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PubMed1991

Modulation of low-density lipoprotein-induced inhibition of intercellular communication by antioxidants and high-density lipoproteins.

In order to study the capacity of antioxidants and high-density lipoproteins (HDL) to modulate the effects of low-density lipoprotein (LDL) on intercellular communication, arterial smooth muscle cells and a dye transfer method were used. LDL, in contrast to HDL, inhibited the communication between arterial smooth muscle cells from human umbilical cord and thoracic aorta in a dose-dependent manner. LDL, which can be oxidized, as detected by the lipid-peroxidation assay and gel electrophoresis, did not influence cell-cell communication in the presence of the antioxidants butylated hydroxytoluene (BHT), alpha-tocopherol and glutathione. The results suggest that LDL must undergo oxidative modification before it can influence intercellular communication. Like antioxidants, HDL diminished the LDL-induced inhibition of cell-cell communication. This study suggests that the modulation of gap-junctional communication by the balance of HDL and LDL in plasma may influence atherogenesis.

Antioxidants↗
PubMed1991

Regulation of gap-junctional intercellular communication in transformation-sensitive and transformation-resistant BALB/c 3T3 cell variants.

BALB/c 3T3 A31-1-13 cells are highly susceptible to chemical-induced cell transformation and their gap-junctional intercellular communication (GJIC) is decreased when these cells become confluent. On the other hand, A31-1-1 cells do not show such a change in GJIC and are more resistant to chemical induction of transformation. In order to see which phenotypes are dominant, cells of these two types were hybridized and the hybrids were analyzed for their phenotypes for GJIC and induction of cell transformation. These two cell lines were tagged with neor gene or hygromycin-resistance gene respectively, and their hybrids were selected in medium containing G418 and hygromycin. Six independently isolated clones were characterized and all showed a loss of intercellular communication at confluence, suggesting that the phenotype of transformation-sensitive cell line A31-1-13 was dominant. However, when these hybrid cells were exposed to 3-methylcholanthrene, no transformed foci were produced, suggesting that the transformation-resistant phenotype is dominant. These results suggest that the regulation of GJIC and the susceptibility to chemical induction of transformation are genetically separate traits, and indirectly suggest that the loss of GJIC alone cannot explain the high susceptibility of A31-1-13 cells to induction of transformation.

3T3 Cells↗
PubMed1998

The rodent nongenotoxic hepatocarcinogen and peroxisome proliferator nafenopin inhibits intercellular communication in rat but not guinea-pig hepatocytes, perturbing S-phase but not apoptosis.

Previously, we have shown that the peroxisome proliferator (PP), nafenopin, induces S-phase in rat hepatocytes and suppresses apoptosis in hepatocytes from both rat and guinea-pig. Here, we confirm and extend these findings by defining the time course of growth perturbation and by correlating this with species differences in loss of gap junctional intercellular communication (GJIC). GJIC is associated with nongenotoxic carcinogenesis, possibly reflecting a tumour suppresser role of the connexins. Fluorescence microscopy of Hoechst 33258-stained rat or guinea-pig hepatocyte monolayers showed 1% apoptosis during the first 8 h of culture, peaking to 2-2.5% at 20-24 h. Nafenopin suppressed apoptosis compared with controls in both rat and guinea-pig, measured at 20 h and 24 h onwards, respectively. The induction of S-phase in rat hepatocytes by nafenopin could be detected as early as 4 h after compound addition whereas S-phase was not altered by nafenopin in guinea-pig hepatocytes. Intercellular communication as measured by intercellular transfer of microinjected Lucifer Yellow CH was observed during the first 14 h of primary rat hepatocyte culture peaking at a maximum value of 88 +/- 3.0% after 7 h. In hepatocyte cultures from guinea-pig, dye-coupling levels were maintained between 88 +/- 3.0 and 93 +/- 3.0% within 2-10 h of culture and by 12 h showed only a slight decrease to 72 +/- 3.0%. In the rat, significant inhibition was observed at 4 h after administration of nafenopin since GJIC was reduced by 20 +/- 5% compared with vehicle control. By contrast, in the presence of nafenopin, the level of dye-coupling between guinea-pig hepatocytes did not decrease but remained between 85 +/- 5 and 93 +/- 3.0%, similar to that observed in control guinea-pig cultures. The data obtained contribute to our understanding of the role of GJIC inhibition in the perturbation of cell survival and proliferation caused by nongenotoxic hepatocarcinogens.

