels. Zn(2+) entry into mitochondria was dependent upon the Ca(2+) uniporter, and the consequent swelling resulted from opening of the mitochondrial permeability transition pore. Confocal imaging of intact neurons revealed entry of Zn(2+) (with Ca(2+)) to cause pronounced mitochondrial swelling, which was far greater than that induced by Ca(2+) entry alone. Further experiments compared the abilities of Zn(2+) and Ca(2+) to induce mitochondrial release of cytochrome c (Cyt-c) or apoptosis-inducing factor. In isolated mitochondria, 10 nm Zn(2+) exposures induced Cyt-c release. Induction of Zn(2+) entry into cortical neurons resulted in distinct increases in cytosolic Cyt-c immunolabeling and in cytosolic and nuclear apoptosis-inducing factor labeling within 60 min. In comparison, higher absolute [Ca(2+)](i) rises were less effective in inducing release of these factors. Addition of the mitochondrial permeability transition pore inhibitors cyclosporin A and bongkrekic acid decreased Zn(2+)-dependent release of the factors and attenuated neuronal cell death as assessed by trypan blue staining 5-6 h after the exposures.

Animals↗

PubMed2026

ARX mutation-associated interneuron defects provide insights into mechanisms underlying developmental epilepsies.

Cortical interneuron (cIN) dysfunction is associated with various neurodevelopmental and neurological disorders, including developmental epilepsies, autism spectrum disorders and intellectual disabilities. Mutations in ARX (aristaless-related homeobox) are linked to these conditions, with or without accompanying structural brain anomalies. We previously demonstrated that the loss of Arx in the mouse ganglionic eminence, the birthplace of cINs, is associated with seizures, whereas its loss in cortical excitatory neuron progenitor cells results in structural anomalies but no seizures. To elucidate the pathophysiological role of ARX in cINs and its relationship to seizure phenotype, Arx conditional mutant mouse lines were investigated using Gad2- and Nkx2.1-Cre drivers to target distinct populations in the cIN lineage. Our data demonstrate that ARX abrogation results in defects in cIN density and distribution, as well as perinatal lethality. In these mice, we observed defects in cell cycle exit, a biased loss of the marginal zone migration stream of cINs, shifts in cell fate from caudal ganglionic eminence to medial ganglionic eminence identity, and a reduced number of parvalbumin⁺ and somatostatin⁺ cINs, with parvalbumin⁺ cINs being more severely affected. Single-cell RNA sequencing combined with chromatin immunoprecipitation and sequencing revealed that ARX regulates key processes involved in cell cycle progression, cIN subtype differentiation and cIN migration. Investigation of one downregulated target gene, Lmo1, uncovered a potential mechanism by which ARX regulates the number and distribution of cINs in the cortex. Cortical slice cultures demonstrate that LMO1 inhibits cIN migration by repressing Cxcr4 expression, which encodes a key receptor involved in cortical guidance. These data indicate that ARX positively regulates cIN migration by derepressing LMO1's repressive role. Consistent with our mouse model, we observed a significant loss of parvalbumin+ and somatostatin+ cINs in the brain of a patient carrying a pathogenic variant of ARX, who was diagnosed with developmental epileptic encephalopathy. Together, our data provide novel insights into how ARX and its target genes regulate cIN development and migration and into the pathogenic mechanisms underlying a spectrum of neurodevelopmental disorders linked to loss of ARX.

Animals↗

PubMed1977

Operative techniques for management of lesions involving the dural venous sinuses.

The basic principles of vascular surgery, adequate exposure, proximal and distal control of hemorrhage, and meticulous approximation of endothelial surfaces should be adhered to in the management of lesions of the dural venous sinuses. Modification of conventional vascular techniques must be made since the major dural venous sinuses are essentially non collapsible and non mobilizable because of the entry of cortical veins at frequent intervals along their course. These problems can be solved by occlusion of the proximal and distal segments of the sinus from within the lumen and by use of a shunt consisting of a siliconized non-collapsible tube with an inflatable balloon cuff at each end. Saphenous vein autografts are used if primary repair is impossible because of loss of tissue. Using these techniques, a patency rate of 91% and a mortality rate of 9% were achieved in eleven cases involving the posterior sagittal and transverse sinuses.

