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At least 379 records · Page 21Linked to original sources
PubMed1999

Glucocorticoids-potent modulators of astrocytic calcium signaling.

Glucocorticoids are the first line of choice in the treatment of cerebral edema associated with brain tumors. High-dose glucocorticoids reduce the extent of edema within hours, often relieving critical increases in intracranial pressure, but the mechanisms by which glucocorticoids modulate brain water content are not well-understood. A possible target of action may be glucocorticoid receptor-expressing astrocytes, which are the primary regulators of interstitial ion homeostasis in brain. In this study, we demonstrate that two glucocorticoids, methylprednisolone and dexamethasone, potentiate astrocytic signaling, via long-range calcium waves. Glucocorticoid treatment increased both resting cytosolic calcium (Ca2+i) level and the extent and amplitude of Ca2+ wave propagation two-fold, compared to matched controls. RU-486, a potent steroid receptor antagonist, inhibited the effects of methylprednisolone. The glucocorticoid-associated potentiation of Ca2+ signaling may result from upregulation of the cellular ability to mobilize Ca2+ and release ATP, because both agonist-induced Ca2+i increments (via ATP and bradykinin) and ATP release were proportionally enhanced by glucocorticoids. In contrast, neither gap junction expression (as manifested connexin 43 immunoreactivity) nor functional coupling was significantly affected by methylprednisolone. Confocal microscopy revealed both the expression of glucocorticoid receptors and nuclear translocation of these receptors when exposed to methylprednisolone. We postulate that the edemolytic effects of glucocorticoids may result from enhanced astrocytic calcium signaling.

Adenosine Triphosphate↗
PubMed1994

The neuroprotective kappa-opioid CI-977 alters glutamate-induced calcium signaling in vitro.

The effect of the neuroprotective kappa opioid agonist CI-977 on glutamate (GLU)-stimulated calcium signaling was studied in individual primary rat cortical neurons. Using laser scanning confocal microscopy and the fluorescent calcium probe fluo-3, both the sustained and biphasic intracellular calcium concentration [Ca2+]i changes induced by GLU (20-40 microM) were altered by CI-977 (25-100 nM), thereby shifting the neuronal population response from unbuffered to buffered patterns of [Ca2+]i flux. This effect was consistent with the previously demonstrated neuroprotective action of CI-977 against glutamate toxicity in vitro. The effect of CI-977 in altering GLU-induced [Ca2+]i signaling was attenuated by naloxone, consistent with a neuroprotective action of CI-977 at opioid receptors, presumably of the kappa subtype.

Animals↗
PubMed2002

[Isolation, expression analysis of a chilling induced cDNA from rice root with differential display: an evidence role for caffeine-sensitive calcium signal].

Chilling-sensitive rice varieties acquire chilling tolerance when their roots are exposed to water stress for short time. Caffeine-sensitive calcium signal was involved in this procedure. By using total RNA differential display, a chilling induced cDNA(ICT: induction of chilling treatment) was isolated from roots of chilling-sensitive rice variety. It was determined that it is a novel cDNA by homology searching. The transcript level of ict mRNA is up-regulated under chilling stress, it is decreased to low level when the samples were transferred to standard culture conditions. Pre-treated with mannitol for two hours is beneficial to inducing ICT level of expression. This chilling induction was inhibited by caffeine, suggesting that it may play a putative role in signal transduction of caffeine-sensitive calcium.

Cold Temperature↗
PubMed1994

The initiation of a calcium signal in Xenopus oocytes.