Animals↗
PubMed2000

Taurine preserves gap junctional intercellular communication in rat hepatocytes under oxidative stress.

Gap junctional intercellular communication (GJIC) between hepatocytes is important for the maintenance of differentiated liver functions. Taurine is known to be cytoprotective, and is used clinically to improve liver functions. We evaluated the effect of taurine on GJIC in hepatocyte doublets under oxidative stress. Hepatocyte doublets were isolated from female Wistar rats, using a collagenase perfusion technique, and cultured in Leibovitz-15 medium containing fetal bovine serum (10%). H2O2 (2 mM) and/or taurine (0.1-1 mM) were added 2 h after inoculation, and the culture was incubated for 3 h. Fluorescent dye (Lucifer Yellow CH) coupling between adjacent cells was evaluated by microinjection. The distribution and quantity of connexin 32 (Cx32) in hepatocytes were detected using indirect immunofluorescence analysis and Western blotting. Steady state mRNA levels of Cx32 were detected by Northern blotting. The percentage of dye coupling 5 h after inoculation was 88 +/- 6.3% in the control. however, this was decreased to almost half the control value by H2O2. Taurine prevented the decrease caused by H2O2 in a dose-dependent manner. Immunofluorescence analysis for Cx32 demonstrated numerous punctate fluorescent spots along the intercellular plasma membrane in controls, which were significantly decreased by H2O2. Taurine prevented the decrease of Cx32. Western blot analysis also showed the decrease of Cx32 protein levels by H2O2 treatment, which decrease was prevented by taurine. Interestingly, H2O2 and/or taurine treatments did not affect Cx32 mRNA levels. Our findings indicated that H2O2 treatment decreased GJIC between hepatocytes, most likely due to augmenting the degradation of Cx32 proteins, whereas taurine prevented this process. This effect of taurine is beneficial for the preservation of differentiated functions in the liver under oxidative stress.

Animals↗
PubMed1983

Intercellular communication in rat seminiferous tubules.

Intercellular electrical coupling in seminiferous tubules from prepubescent and adult Wistar rats has been studied by using conventional techniques. It is found that cells in the seminiferous epithelium are electrically coupled. Experiments performed using "Sertoli cell-enriched" seminiferous tubules indicate the existence of intercellular ionic communication between Sertoli cells. Junctional conductance is independent of the direction of electrical field and it is affected by A23187 Ca ionophore (5 microM) but not by exposure to the neurotransmitter norepinephrine (1-5 X 10(-5) M). Intracellular resistivity (including junctional resistance) is higher in mature as compared to immature germinal epithelium. These findings suggest that cell metabolites or second messenger molecules could be transferred via the low-resistance pathways between epithelium cells to coordinate cellular activity.

Aging↗
PubMed2001

Effect of cadmium on gap junctional intercellular communication in primary cultures of rat renal proximal tubular cells.

Cadmium mainly accumulates in the kidney and causes renal injury. To clarify the mechanism of Cd nephrotoxicity, we investigated the effects of this element on intercellular communication through gap junction channels in primary cultures of rat renal proximal tubular cells. Sixty minutes after exposure to 100 microM Cd, dye coupling experiments showed that gap junctional intercellular communication (GJIC) was significantly inhibited. This inhibition occurred before the appearance of cytotoxicity. Intracellular calcium concentrations [Ca2+]i, which modulate the function of gap junctions, gradually increased after exposure to Cd and reached a maximum after 60 minutes. These results suggest that the inhibition of GJIC as a result of Cd exposure is related to an increase in [Ca2+]i, and that GJIC inhibition may be an indicator of nephrotoxicity.

Acetylglucosaminidase↗
PubMedDate not supplied

Initiation and promotion in cancer formation: the importance of studies on intercellular communication.

Three major theories of cancer--somatic mutation, virus causation, and faulty differentiation--are proposed to involve alterations in DNA structure. Each results finally in terms of failures in the normal intercellular communication that involves feedback between differentiated cells acting on less differentiated cells still capable of proliferation. The historical background of the latter idea is traced to Osgood, Weiss and Kavanau, and to Iversen. The historical background of concepts of initiation and promotion are traced to Berenblum and Mottram and the Boutwell concept of promotion as gene activation is cited. It is proposed that gene activation by promoters is a valid concept and that it results from the blocking of the normal intercellular communication postulated by Osgood and others. The problem of explaining the low probability of cancer following initiators or promoters acting alone is cited as a problem in basic science. A hypothesis to solve the problem is proposed: Cancer results from two of more relevant mutations: promoters enhance proliferation of cells with one relevant mutation, thereby increasing the probability of obtaining a cell with two relevant mutations. A new scheme of five stages of hepatocarcinogenesis is proposed in terms of the hypothesis and available data.