Brain Injuries↗

PubMed1991

Feedback inhibition of cyclic adenosine monophosphate-stimulated Na+ transport in the rabbit cortical collecting duct via Na(+)-dependent basolateral Ca++ entry.

Arginine vasopressin (AVP) transiently stimulates Na+ transport in the rabbit cortical collecting duct (CCD). However, the sustained effect of both AVP and its putative second messenger, cyclic adenosine monophosphate (cAMP), on Na+ transport in the rabbit CCD is inhibitory. Because maneuvers that increase [Ca++]i inhibit Na+ transport, the effects of AVP and cell-permeable cAMP analogues, on [Ca++]i were investigated in fura-2-loaded in vitro microperfused rabbit CCDs. Low-dose AVP (23-230 pM) selectively stimulated Ca++ influx, whereas 23 nM AVP additionally released calcium from intracellular stores. 8-chlorophenylthio-cAMP (8CPTcAMP) and 8-bromo-cAMP (8-Br-cAMP) also increased CCD [Ca++]i. The 8CPTcAMP-stimulated [Ca++]i increase was totally dependent on basolateral [Ca++]. In the absence of cAMP, peritubular Na+ removal produced a marked increase in [Ca++]i, which was also dependent on bath [Ca++], suggesting the existence of basolateral Na+/Ca++ exchange. Luminal Na+ removal in the absence of cAMP did not alter CCD [Ca++]i, but it completely blocked the cAMP-stimulated [Ca++]i increase. Thus the cAMP-dependent Ca++ increase is totally dependent on both luminal Na+ and basolateral Ca++, suggesting the [Ca++]i increase is secondary to cAMP effects on luminal Na+ entry and its coupling to basolateral Na+/Ca++ exchange. 8CPTcAMP inhibits lumen-to-bath 22Na flux [JNa(l-b)] in CCDs bathed in a normal Ca++ bath (2.4 mM). However, when bath Ca++ was lowered to 100 nM, a maneuver that also blocks the 8CPTcAMP [Ca++]i increase, 8CPTcAMP stimulated, rather than inhibited JNa(l-b). These results suggest that cAMP formation initially stimulates CCD Na+ transport, and that increased apical Na+ entry secondarily activates basolateral Ca++ entry. The cAMP-dependent [Ca++]i increase leads to inhibition Na+ transport in the rabbit CCD.

Animals↗

PubMed1999

Zn2+ entry produces oxidative neuronal necrosis in cortical cell cultures.

Evidence has accumulated that Zn2+ plays a central role in neurodegenerative processes following brain injuries including ischaemia or epilepsy. In the present study, we examined patterns and possible mechanisms of Zn2+ neurotoxicity. Inclusion of 30-300 microM Zn2+ for 30 min caused neuronal necrosis apparent by cell body and mitochondrial swelling in cortical cell cultures. This Zn2+ neurotoxicity was not attenuated by antiapoptosis agents, inhibitors of protein synthesis or caspase. Blockade of glutamate receptors or nitric oxide synthase showed no beneficial effect against Zn2+ neurotoxicity. Interestingly, antioxidants, trolox or SKF38393, attenuated Zn(2+)-induced neuronal necrosis. Pretreatment with insulin or brain-derived neurotrophic factor increased the Zn(2+)-induced free radical injury. Kainate or AMPA facilitated Zn2+ entry and potentiated Zn2+ neurotoxicity in a way sensitive to trolox. Reactive oxygen species and lipid peroxidation were generated in the early phase of Zn2+ neurotoxicity. These findings indicate that entry and accumulation of Zn2+ result in generation of toxic free radicals and then cause necrotic neuronal degeneration under certain pathological conditions in the brain.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed2000

Visual loss and central venous catheterization: cortical blindness and hemianopsia after inadvertent subclavian artery entry.

