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PubMed1980

Arachidonic acid-induced swelling in incubated rat brain cortical slices. Effect of bovine serum albumin.

The influence of bovine serum albumin (BSA) on the rat brain cortical swelling induced by sodium arachidonate and polyunsaturated fatty acids has been studied. Coincubation of arachidonate with BSA at a molar ratio of 5 (arachidonate/BSA) or less greater inhibited the arachidonate-induced swelling. As the molar ratio of arachidonate/BSA increased, the degree of swelling increased. The swelling was not reversed by BSA, although the BSA released 46% of the previously incorporated [3H]arachidonic acid from the cortical slices. The entry of [3H]arachidonate into the slice was completely abolished by 0.1 mM BSA or partially inhibited by exogenous arachidonate. It is concluded that the induction of brain swelling by arachidonate requires the intracellular transport of exogenous arachidonate.

Animals↗

PubMed2000

Cell cycle regulation in the course of nodule organogenesis in Medicago.

The molecular mechanisms of de novo meristem formation, cell differentiation and the integration of the cell cycle machinery into appropriate stages of the developmental programmes are still largely unknown in plants. Legume root nodules, which house nitrogen-fixing rhizobia, are unique plant organs and their development may serve as a model for organogenetic processes in plants. Nodules form and are essential for the plant only under limitation of combined nitrogen in the soil. Moreover, their development is triggered by external mitogenic signals produced by their symbiotic partners, the rhizobia. These signals, the lipochitooligosaccharide Nod factors, act as host-specific morphogens and induce the re-entry of root cortical cells into mitotic cycles. Maintenance of cell division activity leads to the formation of a persistent nodule meristem from which cells exit continuously and enter the nodule differentiation programme, involving multiple cycles of endoreduplication and enlargement of nuclear and cell volumes. While the small diploid 2C cells remain uninfected, the large polyploid cells can be invaded and, after completing the differentiation programme, host the nitrogen-fixing bacteroids. This review summarizes the present knowledge on cell cycle reactivation and meristem formation in response to Nod factors and reports on a novel plant cell cycle regulator that can switch mitotic cycles to differentiation programmes.

Cell Cycle↗

PubMed2002

Surgical indications and microsurgical anatomy of the transchoroidal fissure approach for lesions in and around the ambient cistern.

OBJECTIVE: Opening the temporal part of the choroidal fissure (CF) makes it possible to expose the crural cistern, the ambient cistern, and the medial temporal lobe. We examined the microsurgical anatomy and the surgical indications for use of the trans-CF approach. METHODS: The microsurgical anatomy encountered in the trans-CF approach for lesions in and around the ambient cistern was studied in three cadavers. On the basis of these cadaveric studies, the trans-CF approach was used during surgery in three live patients with such lesions. RESULTS: The angiographic "plexal point," which indicates the entrance of the anterior choroidal artery as it enters the temporal horn of the lateral ventricle, was thought to be a key anatomic landmark of the trans-CF approach. A cortical incision for entry into the temporal horn should be made in the inferior temporal gyrus to minimize the potential damage to the optic radiations and to the speech centers. After the CF is opened posteriorly to the plexal point between the tenia fimbria and the choroid plexus, the posterior cerebral artery (PCA) in the ambient cistern can be observed with minimal caudal retraction of the hippocampus. In this study, surgical procedures using the trans-CF approach were successfully performed on patients with high-positioned P2 aneurysms whose PCA ran close to the plexal point or higher, whose medial temporal arteriovenous malformations were fed mainly by the PCA, and whose tentorial hiatus meningiomas protruded into the temporal horn through the CF, with no resulting postoperative visual or memory disturbances. CONCLUSION: The trans-CF approach is especially useful in surgery for lesions in and around the ambient cistern.

Adult↗

PubMed1997

On the relationships between the striatum and the pedunculopontine tegmental nucleus.