Application of acetylcholine to Xenopus oocytes evoked increases in the cytosolic free calcium ion concentration ([Ca2+]i) after latencies of up to several seconds depending on the agonist dose. Higher acetylcholine concentrations evoked responses with larger amplitudes and shorter latencies. The latencies of responses to acetylcholine could be increased by application of caffeine, injection of calcium buffers or depletion of intracellular calcium stores. Acute inhibition of endoplasmic reticulum calcium pumps without substantial reduction of the calcium store content (by application of thapsigargin shortly before agonist stimulation) reduced the latencies of responses to acetylcholine. A schematic and mathematical model are presented to show a possible mechanism by which a calcium signal is initiated following a latent period after the elevation of the inositol trisphosphate concentration. During the latent period, calcium is slowly released from the intracellular stores. The released calcium is rapidly buffered by cytosolic calcium-binding proteins and some is resequestered into the stores by calcium pumps. The [Ca2+]i changes very little until the buffering is locally saturated. The [Ca2+]i then rises above a threshold concentration which evokes an explosive release of calcium due to positive feedback by calcium on the inositol trisphosphate receptor.

Acetylcholine↗
PubMed1999

Estrogen promotes the initial migration and inception of NgCAM-dependent calcium-signaling by new neurons of the adult songbird brain.

The adult avian forebrain continues to generate neurons from ventricular zone (VZ) precursor cells, whose neuronal progeny then migrate into the brain parenchyma. Migrating neurons respond to the Ig-family adhesion molecule NgCAM with increments in cytosolic calcium, and migration is disrupted by anti-NgCAM Ig. The calcium response to NgCAM is developmentally restricted to bipolar migrants during a period spanning 6 to 9 DIV. This period corresponds to the postmitotic age at which new neurons leave the adult VZ to traverse a subjacent layer of estrogen-receptive "gatekeeper" neurons. Since neuronal passage through this layer occurs concurrently with the onset of NgCAM-dependent calcium signaling, we asked whether acquisition of the calcium response to NgCAM required estrogen exposure. Among neurons arising from explants of the adult finch neostriatal VZ, only those supplemented with estrogen developed calcium responses to NgCAM; neither explants raised in the absence of estrogen, nor those supplemented with testosterone, did so. Neurons in all three groups expressed NgCAM, had equivalent baseline calcium levels, and responded identically to K+-depolarization. Nonetheless, many more neurons migrated from explants of both finch and canary VZ raised in estrogen-supplemented media than from their estrogen-deprived counterparts, even though no effect of estrogen on neuronal survival per se was noted. These findings suggest that estrogen encourages the initial departure and assumption of signal competence by neurons arising from the adult avian VZ, thereby promoting their parenchymal recruitment and migration success.

Animals↗
PubMed2003

Spatiotemporal calcium signaling in a Drosophila melanogaster cell line stably expressing a Drosophila muscarinic acetylcholine receptor.

A muscarinic acetylcholine receptor (mAChR), DM1, expressed in the nervous system of Drosophila melanogaster, has been stably expressed in a Drosophila S2 cell line (S2-DM1) and used to investigate spatiotemporal calcium changes following agonist activation. Carbamylcholine (CCh) and oxotremorine are potent agonists, whereas application of the vertebrate M1 mAChR agonist, McN-A-343, results in a weak response. Activation of S2-DM1 receptors using CCh resulted in an increase in intracellular calcium ([Ca(2+)](i)) that was biphasic. Two distinct calcium sources were found to contribute to calcium signaling: (1) internal stores that are sensitive to both thapsigargin and 2-aminoethoxydiphenyl borate and (2) capacitative calcium entry. Spatiotemporal imaging of individual S2-DM1 cells showed that the CCh-induced [Ca(2+)](i) transient resulted from a homogeneous calcium increase throughout the cell, indicative of calcium release from internal stores. In contrast, ionomycin induced the formation of a "calcium ring" at the cell periphery, consistent with external calcium influx.

Animals↗
PubMed1994

Glia-neuron intercellular calcium signaling.