Animals↗
PubMed1998

Methylmercury inhibits gap junctional intercellular communication in primary cultures of rat proximal tubular cells.

Methylmercury (MeHg) causes renal injury in addition to central and peripheral neuropathy. To clarify the mechanism of nephrotoxicity by MeHg, we investigated the effect of this compound on intercellular communication through gap junction channels in primary cultures of rat renal proximal tubular cells. Twenty minutes after exposure to 30 microM MeHg, gap junctional intercellular communication (GJIC), which was assessed by dye coupling, was markedly inhibited before appearance of cytotoxicity. When the medium containing MeHg was exchanged with MeHg-free medium, dye coupling recovered abruptly. However, the dye-coupling was abolished again 30 min after replacement with control medium, and the cells were damaged. Intracellular calcium concentration, [Ca2+]i, which modulates the function of gap junctions, significantly increased following exposure of the cells to 30 microM MeHg and returned to control level following replacement with MeHg-free medium. These results suggest that the inhibiting effect of MeHg on GJIC is related to the change in [Ca2+]i, and may be involved in the pathogenesis of renal dysfunction.

Animals↗
PubMed1996

Connexin expression and intercellular communication in two- and three-dimensional in vitro cultures of human bladder carcinoma.

The identification of gap-junctional proteins (connexins) and the preparation of related antibodies provides new tools to study patterns of intercellular communication in tumors. Focusing on the biology of human bladder carcinoma, we compared the expression of gap-junctional proteins (connexins Cx26, Cx32, and Cx43) with a dye-coupling assay for gap-junctional intercellular communication in three cell lines with different urothelial differentiation. The cell lines HCV-29, RT4, and J82 were initially grown as monolayers of different ages. Connexin expression was found mostly positive over the time of culture and found constantly negative only in J82 cells for Cx26 and HCV-29 cells for Cx32. In HCV-29 cells, Cx26 increased in positivity over the time of culture. Western blotting with the antibodies confirmed the findings. Comparisons of dye transfer using Lucifer Yellow showed an increase of coupling in the normal urothelial cell line HCV-29 in contrast to a decrease of coupling in the tumor cell lines. Data were extended by multicellular spheroid (MCS) co-cultures with the stromal fibroblast line N1. In three-dimensional cultures as MCSs, Cx26 was increased in proximity of RT4 tumor cells to fibroblasts, and positivity was maintained in J82 cells. E-cadherin expression in cell lines showed no change in dependence of growth state. The data suggest that Cx26 plays a role in negative growth control or differentiation of urothelial cells. Preliminary comparative data on normal and neoplastic urothelium show all three connexins in normal urothelium, in contrast to varying amounts of Cx43 and low amounts of Cx32 in tumors and evident loss of Cx26 in low-grade tumors. Discrepancies between monolayer and MCS cultures are most likely due to higher differentiation in MCSs, and the continuation of systematic work with heterologous MCSs is indicated for more information on the role of gap-junctional proteins in human tumors.

Blotting, Western↗
PubMed2000

Gap junctional intercellular communication is not a major mediator in the bystander effect in photodynamic treatment of MDCK II cells.

Photodynamic treatment (PDT) of confluent MDCK II cells resulted in a noticeable clustering of dead cells, consistent with a significant bystander effect. Likewise, PDT of cells in microcolonies resulted in an overabundance of microcolonies that had responded to the treatment as a single unit, that is, in which either all or no cells were dead. Confluent MDCK II cells appeared to communicate via gap junction channels, while cells in microcolonies did not. Monte Carlo simulation models were fitted to the distributions of dead cells in confluent monolayers and in microcolonies. The simulations showed that the degree of the bystander effect was higher in microcolonies than in confluent cells, suggesting that gap junction communication may be involved in the bystander effect. However, when the gap junction hypothesis was tested by treatment of microcolonies with 30 microM dieldrin, an inhibitor of gap junctional intercellular communication, there was no reduction of the bystander effect, indicating that this effect was not mediated by gap junctional intercellular communication. PDT influenced phosphorylation of tyrosine residues in several proteins in the cells. Protein phosphorylation is important in cellular signaling pathways and may be involved in the bystander effect, for example by influencing the mode of cell death.