In this essay we consider the role of the pedunculopontine tegmental nucleus as a striatal output station. We review the relevant anatomical, electrophysiological, behavioral, and pathological studies and conclude that the pedunculopontine tegmental nucleus occupies an important position in striatal outflow, receiving motor output from the dorsal striatum and information from the ventral striatum relating to limbic processes of motivation and reinforcement. The hypothesis we present is that the pedunculopontine tegmental nucleus is at the very least an integral component of the limbic-motor interface, although in discussing this concept we also assess the likelihood that the limbic-motor interface is in fact a distributed system-that is, that limbic-motor interfacing is not all done by a single structure in the central nervous system but that different aspects of it are served by different systems. We present the hypothesis that the pedunculopontine tegmental nucleus is one critical site through which limbic information concerned with motivation, reinforcement, and the construction of novel associations can gain access to a stream of motor outflow coming from the caudate-putamen and directed toward pontomedullary systems without reference back to the cerebral cortex. This hypothesis is important because it highlights striatal outflow, which is not processed through the cortical re-entry systems, and also emphasizes the importance of pontine systems in cognitive processing.

Caudate Nucleus↗

PubMed2002

N-myc promotes survival and induces S-phase entry of postmitotic sympathetic neurons.

In most postmitotic neurons, expression or activation of proteins that stimulate cell cycle progression or DNA replication results in apoptosis. One potential exception to this generalization is neuroblastoma (NB), a tumor derived from the sympathoadrenal lineage. NBs often express high levels of N-myc, a proto-oncogene that can potently activate key components of the cell cycle machinery. Here, we show that in postmitotic sympathetic neurons, N-myc can induce S-phase entry while protecting neurons from death caused by aberrant cell cycle reentry. Specifically, these experiments demonstrate that expression of N-myc at levels similar to those in NBs caused sympathetic neurons to reenter S-phase, as monitored by 5-bromo-2-deoxyuridine incorporation and expression of cell cycle regulatory proteins, and rescued them from apoptosis induced by withdrawal of their obligate survival factor, nerve growth factor. The N-myc-induced cell cycle entry, but not enhanced survival, was inhibited by coexpression of a constitutively hypophosphorylated form of the retinoblastoma tumor suppressor protein, suggesting that these two effects of N-myc are mediated by separate pathways. In contrast, N-myc did not cause S-phase entry in postmitotic cortical neurons. Thus, N-myc both selectively causes sympathetic neurons to reenter the cell cycle and protects them from apoptosis, potentially contributing to their transformation to NBs.

Adenoviridae↗

PubMed1977

Fertilization of immature frog eggs: cleavage and development following subsequent activation.

Frog eggs are normally fertilized after reaching metaphase II. When eggs are inseminated prior to that, several sperm enter, but entry does not activate the egg. When such inseminated, immature eggs were maintained until they became mature and then were artificially activated, the eggs began to cleave. The cleavage furrows were irregular and often multiple, but the eggs developed to blastulae or partial blastulae. About 2 leads to 5% of the eggs developed to tadpoles. Typical asters were not associated with the entering sperm; rather, asters appeared only after activation. The sperm nucleus often formed chromosomes which were attached to small spindles. It is clear that sperm which remain for a time in unactivated egg cytoplasm, retain their ability to promote cleavage and development. Aster formation required not only sperm centrioles but also activated egg cytoplasm. Sperm which entered either near the equator or in the animal half of mature eggs usually produced normal cleavage furrows. Sperm which entered the animal half of immature eggs produced multiple animal half furrows when the egg was subsequently activated. In contrast, sperm which entered near the equator of immature eggs often failed to induce furrowing on subsequent activation or produced unusual equatorial furrows. The difference in the type of furrow between eggs inseminated in the animal half or at the equator is interpreted as a consequence of dissociating sperm entry from the cortical contraction which occurs in activation.

Animals↗

PubMed1993

Rat cortical synaptosomes have more than one mechanism for Ca2+ entry linked to rapid glutamate release: studies using the Phoneutria nigriventer toxin PhTX2 and potassium depolarization.