A case of presumed embolic transient ischemic episodes and multifocal infarcts to the occipital and parietal cortices and the cerebellum of a young woman with ulcerative colitis is reported. These episodes were manifested by multifocal neurologic deficits including cortical blindness, visual hallucinations, and homonymous hemianopsia. They correlated with parenteral nutrition via a central line, presumed venous, but found to be in the subclavian artery. The complications of central venous lines are reviewed. The need for attention to neighborhood structures and unexpected symptoms, in view of the less well-recognized arterial embolic complications is emphasized.

Adult↗

PubMed2004

Drosophila Wee1 kinase regulates Cdk1 and mitotic entry during embryogenesis.

Cyclin-dependent kinases (Cdks) are the central regulators of the cell division cycle. Inhibitors of Cdks ensure proper coordination of cell cycle events and help regulate cell proliferation in the context of tissues and organs. Wee1 homologs phosphorylate a conserved tyrosine to inhibit the mitotic cyclin-dependent kinase Cdk1. Loss of Wee1 function in fission or budding yeast causes premature entry into mitosis. The importance of metazoan Wee1 homologs for timing mitosis, however, has been demonstrated only in Xenopus egg extracts and via ectopic Cdk1 activation . Here, we report that Drosophila Wee1 (dWee1) regulates Cdk1 via phosphorylation of tyrosine 15 and times mitotic entry during the cortical nuclear cycles of syncytial blastoderm embryos, which lack gap phases. Loss of maternal dwee1 leads to premature entry into mitosis, mitotic spindle defects, chromosome condensation problems, and a Chk2-dependent block of subsequent development, and then embryonic lethality. These findings modify previous models about cell cycle regulation in syncytial embryos and demonstrate that Wee1 kinases can regulate mitotic entry in vivo during metazoan development even in cycles that lack a G2 phase.

Animals↗

PubMed2004

Switch from intracellular to intercellular invasion during water stress-tolerant legume nodulation.

Rhizobia colonize their legume hosts by different modes of entry while initiating symbiotic nitrogen fixation. Most legumes are invaded via growing root hairs by the root hair-curl mechanism, which involves epidermal cell responses. However, invasion of a number of tropical legumes happens through fissures at lateral root bases by cortical, intercellular crack entry. In the semiaquatic Sesbania rostrata, the bacteria entered via root hair curls under nonflooding conditions. Upon flooding, root hair growth was prevented, invasion on accessible root hairs was inhibited, and intercellular invasion was recruited. The plant hormone ethylene was involved in these processes. The occurrence of both invasion pathways on the same host plant enabled a comparison to be made of the structural requirements for the perception of nodulation factors, which were more stringent for the epidermal root hair invasion than for the cortical intercellular invasion at lateral root bases.

Ethylenes↗

PubMed1994

Effects of pH on apical calcium entry and active calcium transport in rabbit cortical collecting system.

Rabbit connecting tubules and cortical collecting ducts were isolated by immunodissection and cultured on permeable supports. The monolayers actively transported Ca2+ with a net transcellular rate of 92 +/- 3 nmol.h-1.cm-2. Methoxyverapamil, felodipine, diltiazem, omega-conotoxin GVIA, and omega-agatoxin IVA when added to the apical side had no effect on Ca2+ absorption. Neither hyperpolarization nor depolarization of the apical membrane affected Ca2+ transport rates significantly. Stepwise lowering of the apical pH (pHa) from 8.0 to 5.6 gradually inhibited Ca2+ transport from 88 +/- 5 to 7 +/- 2 nmol.h-1.cm-2. Measuring the intracellular pH (pHi) with 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein revealed that lowering the pHa from 8.0 to 5.6 decreased pHi from 7.8 to 6.7. To determine whether inhibition of Ca2+ absorption results from intracellular acidification, pHi was lowered using an NH4Cl pulse while extracellular pH was kept constant. Intracellular acidification from 7.4 +/- 0.2 to 6.9 +/- 0.1 reduced Ca2+ absorption by 26 +/- 6% only. In addition, lowering of the basolateral pH to 6.2 resulted in a pHi of 6.8 +/- 0.1, without affecting Ca2+ absorption rates. In conclusion, the basal Ca2+ influx mechanism in the apical membrane is most likely a voltage-independent Ca2+ transporter, insensitive to Ca2+ channel blockers, but strongly inhibited by apical acidification.