Animals↗
PubMed2002

Gap junction intercellular communication propagates cell death in cancerous cells.

Gap junction intercellular communication (GJIC) or cell coupling has an important function in maintaining tissue homeostasis and is thus a critical factor in the life and death balance of cells. While the role of GJIC in cell growth regulation has been much studied, its involvement in apoptosis remains unclear. In this study we elucidated the possibility that cell death is propagated via gap junctions, employing the rat bladder carcinoma cell line BC31. BC31 cells proliferate quickly, are tumorigenic, and are well-coupled via gap junctions that contain the gap junction protein Connexin43 (Cx43). In addition, these cells are predisposed to spontaneous death by apoptosis, particularly upon achieving confluency. We found that many dying BC31 cells express Cx43 just as their non-apoptotic counterparts do. Furthermore, Cx43 in apoptotic cells could be functionally competent, supporting coupling of these cells with their non-apoptotic neighbors, and as a result, clusters of coordinately dying cells were observed. The role of Cx43 and GJIC in propagating cell death was shown by analysing clones of BC31 cells expressing a mutant of Cx43 that is a dominant negative inhibitor of GJIC, and by using beta-glycyrrhetinic acid to inhibit intrinsic cell coupling in BC31 cells: in both cases the formation of clusters of dying cells was abrogated, and the intensity of cell death was considerably decreased. These results suggest that GJIC spreads cell-killing signals initially generated by a single cell that spontaneously initiates apoptosis, into healthy surrounding cells, thus increasing the level of cell death. Treatment of BC31 cells with the sleep-inducing lipid Oleamide, which selectively restricts gap junction permeability to Ca(2+) ions, did not abrogate coordinated cell death by clusters, indicating that Ca(2+) ions are the most probable cell-killing signals spread through gap junctions.

Animals↗
PubMed1996

Effect of perchloroethylene and its metabolites on intercellular communication in clone 9 rat liver cells.

Gap junction intercellular communication (IC) is thought to be important in chemical carcinogenesis as abnormalities in IC have been found in cancer cells. Perchloroethylene (PERC) is metabolized in rodent liver to dichloroacetic acid (DCA) and trichloroacetic acid (TCA), which are rodent liver carcinogens. Chloral hydrate (CH) and trichloroethanol (TCEth) are kidney metabolites. We used Lucifer yellow scrape-load dye transfer as a measure of IC to look at the effect of PERC, DCA, TCA, CH, and TCEth on Clone 9 cell cultures (normal rat liver cells). Four independent experiments were performed for each chemical using exposure times of 1, 4, 6, 24, 48, and 168 h. Concentrations for each chemical varied and were based on preliminary data on effect and cytotoxicity. To compare the relative effectiveness of each chemical to cause biological change, we identified the lowest concentration and shortest time to significantly reduce dye transfer. DCA caused a significant change at 10 mM at 6 h; TCA, 1 mM at 1 h; CH and TCEth, 1 mM at 24 h; and PERC, 0.01 mM at 48 h. Over a 24-h treatment period, the relative efficiencies, as defined by the concentration needed to produce 50% reduction in IC, were PERC (0.3 mM) >> TCA (3.8 mM) > TCEth (6.6 mM) = CH (7.0 mM) >> DCA (41 mM). Time-course data indicated that PERC, DCA, and TCA produced reduction in IC in a similar fashion, but 5 mM CH or TCEth exhibited variances from these results and may indicate specific cell responses to these chemicals. The mechanism(s) responsible for inhibition of IC by these structurally related chemicals needs to be established.

Analysis of Variance↗
PubMed1997

Altered gap junctional intercellular communication in neoplastic rat esophageal epithelial cells.