There is increasing evidence for bidirectional communication between glial cells and neurons. In this study, calcium signaling in primary glia/neuron cultures was investigated using video fluorescence imaging and fura-2. Glial cells in culture without neurons showed occasional spontaneous intracellular Ca2+ oscillations but not intercellular Ca2+ waves. By contrast, glial cells in culture with neurons showed frequent spontaneous Ca2+ oscillations as well as propagated intercellular Ca2+ waves. These spontaneous glial intercellular Ca2+ waves often emanated from sites of contact with neurons, but were only occasionally associated with increases in neuronal Ca2+. Mechanical stimulation of a single glial cell induced a glial intercellular Ca2+ wave which was similar in its temporal and spatial characteristics to spontaneous glial Ca2+ waves. Mechanically induced glial Ca2+ waves, but not spontaneous Ca2+ waves, evoked a transient increase in [Ca2+]i or a change in the pattern of spontaneous Ca2+ oscillations in a small percentage (< 10%) of neighboring neurons. Mechanical stimulation of a single neuron consistently evoked an intercellular Ca2+ wave in neighboring glial cells. These results suggest distinct mechanisms for direct glial-neuronal and neuronal-glial communication. These signaling pathways may play important roles in both function and pathology in the central nervous system.

Animals↗
PubMed2001

Comparison of intracellular calcium signals evoked by heat and capsaicin in cultured rat dorsal root ganglion neurons and in a cell line expressing the rat vanilloid receptor, VR1.

The cloning of the receptor for capsaicin, vanilloid receptor 1, has shown it to be non-selective cation channel with a high calcium permeability which can be opened by noxious heat as well as capsaicin. Here we compare the calcium signals produced by native and recombinant capsaicin receptors when activated by either heat or capsaicin by imaging intracellular calcium levels ([Ca2+](i)) in rat dorsal root ganglion neurons and Chinese hamster ovary cells transfected with the rat vanilloid receptor, vanilloid receptor 1. Vanilloid receptor 1 transfected cells and a subset of dorsal root ganglion neurons responded to both capsaicin and to heating to 50 degrees C with rapid, substantial and reversible rises in [Ca2+](i). All except one of the dorsal root ganglion neurons responsive to capsaicin also showed sensitivity to heat, and most, but not all, heat-sensitive neurons also responded to capsaicin. Both capsaicin and heat responses were dependent on the presence of extracellular Ca2+. Non-transfected Chinese hamster ovary cells and non-responsive dorsal root ganglion neurons showed only small rises in [Ca2+](i) in response to heat which did not depend on the presence of external Ca2+. Responsive dorsal root ganglion neurons and vanilloid receptor 1 transfected cells showed a clear temperature threshold, above which [Ca2+](i) increased rapidly. This was estimated to be 42.6+/-0.3 degrees C for vanilloid receptor 1 transfected cells and 42.0+/-0.6 degrees C for dorsal root ganglion neurons. The competitive capsaicin antagonist capsazepine (10microM) abolished [Ca2+](i) increases stimulated by capsaicin in both dorsal root ganglion neurons and vanilloid receptor 1 transfected cells. However, responses to heat of a similar magnitude in the same cells were inhibited by only 37% by capsazepine (10microM). In vanilloid receptor 1 transfected cells, Ruthenium Red (10microM) blocked responses to both capsaicin and heat. These results demonstrate that imaging of [Ca2+](i) can identify dorsal root ganglion neurons which are responsive to both heat and capsaicin. They show that heat and capsaicin responses mediated by native and recombinant capsaicin receptors are similar with respect to the characteristics and pharmacology examined, suggesting that expression of recombinant vanilloid receptor 1 in cell lines accurately reproduces the properties of the native receptor.

Animals↗
PubMed1991

ATP-evoked calcium signal stimulates protein phosphorylation/dephosphorylation in astrocytes.

