Expression of the small conductance Ca 2+ -activated K + channel, SK3, in the olfactory ensheathing glial cells of rat brain

Fujita, Akikazu; Takeuchi, Tadayoshi; Hanai, Jun; Hata, Fumiaki

doi:10.1007/s00441-003-0752-y

Cited by 9 publications

(10 citation statements)

References 38 publications

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“…For comparison, we also examined the SNC and found that in agreement with previous studies using the same antibody, SK3 reactivity is strongly localized to the SNC (Tacconi et al, 2001; Fujita et al, 2003). Like the SON, these observations correlate with mRNA distribution (Köhler et al, 1996; Stocker and Pedarzani, 2000; Tacconi et al, 2001) and the apamin‐sensitivity of an mAHP (Seutin et al, 1993; Wolfart et al, 2003).…”

Section: Discussionsupporting

confidence: 88%

“…The substantia nigra, pars compacta (SNC) is another region known to contain SK3 mRNA (Köhler et al, 1996; Stocker and Pedarzani, 2000; Tacconi et al, 2001) and an apamin‐blockable mAHP (e.g., Seutin et al, 1993; Ping and Sheperd, 1996; Wolfart et al, 2001). SK3 expression is also prominent in the SNC, as judged by studies employing the same antibody as that used here (Tacconi et al, 2001; Fujita et al, 2003). We thus examined the SNC in order to compare the pattern of SK3 expression with that in the SON.…”

Section: Resultssupporting

confidence: 62%

“…Although reports of electrophysiological studies in vitro have noted the presence of CA 2+ ‐dependent K + currents in neuroglia (Barres et al, 1990), including apamin‐blockable currents (Burnard et al, 1990; Jalonen et al, 1997; Bychkov et al, 2001), and although specific apamin binding sites on astrocyte membranes have been found (Seagar et al, 1987), there has been little investigation of the presence of SK‐type channels in astrocytes in situ. A notable exception is a recent report demonstrating SK3‐like immunoreactivity in the glia investing olfactory nerve fascicles in the olfactory bulb (Fujita et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

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Immunocytochemical localization of small‐conductance, calcium‐dependent potassium channels in astrocytes of the rat supraoptic nucleus

Armstrong

Rubrum

Teruyama

et al. 2005

J of Comparative Neurology

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Supraoptic nucleus (SON) neurons possess a prominent afterhyperpolarization (AHP) that contributes to spike patterning. This AHP is probably underlain by a small-conductance, CA2+-dependent, K+ type 3 (SK3) channel. To determine the distribution of SK3 channels within the SON, we used immunocytochemistry in rats and in transgenic mice with a regulatory cassette on the SK3 gene, allowing regulated expression with dietary doxycycline (DOX). In rats and wild-type mice, SK3 immunostaining revealed an intense lacy network surrounding SON neurons, with weak staining in neuronal somata and dendrites. In untreated, conditional SK3 knockout mice, SK3 was overexpressed, but the pericellular pattern in the SON was similar to that of rats. DOX-treated transgenic mice exhibited no SK3 staining in the SON. Double staining for oxytocin or vasopressin neurons revealed weak co-localization with SK3 but strong staining surrounding each neuron type. Electron microscopy showed that SK3-like immunoreactivity was intense between neuronal somata and dendrites, in apparent glial processes, but weak in neurons. This was confirmed by using confocal microscopy and double staining for glial fibrillary acidic protein (GFAP) and SK3: many GFAP-positive processes in the SON, and in the ventral dendritic/glial lamina, were shown to contain SK3-like immunoreactivity. These studies suggest a prominent role of SK3 channels in astrocytes. Given the marked plasticity in glial/neuronal relationships, as well as studies suggesting that astrocytes in the central nervous system can generate prominent CA2+ transients to various stimuli, a CA2+-dependent K+ channel may help SON astrocytes with K+ buffering whenever astrocyte intracellular CA2+ is increased.

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Section: Discussionsupporting

confidence: 88%

Section: Resultssupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

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Immunocytochemical localization of small‐conductance, calcium‐dependent potassium channels in astrocytes of the rat supraoptic nucleus

Armstrong

Rubrum

Teruyama

et al. 2005

J of Comparative Neurology

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“…SK3 is preferentially expressed in phylogenetically older brain regions (thalamus, basal ganglia, cerebellum, brainstem) [47-50]; for instance, KCNN3 mRNA [47] is relatively high in the caudate putamen and in dopaminergic neurons of the substantia nigra, and SK3 immunoreactivity [49] is present in the caudate putamen. Reports of SK3 expression in non-neuronal cells are very limited; it is expressed in astrocytes in the supraoptic nucleus and in olfactory ensheathing glial cells [51,52], and it contributes to vasodilation in response to endothelium-derived hyperpolarizing factor (EDHF) [53]. Here, we observed widely distributed and punctate SK3 immunostaining in the healthy adult rat striatum (except in white matter tracts), and for the first time, have shown SK3 immunoreactivity in microglia in vivo and in vitro .…”