Gap junctional intercellular communication (GJIC) is reduced in many neoplastic cells, but few data exist for esophageal neoplasms. GJIC was examined by fluorescent dye microinjection in two nontumorigenic and two highly tumorigenic rat esophageal epithelial cell lines. All lines expressed high levels of dye coupling in homologous cell culture. In cocultures of nontumorigenic and tumorigenic cells, however, only one of six cell combinations displayed significant heterologous GJIC. Northern, Western, and immunohistochemical analyses indicated that all four cell lines expressed comparable levels of connexin43 (Cx43), but not connexin32 or connexin26, and formed Cx43-containing gap junction plaques at cell-cell interfaces. Immunostaining of rat esophageal frozen sections demonstrated that esophageal epithelial cells expressed Cx43 in vivo. In normal epithelium, the highest expression was seen in the basal cells and little suprabasal staining was evident. In preneoplastic and neoplastic lesions of the esophageal epithelium which were induced by treating rats with N-nitrosomethylbenzylamine, Cx43 staining of the basal layer was also seen but appeared to be more diffuse compared to normal epithelium. In addition, suprabasal Cx43 staining was apparent in dysplastic and papillomatous lesions. These results indicate that Cx43 is expressed in normal and neoplastic rat esophageal cells and that the cells exhibit extensive homologous GJIC, but little heterologous GJIC. This lack of heterologous GJIC may be due to differences in cell adhesion proteins or other factors.

Animals↗
PubMed2003

Gap junctional intercellular communication and cellular response to heat stress.

Gap junctional intercellular communication (GJIC) is essential in the maintenance of tissue homeostasis and has been implicated in tumor suppression. Recent studies have indicated that GJIC is also involved in cellular stress responses to low dose ionizing radiation, UV light and hydrogen peroxide. However, the contribution of GJIC to the heat stress response has not yet been elucidated. We here demonstrate a potential link between GJIC and the heat stress response. First, we investigated whether the abolition of GJIC by lindane affects heat sensitivity in normal human cells. Lindane potentiated cell killing by heat shock at 43 degrees C, whereas little or no cytotoxicity was observed at 37 degrees C. Nuclear translocation of heat shock protein 72 (HSP72) was interrupted by lindane, although its induction was not affected. These results indicate that lindane exacerbates hyperthermic lethality via disrupted nuclear translocation of HSP72 protein. Second, we assessed whether heat shock alters GJIC and phosphorylation of gap junction connexin (Cx) proteins in normal human cells. Persistent heat treatment augmented Cx43 phosphorylation in a heat- and time-dependent fashion and this phosphorylation was recovered after heat shock. GJIC was also disturbed by heat shock. These results indicate that heat shock augments Cx43 phosphorylation leading to GJIC abrogation. Our present results imply that GJIC contributes to protection against heat stress and that loss of GJIC function during carcinogenesis exacerbates hyperthermic lethality.

Cell Communication↗
PubMed2002

Intercellular communication and human prostate carcinogenesis.

Gap-junction-mediated intercellular communication (GJIC) is required for completion of embryonic development, tissue homeostasis, and regulation of cell proliferation and death. Although, as emphasized in several reports, defects or disruption of GJIC may be important in carcinogenesis, the potential role of GJIC in the onset and progression of human prostate cancer remains ill-defined. The gap junction channel-forming connexins (Cx) comprise a multigene family of highly conserved proteins that are differentially expressed in a tissue- and development-specific manner; changes in connexin expression are also commonly seen during cellular differentiation. However, when multiple connexins are concurrently expressed, gap junction channels may consist of more than one connexin species. This is important, because only certain pairings give rise to functional channels. In our studies, we investigated GJIC in a panel of both nontumorigenic (RWPE-1) and malignant (RWPE-2, LNCaP, DU-145) human prostate epithelial cells, compared to a normal rat liver epithelial F344 (WB-1) cell line, as it was found to be junctionally proficient. In addition, expression and regulation of Cx43 and Cx32 were also inspected using western blot analysis. The ability of hormones, antihormones, and the antihypertensive drug forskolin to restore GJIC in nontumorigenic and malignant human prostate epithelial cells was examined by the scrape-loading/dye transfer (SL/DT) or fluorescence recovery after photobleaching (FRAP) methods using an Ultima laser cytometer. Results from both assays showed that neither nontumorigenic nor malignant prostate cells have functional GJIC. However, both estrone (E1) and forskolin (FK) induced a significant increase (4.4- and 2.8-fold, respectively) in cell-cell communication only in the RWPE-1 cells. Interestingly, the use of Matrigel, a solubilized basement membrane, as substrate for cell attachment and growth resulted in the rescue of GJIC activity in RWPE-1 cells, as revealed by the SL/DT method. Furthermore, E1 induced a twofold increase in connexin 43 (Cx43), whereas forskolin caused a 50% reduction in Cx32 expression in RWPE-1 cells. These data suggest that agents that increase Cx43:Cx32 ratio may restore GJIC in junctionally deficient cells, providing a basis for the development of new strategies for the prevention and treatment of human prostate cancer.