Extracellular adenosine 5'-triphosphate (ATP)-evoked increases in intracellular calcium and the consequent stimulation of calcium-mediated protein phosphorylation systems were investigated in primary cultures of rat cerebral cortical astrocytes. Measurement of calcium responses in fura-2-loaded astrocytes indicated that extracellular ATP stimulated a transient calcium peak followed by a sustained increase in intracellular calcium which declined to baseline when external calcium was removed, thereby indicating that ATP evokes mobilization of internal calcium as well as influx of external calcium. Protein phosphorylation studies revealed that application of extracellular ATP resulted in increased phosphorylation of 55 and 52 kDa proteins (4-fold and 2-fold, respectively) and decreased phosphorylation of 24 and 21 kDa proteins (approximately 50% for each protein). These effects were time- and dose-dependent. The changes in phosphate incorporation were (a) inhibited by lanthanum, (b) reduced when calcium was omitted from the bath and (c) mimicked by ionomycin, thus suggesting that the ATP-induced changes in protein phosphorylation were dependent on increased levels of intracellular calcium. Adenosine diphosphate (ADP) gave similar, but reduced, effects while adenosine and guanosine triphosphate (GTP) were ineffective, findings consistent with activation of P2 purinergic receptors. The 52 kDa protein co-migrated with glial fibrillary acidic protein. These results support the premise that calcium-dependent protein kinases and phosphatases are transducing elements for the calcium signal brought about by activation of P2 purinergic receptors in astrocytes. Since ATP is released from neurons and endothelial cells, this signal transduction mechanism may be an important component of neuronal- and endothelial-astrocytic communication.

Adenosine Triphosphate↗
PubMed2005

Calcium signaling is involved in ethanol-induced volume decrease and gap junction closure in cultured rat gastric mucosal cells.

Ethanol is a well-established "barrier breaker" in gastric mucosa, but its detailed effects at the cellular level remain unclear. We have previously shown that the intracellular free calcium concentration is increased, gap junctions are closed, and cell volume is decreased after exposure to 5% (v/v) ethanol in primarily cultured rabbit gastric epithelial cells. Rat gastric mucosal (RGM) cells were grown to confluence on a coverslip or on a filter membrane. Gap junctional diffusion was measured in 5-carboxyfluorescein-loaded cells by bleaching a small area with a laser and measuring the recovery with confocal microscope. Intracellular calcium was measured spectrofluorometrically in fura-2-loaded cells. For cell volume measurements the cell monolayer was loaded with calcein and imaged along the Z-axis with a confocal microscope. The changes in fluorescence intensity were intercepted as a measure of cell volume change. TMB-8 was used to inhibit intracellular calcium release and lanthanum to block plasma membrane calcium selective ion channels, while BABTA served as an intracellular calcium chelating agent. Results showed that ethanol (7.5%, v/v) exposure increased intracellular calcium from 69 +/- 7 to 142 +/- 11 nM (N = 5; P < 0.05), decreased cell volume by -23 +/- 5% (N = 8; P < 0.05), and induced gap junction closure (fluorescence recovery from 37 +/- 9 to 15 +/- 3%; N = 6; P < 0.05). A serosal potassium channel blocker, quinine, almost completely prevented the ethanol-induced cell volume decrease (from -23 +/- 5 to -3 +/- 3%), suggesting that opening of basolateral potassium channels underlies cell shrinkage. BABTA inhibited completely (from 35 +/- 3 to 39 +/- 4 nM; N = 6; P < 0.05), and TMB-8 + lanthanum partially (from 60 +/- 6 to 92 +/- 12 nM; N = 6; P < 0.05), the ethanol-induced intracellular calcium increase. BABTA also abolished the ethanol-induced volume decrease (from -23 +/- 5 to 1 +/- 4%; N = 6; P < 0.05), while TMB-8 + lanthanum had a lesser effect on it (from -23 +/- 5 to -11 +/- 3%; N = 9; P < 0.05). They also abolished the closure of gap junctions induced by ethanol (fluorescence recovery, 38 +/- 5% for BABTA and 30 +/- 4% for TMB-8 + lanthanum). We conclude that luminal ethanol opens basolateral calcium-dependent potassium selective channels with resultant shrinkage of the cells and blocks the intercellular gap junctions. These actions are mediated by intracellular calcium signaling.