PhTX2, one of the components of the venom of the South American spider Phoneutria nigriventer, inhibits the closure of voltage-sensitive Na+ channels. Incubation of cerebral-cortical synaptosomes with PhTX2 causes a rapid increase in the intrasynaptosomal free Ca2+ concentration and a dose-dependent release of glutamate. This release is made up of a slow component, which appears to be due to reversal of Na(+)-dependent glutamate uptake, and more rapid component that is dependent on the entry of extrasynaptosomal Ca2+. It has previously been shown that membrane depolarization using KCl can cause rapid Ca(2+)-dependent release of glutamate from synaptosomes. This requires Ca2+ entry through a specific type of Ca2+ channel that is sensitive to Aga-GI, a toxic component of the venom of the spider Agelenopsis aperta. We have compared the effects of PhTX2 and KCl on elevation of intrasynaptosomal free Ca2+ and glutamate release, and a number of differences have emerged. Firstly, PhTX2-mediated Ca2+ influx and glutamate release, but not those caused by KCl, are inhibited by tetrodotoxin. Secondly, KCl produces a clear additional increase in Ca2+ and glutamate release following those elicited by PhTX2. Finally, 500 microM MnCl2 abolishes PhTX2-mediated, but not KCl-mediated, glutamate release. These findings suggest that more than one mechanism of Ca2+ entry may be coupled to glutamate release from nerve endings.

Animals↗

PubMed1991

Quantitative microfocal radiographic assessment of disease and progression in osteoarthritis of the hand.

Macroradiographic examination of the wrists and hands of 32 patients with osteoarthritis (OA) over an 18 month period showed that, compared with healthy control subjects, 44% of the patients had significant joint space narrowing at entry, which increased to 65%. Subchondral cortical thickness was greater in all patients at entry and increased with time. Osteophytes and juxtaarticular radiolucencies were present in all patients at study entry; by the end, osteophytes had increased in number and area, and juxtaarticular radiolucencies in area only. We conclude that in OA of the hand, bony changes have progressed significantly before joint space narrowing.

Aged↗

PubMed2003

ATP-induced, sustained calcium signalling in cultured rat cortical astrocytes: evidence for a non-capacitative, P2X7-like-mediated calcium entry.

The receptor mechanisms regulating the ATP-induced free cytosolic Ca(2+) concentration ([Ca(2+)](i)) changes in cultured rat cortical type-1 astrocytes were analyzed using fura-2-based Ca(2+) imaging microscopy. Upon prolonged ATP challenge (1-100 microM), astroglial cells displayed a biphasic [Ca(2+)](i) response consisting of an initial peak followed by a sustained elevation. Suramin and pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid blocked both components, albeit to a different extent. By contrast, the selective P2X7 antagonist oxidized ATP irreversibly abrogated the sustained [Ca(2+)](i) signal without affecting the transient phase. Finally, astrocyte challenge with the selective P2X7 agonist 3'-O-(4-benzoyl)benzoyl-ATP evoked a sustained [Ca(2+)](i) elevation, which occluded that induced by ATP. We can conclude that in cultured cortical astrocytes the ATP-mediated sustained [Ca(2+)](i) rise does not implicate capacitative Ca(2+) entry but involves Ca(2+) influx through P2X7-like receptors.

Adenosine Triphosphate↗

PubMed2001

Inositol 1,4,5-triphosphate receptor-sensitive Ca(2+) release, store-operated Ca(2+) entry, and cAMP responsive element binding protein phosphorylation in developing cortical cells following exposure to polychlorinated biphenyls.

The present study assessed intracellular Ca(2+) signaling pathways sensitive to polychlorinated biphenyls (PCBs), xenobiotics that perturb neural development and plasticity. Mobilization of intracellular Ca(2+) stores after acute exposure to a PCB mixture, Aroclor 1254 (A1254), as well as selected PCB congeners, was studied in P0 rat cortical neuronal culture using fluorescence microscopy. Ca(2+) responses to A1254 progressed from a transient intracellular Ca(2+) increase (lasting 3--5 min) at 1 to 2 microM (0.3-0.6 ppm) to a Ca(2+) transient with store-operated Ca(2+) influx and later disturbances of basal Ca(2+) concentration; this latter pattern occurred more often with 10 to 20 microM (3--6 ppm) A1254. Thapsigargin, xestospongin C, and carbachol/Ca(2+)-free buffer blocked significantly the PCB-induced Ca(2+) transient, whereas both ryanodine (to deplete ryanodine-sensitive stores) and the L-type Ca(2+) channel blocker nifedipine were without effect on the A1254 initial Ca(2+) transient. Both thapsigargin and xestospongin also blocked latent elevations (at 0.5 h) in Ca(2+), disturbances that depend upon extracellular Ca(2+) entry via ion channels. Two possible consequences were explored. Phosphorylation of cAMP responsive element binding protein, a Ca(2+)-activated nuclear transcription factor (CREB), occurred in an A1254 concentration-dependent manner and persisted at least 1 h. Cell viability following a 24-h exposure to A1254 (2-20 microM) was decreased at 20 microM, but only in cells cultured >6 days. This cell death did not occur via an apoptotic mechanism. These results indicate that Ca(2+) disturbances following PCB exposure are associated with 1) discrete alterations in IP(3) receptor-mediated signals and 2) activation of downstream events that impact developing cortical cells.

