Heparin prevents M-current over-recovery but not M-current suppression in bullfrog sympathetic ganglion neurones

Chen, Hsinyo; Kurenny, Dmitry E.; Smith, Peter A.

doi:10.1016/0006-8993(93)91075-4

Cited by 11 publications

(9 citation statements)

References 12 publications

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“…Since the response to 200 nM PMA in the presence of the kinase inhibitor is larger that in its absence, H-7 does not antagonize phorbol ester responses. These data also confirm that the maximal IM suppression which can be attained following brief (1-2 min) applications of PMA is less than that which can be attained with muscarine (Bosma & Hille, 1989;Selyanko et al, 1990 obvious 'over-recovery' (Pfaffinger, 1988;Chen et al, 1993 As with acute responses, the presence of 50 JM H-7 on both sides of the membrane had no obvious effect on the response to the long-term application of PMA. Figure 3c compares the amount of IM remaining after 10-20min in 20nM PMA (data points were collected from 6 cells) with that remaining in the presence of PMA plus H-7 (data from 4 cells; 50 JM H-7 on both sides of the membrane).…”

Section: Resultssupporting

confidence: 69%

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Phorbol ester‐induced M‐current suppression in bull‐frog sympathetic ganglion cells: insensitivity to kinase inhibitors

Chen

Jassar

Kurenny

et al. 1994

British J Pharmacology

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1The effects of l-oleoyl-2-acetyl-sn-glycerol (OAG), phorbol 12-myristate 13-acetate (PMA), 4--phorbol and muscarine on B-neurones from bull-frog sympathetic ganglion were studied by means of whole-cell patch-clamp recording. With the exception of 4-x-phorbol, all of these agonists reduced the steady-state outward current recorded at -30 mV as a result of suppression of a voltage-dependent, non-inactivating K+-current, the M-current, (IM).2 Of the cells tested, 34% displayed bona fide responses to OAG (20 fLM). The chance of recording a response was not decreased when the protein kinase inhibitor, l-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7; 50 or 75 tLM) was included simultaneously in the extracellular solution and in the pipette solution. 3 The presence of 50 pM H-7 on both sides of the membrane or 500 nM staurosporine in the pipette solution did not prevent responses to brief (1-2 min) or prolonged (>20 min) applications of PMA.4 Brief (1-2min) extracellular application of H-7 (300t9M) suppressed IM by about 29%.5 The most likely explanation of these data is that PMA and OAG modulate IM via a mechanism that is independent of protein kinase C (PKC). The availability of such a mechanism poses new questions as to the mechanism of muscarine-induced IM suppression.

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Section: Resultssupporting

confidence: 69%

“…For abbreviations, see text. obvious 'over-recovery' (Pfaffinger, 1988;Chen et al, 1993). Long-term application of 20 nM PMA slowly suppresses IM to almost the same level as seen with muscarine.…”

Section: Resultsmentioning

confidence: 85%

Phorbol ester‐induced M‐current suppression in bull‐frog sympathetic ganglion cells: insensitivity to kinase inhibitors

Chen

Jassar

Kurenny

et al. 1994

British J Pharmacology

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“…7A). This phenomenon (over-recovery) has also been observed for M-channels after inhibition by muscarine (Marrion et al 1991;Chen et al 1993;Tokimasa et al 1996;Kurennyi et al 1997), suggesting that some K + channels share the same properties. We considered that the over-recovery of the outward K + channels after CCK-mediated inhibition was at least part of the mechanism underlying the CCK-induced late phase of reduction (see Discussion).…”

Section: Cck Inhibits Camentioning

confidence: 78%

“…The possible reason for this discrepancy is that the change in AHP amplitude is so subtle that it could not reliably be detected after averaging the action potentials. Interestingly, over-recovery of M-channel currents has also been observed after agonist-induced inhibition, and it is related to agonist-induced intracellular Ca 2+ release (Marrion et al 1991;Chen et al 1993;Tokimasa et al 1996;Kurennyi et al 1997). Whether intracellular Ca 2+ release underlies CCK-induced over-recovery of I K(Ca) remains to be determined.…”

Section: Ionic Mechanisms Underlying Cck-mediated Modulation Of Gaba mentioning

confidence: 99%

Bidirectional modulation of GABAergic transmission by cholecystokinin in hippocampal dentate gyrus granule cells of juvenile rats