Animals↗
PubMed1999

Bruton's tyrosine kinase controls a sustained calcium signal essential for B lineage development and function.

Genetic data support a role for Btk during the B lineage development transitions regulated by signaling through both the pre-B and the B cell antigen receptors. Dysregulated signaling at each of these transitions can result in failure of these cell populations to proliferate and subsequent cell death. Btk-dependent IP3 production is crucial for maintaining the sustained calcium signal in response to BCR engagement and is likely to regulate a subset of transcriptional events essential for B lineage growth or survival. Identification of these Btk-dependent signals will be important in understanding B cell activation, differentiation, and cell death. This information may lead to therapies specifically targeting these events in B cell autoimmunity or malignancy and provide a fuller understanding of the appropriate target populations and potential negative consequences of Btk gene therapy in XLA. Identification of Btk/Tec family kinases in an increasing number of vertebrate and invertebrate cell lineages suggests that the link between Btk and the PLC gamma/IP3/calcium signaling pathways may be broadly conserved.

Agammaglobulinaemia Tyrosine Kinase↗
PubMed2004

Differential modulation of ATP-induced calcium signalling by A1 and A2 adenosine receptors in cultured cortical astrocytes.

1. Despite the accumulating evidence that under various pathological conditions the extracellular elevation of adenine-based nucleotides and nucleosides plays a key role in the control of astroglial reactivity, how these signalling molecules interact in the regulation of astrocyte function is still largely elusive. 2. The action of the nucleoside adenosine in the modulation of the intracellular calcium signalling ([Ca(2+)](i)) elicited by adenosine 5'-triphosphate (ATP)-induced activation of P2 purinoceptors was investigated on neocortical type-1 astrocytes in primary culture by using single-cell microfluorimetry. 3. Astrocyte challenge with ATP (1-10 microm) elicited biphasic [Ca(2+)](i) responses consisting of an initial peak followed by a sustained elevation. The stable adenosine analogue 2-chloroadenosine (2-ClA) potentiated the transient [Ca(2+)](i) rise induced by activation of metabotropic P2Y receptors. Among the various P1 receptor agonists tested, the nonselective agonist 5'-N-ethylcarboxamidoadenosine (NECA) mimicked the 2-ClA action, whereas the selective A1 R(-) N6-(2-phenylisopropyl)-adenosine (R-PIA), the A2A 2-[4-(2-carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS-21680) and A3 1-deoxy-1-(6-[([3-lodophenyl]methyl)-amino]-9H-purin-9-yl)-N-methyl-beta-d-ribofuranuronamide (IB-MECA) agonists were ineffective. 4. Application of R-PIA>NECA>or=2-ClA depressed the [Ca(2+)](i) plateau reversibly. Moreover, in the presence of R-PIA or 2-ClA, the prolonged [Ca(2+)](i) signal was maintained by application of the A1 antagonist 1,3-diethyl-8-phenylxanthine (DPX). Finally, preincubation of the astrocytes with pertussis toxin abrogated the 2-ClA inhibition of the ATP-elicited sustained [Ca(2+)](i) rise without affecting the transient [Ca(2+)](i) potentiation. 5. Taken together, these findings indicate that stimulation of A1 and A2 adenosine receptors mediates a differential modulation of [Ca(2+)](i) signalling elicited by P2 purinoceptors. Since variations in [Ca(2+)](i) dynamics also affect cell proliferation and differentiation, our data suggest that tuning of the extracellular levels of adenosine may be relevant for the control of astrogliosis mediated by adenine nucleotides.

2-Chloroadenosine↗
PubMed2002

Calcium signaling is required for ultrasound-stimulated aggrecan synthesis by rat chondrocytes.