Animals↗

PubMed1990

Sodium entry routes in principal and intercalated cells of the isolated perfused cortical collecting duct.

Transmembrane sodium transport pathways were studied in principal and intercalated cells of the isolated perfused rabbit cortical collecting duct. Intracellular electrolyte concentrations in individual collecting duct cells were measured by electron microprobe analysis during blockage of basolateral Na-K-ATPase by ouabain and simultaneous inhibition of sodium entry across the apical and/or basolateral cell membrane. In principal cells the ouabain-induced rise in cell sodium concentration could only partially be blocked by amiloride (10(-4) mol/l) in the perfusion fluid. Amiloride (10(-3) mol/l) added to the bathing solution produced a further, significant reduction of sodium influx. In principal cells the ouabain-induced increase in sodium concentration was completely prevented by amiloride in the perfusion solution in combination with omission of sodium from the peritubular bathing solution. In intercalated cells ouabain caused a less pronounced increase in sodium concentration than in principal cells. Neither amiloride in the perfusate, nor amiloride in both bathing and perfusion solution, significantly reduced the ouabain-induced rise in intercalated cell sodium concentration. These results indicate that in principal cells amiloride-sensitive sodium channels constitute the predominant pathway for sodium entry across the apical cell membrane. In addition, substantial amounts of sodium enter principal cells across the basolateral cell membrane, probably via Na-H exchange. Finally, the data suggest that in intercalated cells sodium channels and the Na-H exchange are sparse or even absent.

Amiloride↗

PubMed1997

Electrophysiological changes during the sleep onset period of psychophysiological insomniacs, psychiatric insomniacs, and normal sleepers.

The electroencephalograms (EEGs) of the sleep onset period (SOP) of psychophysiogical insomniacs. psychiatric insomniacs, and controls were compared using power spectral analysis. We predicted that psychophysiological insomniacs would show elevated cortical arousal throughout their entry into sleep. Electroencephalograms, electrooculograms (EOGs), and electromyograms (EMGs) were recorded for two consecutive nights. Power spectral analysis of EEG from the sleep onset period was performed on all standard frequency bands. Psychophysiological insomniacs had less alpha during the first part of the SOP and did not show the dramatic drop in alpha across the SOP that characterizes normal sleep. They showed less delta in the last quartile of the chronological analysis of the SOP. Psychiatric insomniacs showed lower relative beta power values overall, while psychophysiological insomniacs showed higher relative beta power values during wakefulness. This microanalysis indicates that the SOP is generally similar for psychiatric insomniacs and normal sleepers but that clear differences in the SOP of psychophysiological insomniacs exist. They have higher cortical arousal during the SOP than do psychiatric insomniacs and controls. The dramatic changes in power values in the latter two groups as sleep begins are not seen in the psychophysiological insomniacs, which may help explain the difficulty that psychophysiological insomniacs have discriminating between wakefulness and sleep.

Adult↗

PubMed1999

Cortical auditory signal processing in poor readers.

Magnetoencephalographic responses recorded from auditory cortex evoked by brief and rapidly successive stimuli differed between adults with poor vs. good reading abilities in four important ways. First, the response amplitude evoked by short-duration acoustic stimuli was stronger in the post-stimulus time range of 150-200 ms in poor readers than in normal readers. Second, response amplitude to rapidly successive and brief stimuli that were identical or that differed significantly in frequency were substantially weaker in poor readers compared with controls, for interstimulus intervals of 100 or 200 ms, but not for an interstimulus interval of 500 ms. Third, this neurological deficit closely paralleled subjects' ability to distinguish between and to reconstruct the order of presentation of those stimulus sequences. Fourth, the average distributed response coherence evoked by rapidly successive stimuli was significantly weaker in the beta- and gamma-band frequency ranges (20-60 Hz) in poor readers, compared with controls. These results provide direct electrophysiological evidence supporting the hypothesis that reading disabilities are correlated with the abnormal neural representation of brief and rapidly successive sensory inputs, manifested in this study at the entry level of the cortical auditory/aural speech representational system(s).