Carcinogenicity Tests↗
PubMed1991

Intercellular communication in the early human embryo.

A preliminary study on intercellular communicative devices in the early human embryo has been made using dye-coupling techniques and electron microscopy (EM). Lucifer yellow injected into single blastomeres of embryos at the 4-cell stage up to the late morula stage did not spread to neighbouring cells, indicating that gap junctions and cytoplasmic bridges are not significant pathways for information transfer. Dye spread was first observed in the blastocyst stage, where trophectoderm cells and inner mass cells were shown to be in communication through gap junctions. Studies at the EM level confirmed this finding. Tight junctions and desmosome-like structures, apparent from the 6-cell stage onward, were located both peripherally and centrally and were initially nonzonular. The role of intercellular devices in the primary differentiation of the human embryo is discussed.

Blastocyst↗
PubMed1998

Inhibition of intrinsic gap-junction intercellular communication and enhancement of tumorigenicity of the rat bladder carcinoma cell line BC31 by a dominant-negative connexin 43 mutant.

The tumor-suppressive property of the connexin gap-junction proteins was postulated from the fact that their function of cell coupling is impaired in most cancer cells. However, in conflict with this notion, certain cancer cells are able to communicate through gap junctions despite their malignancy. To explain this phenomenon, we studied by using a dominant-negative strategy the effect on tumorigenicity of loss of intrinsic gap-junction intercellular communication (GJIC) in the rat bladder carcinoma cell line BC31, which shows both expression of connexin 43 (Cx43) and intercellular communication. In cells transfected with a mutant Cx43 with seven residues deleted from the internal loop at positions 130-136 (Cx43delta), transport of the resulting connexin protein to the plasma membrane occurred normally, but the GJIC of the cells was effectively abolished at the level of permeability of established gap junctions. Dominant-negative inhibition of GJIC by Cx43delta accelerated growth of BC31 cells in nude mice. In contrast, when GJIC in BC31 cells was artificially enforced by transfection of wild-type Cx43, the cells lost the capacity to grow in vivo. Decreased phosphorylation of Cx43delta suggested close interaction of the internal loop of connexin with its commonly phosphorylated domains in the C-terminal tail and involvement of this interaction in gap-junction permeability. Therefore, we conclude that the intrinsic GJIC observed in cancer cells should be considered a tumor-suppressor factor and that its level may influence malignant growth capacity.

Animals↗
PubMed2003

[Effects of power frequency magnetic field on gap junction intercellular communication of astrocytes].

OBJECTIVE: In order to explore if power frequency magnetic field (PFMF) can act as cancer promoter or be synergistic with phorbol 12-myristate 13-acetate (TPA) in cancer promotion, the effects of 50 Hz MF on gap junction intercellular communication (GJIC) of astrocytes were observed. METHODS: Fluorescence redistribution after photobleaching (FRAP) was adopted to observe the recovery of fluorescence intensity in the bleached cells thus to estimate intercellular communication by gap junction. Comparative fluorescence intensity recovery rate (CFIRR) was as evaluation index. The effects of 50 Hz MF alone or with TPA on GJIC of astrocytes were studied. RESULTS: After 3 ng/ml TPA treatment for 1 hour, M(d) of CFIRR was 4.53%/min, whereas that in the control group was 9.74%/min (H = 12.084, P < 0.005). After exposure to 0.8 and 1.6 mT magnetic field for 24 hours respectively, M(d) of CFIRR was 8.25%/min and 6.68%/min respectively, no significant difference from that of control (H = 32.617, P > 0.05). After exposure to 0.8 and 1.6 mT magnetic field for 23 hours then combined with 3 ng/ml TPA treatment for 1 hour, M(d) of CFIRR was 3.32%/min and 2.85%/min respectively, also no significant difference from that in the group treated with 3 ng/ml TPA alone (H = 2.589, P > 0.05). CONCLUSION: 50 Hz MF (within 0 - 1.6 mT) alone could not inhibit GJIC of astrocytes; with TPA, could not enhance the inhibition of TPA on GJIC of astrocytes. But with MF intensity increasing, the inhibition of MF on GJIC showed elevated tendency.

Animals↗