Deng

Lei

2006

The Journal of Physiology

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A receptor-mediated synaptic transmission in the hippocampal formation and then explored the underlying cellular mechanisms by focusing on the dentate gyrus region, where the highest levels of CCK-binding sites have been detected. Our results indicate that activation of CCK-B receptors initially and transiently increased spontaneous IPSC (sIPSC) frequency, followed by a persistent reduction. The effects of CCK were more evident in juvenile rats, suggesting that they are developmentally regulated. Cholecystokinin failed to modulate the miniature IPSCs recorded in the presence of TTX and the amplitude of the evoked IPSCs, but produced a transient increase followed by a reduction in action potential firing frequency recorded from GABAergic interneurons, suggesting that CCK acts by modulating the excitability of the interneurons to regulate GABA release. Cholecystokinin reduced the amplitude of the after-hyperpolarization of the action potentials, and application of paxilline or charybdotoxin considerably reduced CCK-mediated modulation of sIPSC frequency, suggesting that the effects of CCK are related to the inhibition of Ca 2+ -activated K + currents (I K(Ca) ). The effects of CCK were independent of the functions of phospholipase C, intracellular Ca 2+ release, protein kinase C or phospholipase A 2 , suggesting a direct coupling between the G proteins of CCK-B receptors and I K(Ca) . Our results provide a novel mechanism underlying CCK-mediated modulation of GABA release.

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“…Note added in proof Recently, Chen et al (1993) reported that overrecovery is attenuated by intracellular application of 150 PM heparin. This observation has been taken as support of the hypothesis that IP,-mediated intracellular calcium release mediates overrecovcry, because heparin competitively inhibits the interaction of IP, with its receptor (K, = 2.7 nM).…”

Section: Discussionmentioning

confidence: 99%

On the role of arachidonic acid in M-current modulation by muscarine in bullfrog sympathetic neurons

Villarroel

1994

J. Neurosci.

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The modulation by muscarine or LHRH of the potassium M-current (IM) in whole-cell voltage-clamped bullfrog sympathetic neurons presents an initial phase of current reduction, followed, after agonist removal, by a transient enhancement or “overrecovery.” Employing a fast solution exchange system, an inhibitory process and an enhancing process were distinguished kinetically. The extent of overrecovery increased with the extent of the preceding inhibition. The rate and degree of inhibition increased with the concentration of agonist. In contrast, the rate of recovery and the extent of overrecovery were independent. The half-lives of the inhibitory and enhancing processes were 21 and 53 sec, respectively. Several observations suggest that arachidonic acid (AA) may be involved in overrecovery: (1) AA enhanced IM in a dose- dependent and reversible manner, with an IC50 of 2.8 microM. (2) Muscarine inhibited the A-current (IA), a potassium current that is blocked by AA. (3) Phospholipase A2 inhibitors (quinacrine and bromophenacyl bromide) and a lipoxygenase inhibitor (nordihydroguaiaretic acid) prevented overrecovery, without affecting the rate or extent of IM inhibition significantly. However, kinetic analysis indicates that these drugs were preventing overrecovery by prolonging the half-life of the inhibitory process to > 80 sec (e.g., not necessarily by blocking the enhancing pathway). In addition, the extent of IA inhibition was less than expected if AA was mediating both IM enhancement and IA inhibition. The observed relation between extent and rate of overrecovery, and the action of arachidonic acid metabolism inhibitors can be accounted for by a model proposing that the agonist alters the equilibrium between three pools of M-channels.

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Heparin prevents M-current over-recovery but not M-current suppression in bullfrog sympathetic ganglion neurones

Cited by 11 publications

References 12 publications

Phorbol ester‐induced M‐current suppression in bull‐frog sympathetic ganglion cells: insensitivity to kinase inhibitors

Phorbol ester‐induced M‐current suppression in bull‐frog sympathetic ganglion cells: insensitivity to kinase inhibitors

Bidirectional modulation of GABAergic transmission by cholecystokinin in hippocampal dentate gyrus granule cells of juvenile rats

On the role of arachidonic acid in M-current modulation by muscarine in bullfrog sympathetic neurons

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