Acoustic Stimulation↗

PubMed2005

Nitric oxide modulates calcium entry through P/Q-type calcium channels and N-methyl-d-aspartate receptors in rat cortical neurons.

Voltage-gated calcium channels (VGCC) and N-methyl-d-aspartate receptors (NMDAR) account for most of the depolarization-induced neuronal calcium entry. The susceptibility of individual routes of calcium entry for nitric oxide (NO) is largely unknown. We loaded cultured rat cortical neurons with fluo-4 acetoxymethylester to study the effect of the NO synthase inhibitor Nomega-nitro-l-arginine and the NO donor S-nitroso-N-acetylpenicillamine on the intracellular calcium concentration ([Ca2+]i). The potassium-induced [Ca2+]i increase was amplified by Nomega-nitro-l-arginine and attenuated by S-nitroso-N-acetylpenicillamine. This modulation was abolished by either the P/Q-type VGCC antagonist omega-agatoxin IVA or by the NMDAR antagonist MK-801, but not by N-type (omega-conotoxin GVIA) or L-type (nimodipine) VGCC blockers. These results suggest that NO can modulate neuronal calcium entry during depolarization by interacting with P/Q-type VGCC and NMDAR.

Action Potentials↗

PubMed1997

Behavioral consequences of abnormal cortical development: insights into developmental disabilities.

Cerebral cortical development occurs in precisely-timed stages that can be divided into neurogenesis, neuronal migration and neuronal differentiation. These events occur during discrete time windows that span the late prenatal and early postnatal periods in both rodents and primates, including humans. Insults at particular developmental stages can lead to distinctive cortical abnormalities including cortical hypoplasia (reduced cell number), cortical ectopias (abnormalities in migration) and cortical dysplasias (abnormalities in the shapes or numbers of dendrites). In this review, we examine some of the most extensively-studied animal models of disrupted stages of cortical development and we compare long-term anatomical, neurochemical, and behavior abnormalities in these models. The behavioral abnormalities in these models range from alterations in simple motor behaviors to food hoarding and maternal behaviors as well as cognitive behaviors. Although we examine concisely animal models of cortical hypoplasia and cortical ectopias, we focus here on developmental manipulations that affect cortical differentiation, particularly, those that interrupt the normal ontogeny of the neurotransmitter-defined cortical afferent systems: norepinephrine, serotonin, dopamine and acetylcholine. All of these afferents presumably play a critical role in the maturation of their cortical targets; the timing of the afferents' entry into the cortex and their effects on their cortical targets, however, are different. We, therefore, compare the specific anatomical, neurochemical and behavioral effects of manipulations of the different cortical afferents. Because of the considerable evidence that cortical development proceeds differently in the two sexes, when data are available, we address whether perinatal insults differentially affect the sexes. Finally, we discuss how these developmental studies provide insights into cellular and neurochemical correlates of behavioral functional abnormalities and the relevance of these data to understanding developmental disabilities in humans.

Animals↗

PubMed2005

GABAB heterodimeric receptors promote Ca2+ influx via store-operated channels in rat cortical neurons and transfected Chinese hamster ovary cells.