Animals↗

PubMed2003

Recognition by top-down and bottom-up processing in cortex: the control of selective attention.

Visual recognition is achieved by a hierarchy of bidirectionally connected cortical areas. The entry of signals into higher areas involves the serial sampling of information within a movable window of attention. Here we explore how the cortex can move this window and integrate the sampled information. To make this concrete, we modeled the process of visual word recognition by hierarchical cortical areas representing features, letters, and words. At the start of the recognition process, nodes representing all contextually possible words are active. Simple connectivity rules allow a parallel top-down (T-D) computation of the relative probability of each feature at each location given the set of active words. This information is then used to guide the window of attention to information-rich features (e.g., a feature that is present in the visual image but has lowest probability). Bottom-up processing of this feature excludes words that do not contain it and leads to T-D recomputation of feature probabilities. Recognition occurs after several such cycles when all but one word has been excluded. We show that when 950 words are stored in long-term memory, recognition occurs after an average of 4.9 cycles. Because covert attention can be moved every 20-30 ms, word recognition could be as fast as determined experimentally (<200 ms of cortical processing). This model accounts for the findings that recognition time depends logarithmically on set size, recognition time is reduced when context reduces the number of possible targets, the time to classify a nonword decreases when its approximation to English decreases, and in high level cortex, the firing of neurons tuned to an object increases progressively as its recognition occurs. More generally the model provides a physiologically plausible view of how bi-directional signal flow in cortex guides attention to produce efficient recognition.

Animals↗

PubMed1999

An investigation of the latency period between sperm oolemmal adhesion and oocyte penetration.

In clinical studies of the ability of capacitated human sperm to penetrate zona-free hamster eggs, we have previously observed that the ratio of oolemmal adherent to penetrating sperm varied between men. Sperm incorporation did not occur immediately following gamete adhesion and not all adherent sperm penetrated the egg. To further investigate this phenomenon, comparisons were made of the kinetics of gamete adhesion, membrane fusion, and sperm incorporation of capacitated mouse and human spermatozoa by zona-free hamster eggs and of mouse sperm by zona-free mouse and hamster eggs. Eggs were inseminated with either capacitated human or mouse sperm or combinations of both, washed out of sperm suspension after initial gamete adherence, and further incubated in sperm-free medium. Gamete membrane fusion was judged by dye transfer of Hoechst 33342 and sperm entry of the cortical ooplasm by observation of expanded sperm heads within acridine orange stained eggs. Oolemmal adherent mouse and human sperm fused with and penetrated zona-free hamster eggs at different times whether eggs were inseminated in parallel or with combinations of sperm of both species. Oolemmal adherent mouse sperm penetrated zona-free hamster eggs prior to their penetration of zona-free mouse eggs. Ultrastructural studies of zona-free human eggs inseminated with human sperm confirmed prior observations with hamster eggs that only acrosome-reacted human sperm adhere to the oolemma. These results have lead us to postulate that sperm entry into the egg may occur through a "zipper" mechanism involving the ligation of local gamete receptors similar to the incorporation of target particles by phagocytes and suggest that not all oolemmal adherent human sperm are capable of being incorporated although they have undergone an acrosome reaction.

Animals↗

PubMed2005

Is the failure to detect stimulus deviance during sleep due to a rapid fading of sensory memory or a degradation of stimulus encoding?