Section: Discussionmentioning

confidence: 99%

The Ca2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro

Schlichter

Kaushal

Moxon‐Emre

et al. 2010

J Neuroinflammation

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BackgroundSmall-conductance Ca2+ activated K+ channels are expressed in the CNS, where KCNN2/SK2/KCa2.2 and KCNN3/SK3/KCa2.3 help shape the electrical activity of some neurons. The SK3 channel is considered a potential therapeutic target for diseases and disorders involving neuron hyper-excitability but little is known about its expression and roles in non-neuronal cells in either the healthy or damaged CNS. The purpose of this study was to examine expression of KCNN3/SK3 in CNS microglia in vivo and in vitro, and to use an established in vitro model to determine if this channel contributes to the neurotoxic capacity of activated microglia.MethodsKCNN3 mRNA (real-time RT-PCR) and SK3 immunoreactivity were examined in rat microglia. Lipopolysaccharide was then used to activate microglia (monitored by iNOS, nitric oxide, activation of NF-κB and p38 MAPK) and transform them to a neurotoxic state. Microglia-mediated neuron damage (TUNEL, activated caspase 3) and nitrotyrosine levels were quantified using a two-chamber system that allowed microglia to be treated with channel blockers, washed and then added to neuron/astrocyte cultures. Contributions of SK3 to these processes were discriminated using a subtractive pharmacological approach with apamin and tamapin. ANOVA and post-hoc tests were used to assess the statistical significance of differences between treatment groups. SK3 immunoreactivity was then compared in the normal and damaged adult rat striatum, by injecting collagenase (a hemorrhagic stroke) or endothelin-1 (a transient ischemic stroke).ResultsKCNN3 mRNA was prevalent in cultured microglia and increased after lipopolysaccharide-induced activation; SK3 channel blockade inhibited microglial activation and reduced their ability to kill neurons. SK3 immunoreactivity was prevalent in cultured microglia and throughout the adult rat striatum (except white matter tracts). After strokes, SK3 was highly expressed in activated microglia/macrophages within the lesions, but reduced in other cells.ConclusionsSK3 is expressed in microglia in both the healthy and damaged adult striatum, and mechanistic in vitro studies show it contributes to transformation of microglia to an activated neurotoxic phenotype. Thus, SK3 might be a therapeutic target for reducing inflammation-mediated acute CNS damage. Moreover, its roles in microglia must be considered when targeting this channel for CNS diseases, disorders and reducing neuron hyper-excitability.

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“…The immunohistochemical study was carried out by the method described previously [13]. Briefly, wild-type mice were deeply anesthetized with pentobarbital sodium (50 mg/kg À1 , i.p.)…”

Section: Immunohistochemical Studymentioning

confidence: 99%

Roles of PACAP and PHI as inhibitory neurotransmitters in the circular muscle of mouse antrum

Toyoshima

Takeuchi

Goto

et al. 2005

Pflugers Arch - Eur J Physiol

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Mediators of neurogenic responses of the gastric antrum were studied in wild-type and pituitary adenylate cyclase-activating polypeptide (PACAP) -knockout (KO) mice. Electrical field stimulation (EFS) to the circular muscle strips of the wild-type mouse antrum induced a triphasic response; rapid transient relaxation and contraction, and sustained relaxation that was prolonged for an extended period after the end of EFS. The transient relaxation and contraction were completely inhibited by L-nitroarginine and atropine, respectively. The sustained relaxation was significantly inhibited by a PACAP receptor antagonist, PACAP(6-38). The antral strips prepared from PACAP-KO mice unexpectedly exhibited a tri-phasic response. However, the sustained relaxation was decreased to about one-half of that observed in wild-type mice. PACAP(6-38) inhibited EFS-induced sustained relaxation (33.5% of control) in PACAP-KO mice. Anti-peptide histidine isoleucine (PHI) serum partially (the 30% inhibition) or significantly (the 60% inhibition) inhibited the sustained relaxations in the wild-type and PACAP-KO mice, respectively. The immunoreactivities to the anti-PACAP and anti-PHI serums were found in myenteric ganglia of the mouse antrum. These results suggest that nitric oxide and acetylcholine mediate the transient relaxation and contraction, respectively, and that PACAP and PHI separately mediate the sustained relaxation in the antrum of the mouse stomach.

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Expression of the small conductance Ca 2+ -activated K + channel, SK3, in the olfactory ensheathing glial cells of rat brain

Cited by 9 publications

References 38 publications

Immunocytochemical localization of small‐conductance, calcium‐dependent potassium channels in astrocytes of the rat supraoptic nucleus

Immunocytochemical localization of small‐conductance, calcium‐dependent potassium channels in astrocytes of the rat supraoptic nucleus

The Ca2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro

Roles of PACAP and PHI as inhibitory neurotransmitters in the circular muscle of mouse antrum

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