Inhibition of BK channels contributes to the second phase of the response to TRH in clonal rat anterior pituitary cells

Haug, Trude M.; Hafting, Torkel; Sand, Olav

doi:10.1111/j.1365-201x.2004.01266.x

Cited by 9 publications

(6 citation statements)

References 55 publications

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“…Tandem-pore domain K + channels have previously been described in Hcrt neurons and K 2P channels are thought to mediate inhibition of Hcrt neurons by glucose (Burdakov et al, 2006). However, TRH has also been reported to inhibit Ca 2+ -dependent K + (BK) channels in pituitary cells (Haug et al, 2004), observations consistent with Ca 2+ -dependent effects of TRH in Hcrt cells (Fig. 2C and D).…”

Section: Discussionsupporting

confidence: 80%

Thyrotropin-Releasing Hormone Increases Behavioral Arousal through Modulation of Hypocretin/Orexin Neurons

Hara¹,

Gerashchenko²,

Wisor³

et al. 2009

J. Neurosci.

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Thyrotropin-releasing hormone (TRH) has previously been shown to promote wakefulness and to induce arousal from hibernation. Expression of TRH-R1 (TRH receptor 1) is enriched in the tuberal and lateral hypothalamic area (LHA), brain regions in which the hypocretin/orexin (Hcrt) cells are located. Because the Hcrt system is implicated in sleep/wake control, we hypothesized that TRH provides modulatory input to the Hcrt cells. In vitro electrophysiological studies showed that bath application of TRH caused concentration-dependent membrane depolarization, decreased input resistance, and increased firing rate of identified Hcrt neurons. In the presence of tetrodotoxin, TRH induced inward currents that were associated with a decrease in frequency, but not amplitude, of miniature postsynaptic currents (PSCs). Ion substitution experiments suggested that the TRH-induced inward current was mediated in part by Ca 2ϩ influx. Although TRH did not significantly alter either the frequency or amplitude of spontaneous excitatory PSCs, TRH (100 nM) increased the frequency of spontaneous inhibitory PSCs by twofold without affecting the amplitude of these events, indicating increased presynaptic GABA release onto Hcrt neurons. In contrast, TRH significantly reduced the frequency, but not amplitude, of miniature excitatory PSCs without affecting miniature inhibitory PSC frequency or amplitude, indicating that TRH also reduces the probability of glutamate release onto Hcrt neurons. When injected into the LHA, TRH increased locomotor activity in wild-type mice but not in orexin/ataxin-3 mice in which the Hcrt neurons degenerate postnatally. Together, these results are consistent with the hypothesis that TRH modulates behavioral arousal, in part, through the Hcrt system.

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Section: Discussionsupporting

confidence: 80%

Thyrotropin-Releasing Hormone Increases Behavioral Arousal through Modulation of Hypocretin/Orexin Neurons

Hara¹,

Gerashchenko²,

Wisor³

et al. 2009

J. Neurosci.

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“…Under current-clamp condition, cilostazol could also reduce the firing of action potentials in GH 3 cells. These results were further verified by using cell-attached patch recordings to examine the firing of action potentials and the activity of BK Ca channels simultaneously [55,56]. Cilostazol applied to the bath significantly increased the probability of channel openings.…”

Section: Cilostazolmentioning

confidence: 57%

Pharmacological Roles of the Large-Conductance Calcium-Activated Potassium Channel

Wu¹,

Wu²,

Lin³

2006

CTMC

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The gating of large-conductance Ca(2+)-activated K(+) (BK(Ca)) channel is primarily controlled by intracellular Ca(2+) and/or membrane depolarization. These channels play a role in the coupling of excitation-contraction and stimulus-secretion. A variety of structurally distinct compounds may influence the activity of these channels. Squamocin, an Annonaceous acetogenin, could interact with the BK(Ca) channel to increase the amplitude of Ca(2+)-activated K(+) current in coronary smooth muscle cells. Its stimulatory effect is related to intracellular Ca(2+) concentrations. In inside-out patches, application of ceramide to the bath suppressed the activity of BK(Ca) channels recorded from pituitary GH(3) cells and from retinal pigment epithelial cells. ICI-182,780, an estrogen receptor antagonist, was found to modulate BK(Ca)-channel activity in cultured endothelial cells and smooth muscle cells in a mechanism unlinked to the inhibition of estrogen receptors. Caffeic acid phenethyl ester (CAPE) and its analogy, cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate, could directly increase the activity of BK(Ca) channels in GH(3) cells. CAPE also reduced the frequency and amplitude of intracellular Ca(2+) oscillations in these cells. The CAPE-stimulated activity in BK(Ca) channels is thought to be unassociated with its inhibition of NF-kappaB activation. Cilostazol, an inhibitor of cyclic nucleotide phosphodiesterase, could stimulate BK(Ca) channel-activity and reduce the firing of action currents simultaneously in GH(3) cells. Therefore, the regulation by these compounds of BK(Ca) channels may in part be responsible for their regulatory actions on cell functions.

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“…CCK increases action potential firing and GABA release in the dentate gyrus by inhibiting a Ca 2+ ‐dependent K + channel (Deng & Lei, 2006). Similarly, TRH has been reported to inhibit Ca 2+ ‐dependent K + channels (Haug et al 2004). The mechanisms underlying TRH‐mediated increase in GABA release in the dentate gyrus granule cells will be examined in the future.…”

Section: Discussionmentioning

confidence: 98%

Thyrotropin‐releasing hormone increases GABA release in rat hippocampus

Deng

Porter

Shin

et al. 2006

The Journal of Physiology

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Thyrotropin-releasing hormone (TRH) is a tripeptide that is widely distributed in the brain including the hippocampus where TRH receptors are also expressed. TRH has anti-epileptic effects and regulates arousal, sleep, cognition, locomotion and mood. However, the cellular mechanisms underlying such effects remain to be determined. We examined the effects of TRH on GABAergic transmission in the hippocampus and found that TRH increased the frequency of GABA A receptor-mediated spontaneous IPSCs in each region of the hippocampus but had no effects on miniature IPSCs or evoked IPSCs. TRH increased the action potential firing frequency recorded from GABAergic interneurons in CA1 stratum radiatum and induced membrane depolarization suggesting that TRH increases the excitability of interneurons to facilitate GABA release. TRH-induced inward current had a reversal potential close to the K + reversal potential suggesting that TRH inhibits resting K + channels. The involved K + channels were sensitive to Ba 2+ but resistant to other classical K + channel blockers, suggesting that TRH inhibits the two-pore domain K + channels. Because the effects of TRH were mediated via Gα q/11 , but were independent of its known downstream effectors, a direct coupling may exist between Gα q/11 and K + channels. Inhibition of the function of dynamin slowed the desensitization of TRH responses. TRH inhibited seizure activity induced by Mg 2+ deprivation, but not that generated by picrotoxin, suggesting that TRH-mediated increase in GABA release contributes to its anti-epileptic effects. Our results demonstrate a novel mechanism to explain some of the hippocampal actions of TRH.

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Inhibition of BK channels contributes to the second phase of the response to TRH in clonal rat anterior pituitary cells

Cited by 9 publications

References 55 publications

Thyrotropin-Releasing Hormone Increases Behavioral Arousal through Modulation of Hypocretin/Orexin Neurons

Thyrotropin-Releasing Hormone Increases Behavioral Arousal through Modulation of Hypocretin/Orexin Neurons

Pharmacological Roles of the Large-Conductance Calcium-Activated Potassium Channel

Thyrotropin‐releasing hormone increases GABA release in rat hippocampus

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