Low-intensity ultrasound accelerates fracture healing in humans. In rat femur fracture models, ultrasound advanced healing is associated with increased proteoglycan expression. Here we report that ultrasound stimulation of primary rat chondrocytes elevated the intracellular concentration of calcium [Ca2+]i. The [Ca2+]i increase was rapid and transient at lower pressures (175-320 kPa), but rapid and sustained at higher ultrasound exposures (350-500 kPa). Chelating internal [Ca2+]i with 1,2-bis(2-aminophenoxy) ethane-N-N-N',N'-tetraacetic acid (BAPTA-AM), stopping the Ca2+/ATP-ase induced mitochondrial release of [Ca2+]i with Thapsigargin, or removing [Ca2+]i from the medium with EGTA inhibited the stimulatory effects of ultrasound on proteoglycan synthesis. These results imply that ultrasound-stimulated synthesis of cell matrix proteoglycan, associated with accelerated fracture healing, is mediated by intracellular calcium signaling.

Aggrecans↗
PubMed2004

Comparative analysis of plant and animal calcium signal transduction element using plant full-length cDNA data.

We obtained 32K full-length cDNA sequence data from the rice full-length cDNA project and performed a homology search against NCBI GenBank data. We have also searched homologs of Arabidopsis and other plants' genes with the databases. Comparative analysis of calcium ion transport proteins revealed that the genes specific for muscle and nerve calcium signal transduction systems (VDCC, IP3 receptor, ryanodine receptor) are very different in animals and plants. In contrast, Ca elements with basic functions in cell responses (CNGC, iGlu receptor, Ca(2+)ATPase, Ca2+/Na(+)-K+ ion exchanger) are basically conserved between plants and animals. We also performed comparative analyses of calcium ion binding and/or controlling signal transduction proteins. Many genes specific for muscle and nerve tissue do not exist in plants. However, calcium ion signal transduction genes of basic functions of cell homeostasis and responses were well conserved; plants have developed a calcium ion interacting system that is more direct than in animals. Many species of plants have specifically modified calcium ion binding proteins (CPK, CRK), Ca2+/phospholipid-binding domains, and calcium storage proteins.

Animals↗
PubMed2001

Inhibitors of arachidonic acid metabolism have variable effects on calcium signaling pathways.

The metabolic pathways of arachidonic acid (AA) have been shown to be important in the regulation of cellular function. Several studies have demonstrated both direct and indirect effects of products of these pathways in the regulation of vascular actions, and in particular on signaling pathways. Because intracellular calcium concentration is a significant mediator of stimulus-coupled signal transduction, we investigated the effects of AA pathway inhibitors on angiotensin II (Ang II)-induced calcium mobilization in cultured rat vascular smooth muscle cells (VSMC). Thus, specific calcium pools were examined for differential effects resulting from inhibitors of the three major pathways of AA metabolism. Inhibition of lipoxygenase (LO) with 2.5 micromol/L of 5,8,11 eicosatriynoic acid (ETI), cyclooxygenase (CO) with 2 micromol/L of ibuprofen (IBU), and cytochrome P-450 (P450) with 1 micromol/L of 7-ethoxyresorufin (7ER) all reduced total Ang II-induced intracellular calcium transients ([Ca2+]i) in fura 2-loaded cultured rat VSMC. However, the sites of action affected were unique for each inhibitor. Pretreatment of VSMC with either ETI or IBU inhibited thapsigargin (TG) (1 micromol/L)-sensitive calcium increments (control; 118.0 +/- 33.1 nmol/L, n = 9, ETI; 34.7 +/- 4.8 nmol/L, n = 9, IBU; 40.3 +/- 8.8 nmol/L, n = 8, P < .05 v control). Both caffeine (CAF) and ryanodine (RY) treatment attenuated Ang II-induced [Ca2+]i; however, pretreatment with ETI, IBU, or 7ER did not alter this effect. In other studies, the LO inhibitor ETI attenuated Ang II-induced Ca2+ influx, whereas inhibitors of CO and P450 pathways had no effect. These data show that 1) E

8,11,14-Eicosatrienoic Acid↗
PubMed2001

Effects of Sclerocarya birrea (A. rich) hochst (anacardiaceae) leaf extracts on calcium signalling in cultured rat skeletal muscle cells.