The mismatch negativity (MMN) is thought to reflect the outcome of a system responsible for the detection of change in an otherwise repetitive, homogenous acoustic environment. This process depends on the storage and maintenance of a sensory representation of the frequently presented stimulus to which the deviant stimulus is compared. Few studies have been able to record the MMN in non-rapid eye movement (NREM) sleep. This pattern of results might be explained by either a rapid fading of sensory memory or an inhibition of stimulus input prior to entry into the cortical MMN generator site. The present study used a very rapid rate of presentation in an attempt to capture mismatch-related negativity prior to the fading of sensory memory. Auditory event-related potentials were recorded from 12 subjects during a single sleep period. A 1000 Hz standard stimulus was presented every 150 ms. At random, on 6.6% of the trials, the standard was changed to either a large 2000 Hz or a small 1100 Hz deviant. In wakefulness, the large deviant elicited an extended negativity that was reduced in amplitude following the presentation of the small deviant. This negativity was also apparent during REM sleep following the presentation of the large deviant. These deviant-related negativities (DRNs) were probably a composite of N1 and MMN activity. During NREM sleep (stage 2 and slow-wave sleep), only the large deviant continued to elicit a DRN. However this DRN might be overlapped by the initial activity of a component that is unique to sleep, the N350. There was little evidence of the DRN or the MMN during sleep following the presentation of the small deviant. A rapid rate of presentation, therefore, does not preserve the MMN following small deviance within sleep. It is possible that inhibition of sensory input occurs before entry into the MMN generating system in the temporal cortex.

Adolescent↗

PubMed1984

A stereotaxic atlas of the brain of the cynomolgus monkey (Macaca fascicularis).

Outline drawings of representative frontal sections of the Macaca fascicularis brain are presented in stereotaxic coordinates. The levels extend from the rostral tip of the neostriatum to the posterior end of the deep cerebellar nuclei. The illustrations are based on the photographs of unstained frozen sections of three formalin-fixed brains in which stainless steel needles were inserted to mark the horizontal zero and several anteroposterior positions. The sections were not stained in order to prevent shrinkage. Stereotaxic measurements were taken in situ of the highest points on the cortical surface, the position of the central and lunate sulcus, and of certain landmarks at the base of the cranium in a large number of monkeys. These data along with brain dimensions and the weight of animals are displayed in tables to indicate individual variations and to aid investigators in determining the best stereotaxic coordinates for a given structure. It is recommended that the cortical point of entry for an electrode or needle be routinely noted and be compared to the parameters in the atlas to compensate for deviations in the horizontal plane.

Animals↗

PubMed1994

A Xenopus maternal effect mutant gene affects oocyte meiotic reinitiation and fertilization.

No cleavage (nc) is a maternal effect mutant gene, recessive and sex limited. It affects the eggs laid by homozygous mutant females, independently of the male genotype. Contrary to normal oocytes, following germinal vesicle breakdown (GVBD) during maturation, the transient microtubular array (TMA) is not formed, nor are the meiotic spindles. Cytoplasmic asters with condensed chromosomes are present in the majority of oocytes, as well as microtubular bundles and sometimes cytoplasmic spindle-like asters. These mature oocytes exhibit a disturbance in yolk platelet arrangements. The white spot is rather irregular, and the maturation period is longer than normal. Transfers of cytoplasm from nc mature oocytes into normal stage VI oocytes resulted in abnormal maturation of the normal oocytes. Reciprocal transfers (cytoplasm from normal mature oocytes into nc stage VI oocytes) induce the formation of spindles, usually cytoplasmic; this indicates that the deficiency can be partly rescued. Following fertilization, the nc eggs show neither contraction nor rotation; polyspermy is present in the majority of cases. Even in the same egg, simultaneous spindles and nuclei can be observed, revealing a disturbance in the spatial localization of regulators of the cell cycle. Cytokinesis never occurs. Polyspermy results from the absence of cortical reaction following sperm entry. However, when mature nc oocytes are treated with PMA, they show cortical granule exocytosis and the formation of an altered vitelline envelope. The different factors possibly involved in these anomalies are discussed in relation to cytoarchitectural disorganization of the cell and abnormal cell cycle regulation.

Animals↗