The GABAB receptors are generally considered to be classical Gi-coupled receptors that lack the ability to mobilize intracellular Ca2+ without the aid of promiscuous G proteins. Here, we report the ability of GABAB receptors to promote calcium influx into primary cultures of rat cortical neurons and transfected Chinese hamster ovary cells. Chinese hamster ovary cells were transfected with GABAB1(a) or GABAB1(b) subunits along with GABAB2 subunits. In experiments using the fluorometric imaging plate reader platform, GABA and selective agonists promoted increases in intracellular Ca2+ levels in transfected Chinese hamster ovary cells and cortical neurons with the expected order of potency. These effects were fully antagonized by selective GABAB receptor antagonists. To investigate the intracellular pathways responsible for mediating these effects we employed several pharmacological inhibitors. Pertussis toxin abolished GABAB mediated Ca2+ increases, as did the phospholipase Cbeta inhibitor U73122. Inhibitor 2-aminethoxydiphenyl borane acts as an antagonist at inositol 1,4,5-trisphosphate receptors and at store-operated channels. In all cell types, 2-aminethoxydiphenyl borane prevented Ca2+ mobilization. The selective store-operated channel inhibitor 1-[2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl-1H-imidazole hydrochloride prevented increases in intracellular Ca2+ levels as did performing the assays in Ca2+ free buffers. In conclusion, GABAB receptors expressed in Chinese hamster ovary cells and endogenously expressed in rat cortical neurons promote Ca2+ entry into the cell via the activation of store-operated channels, using a mechanism that is dependent on Gi/o heterotrimeric proteins and phospholipase Cbeta. These findings suggest that the neuronal effects mediated by GABAB receptors may, in part, rely on the receptor's ability to promote Ca2+ influx.

Animals↗

PubMed1995

Functional mapping of the early stages of status epilepticus: a 14C-2-deoxyglucose study in the lithium-pilocarpine model in rat.

Continuous convulsive activity in status epilepticus generally does not occur suddenly in response to the inciting epileptogenic agent, but is rather the culmination of a stereotyped sequence of stages. Initially seizures are discrete, then undergo waxing-and-waning of convulsive/electroencephalographic severity. Following a transitional EEG-recorded fast-and-slow spiking phase, continuous fast spiking with invariant convulsive behavior ensues. We sought to map the seizure anatomic substrates corresponding to these stages, utilizing the 14C-2-deoxyglucose technique, in order to make inferences about underlying mechanisms. The lithium-pilocarpine status epilepticus model in rat was employed. Cerebral autoradiographs associated with discrete seizures revealed non-uniform cerebral metabolic activation, with rostral cortical and olfactory areas especially involved. Portions of basal ganglia were also activated, consistent with projections from seizure-activated areas. Successive stages of status entry displayed additional limbic and cortical activation, along with subcortical projection sites, so that by fast-and-slow spiking most forebrain areas were recruited. Based on these results, a model is proposed whereby cyclical seizure-attenuating mechanisms cause, in the initial stages of status entry, fluxing of seizure anatomic extents between small and large cerebral domains, with corresponding cycling of convulsive severity. In the later stages of status entry, these mechanisms become ineffective, resulting in steady-state maximal forebrain recruitment, associated with continuous and invariant convulsive behavior and electrographic fast spiking.

Animals↗

PubMed2001

Modulation of aldosterone-induced stimulation of ENaC synthesis by changing the rate of apical Na+ entry.

Primary cultures of immunodissected rabbit connecting tubule and cortical collecting duct cells were used to investigate the effect of apical Na+ entry rate on aldosterone-induced transepithelial Na+ transport, which was measured as benzamil-sensitive short-circuit current (I(sc)). Stimulation of the apical Na+ entry, by long-term short-circuiting of the monolayers, suppressed the aldosterone-stimulated benzamil-sensitive I(sc) from 320 +/- 49 to 117 +/- 14%, whereas in the presence of benzamil this inhibitory effect was not observed (335 +/- 74%). Immunoprecipitation of [(35)S]methionine-labeled beta-rabbit epithelial Na+ channel (rbENaC) revealed that the effects of modulation of apical Na+ entry on transepithelial Na+ transport are exactly mirrored by beta-rbENaC protein levels, because short-circuiting the monolayers decreased aldosterone-induced beta-rbENaC protein synthesis from 310 +/- 51 to 56 +/- 17%. Exposure to benzamil doubled the beta-rbENaC protein level to 281 +/- 68% in control cells but had no significant effect on aldosterone-stimulated beta-rbENaC levels (282 +/- 68%). In conclusion, stimulation of apical Na+ entry suppresses the aldosterone-induced increase in transepithelial Na+ transport. This negative-feedback inhibition is reflected in a decrease in beta-rbENaC synthesis or in an increase in beta-rbENaC degradation.

Aldosterone↗