Sclerocarya birrea is a plant used widely to treat many diseases in Burkina Faso, although no scientific data has been reported about its mechanism of action. In the present study the effects of its leaf extracts were investigated on calcium signalling in rat cultured skeletal muscle cells. The results show that the different extracts (crude decoction, aqueous, ethanolic and chloroformic extracts) have significant antagonistic effect on caffeine-induced calcium release from sarcoplasmic reticulum. Crude decoction is the most active followed by ethanolic, aqueous and chloroformic extracts in dose-dependent manner and can partly justify the use of the plant in traditional medicine.

Animals↗
PubMed2000

Sodium-calcium exchange affects local calcium signal decay and the rate of exocytotic secretion in single chromaffin cells.

The effects of Na+ deprivation on local calcium signal decay and the rate of exocytotic secretion were measured in single bovine chromaffin cells to determine whether Na-Ca exchange influences the local cytosolic Ca2+ signal for neurohormone release. Na+ replacement with N-methylglucamine caused a marked slowing of the decay of the local Ca2+ signal near points of its initiation, as measured by high-resolution fluorescent Ca2+ imaging in the confocal laser scanning microscope. Na+ replacement also resulted in a doubling of the rate and magnitude of exocytotic secretion measured in single cells by high-resolution microamperometry. Release rates provide an independent measure of local active zone Ca2+. Five repetitive stimulations of the same cell in Na+-free, but not in Na+-containing, medium resulted in a progressively increasing rate of catecholamine release, suggesting an increasing level of active zone Ca2+ and a role of Na-Ca exchange activity in Ca2+ clearance between stimulations. As secretory activity and its triggering Ca2+ signals are known to be co-localized in active zones along the plasma membrane, the results suggest that Na-Ca exchange may influence the decay of the local Ca2+ signal for exocytotic secretion. This would be consistent with a contribution to local Ca2+ clearance by a novel mechanism utilizing the insertion of secretory vesicle Na-Ca exchangers into the plasma membrane during exocytosis.

Animals↗
PubMed1996

Immunoreactivities for calcium signaling components and neural-like properties of a Colorado potato beetle cell line.

Of the approximately 400 described insect cell lines, only three are derived from beetles (Coleoptera), and none are neural in origin. The present work was undertaken to characterize further a new cell line, designated IPLB-CPB2, derived from eggs of the Colorado potato beetle, Leptinotarsa decimlineata. Indirect immunofluorescent studies reported here indicate that these cells express neurofilament (Nf)-like immunoreactivities to antibodies directed against mammalian Nf-Medium (MW 150,000) and a heavily phosphorylated form of Nf-Heavy (MW 200,000; detected using the axonal monoclonal antibody SMI 31). This appears to be the first report of neurofilament-like immunoreactivity in an arthropod. Immunofluorescent analyses also indicate that IPLB-CPB2 cells express an antigenic epitope characteristic of the mammalian type 1 inositol trisphosphate (IP3) receptor, the ryanodine receptor (RyR) (also termed calcium-induced calcium release receptor channel, or CICR) and the sarco(endo)plasmic reticulum Ca2+ pump (SERCA). Patch-clamp recordings indicate that some IPLB-CPB2 cells are capable of producing spontaneous action potentials, while others may be photosensitive. Taken together, the findings reported here suggest that IPLB-CPB2 cells are of neural origin and that they express the major receptor channels and pumps known to be localized in the ER of the cell, which are required for receptor-mediated calcium signaling. Thus, the IPLB-CPB2 cell line may prove to be an excellent model system for studies of insect neurobiology and calcium-based signal transduction.

Animals↗