Effects of various K+ channel blockers on spontaneous glycine release at rat spinal neurons

Shoudai, Kiyomitsu; Nonaka, Kiku; Maeda, Megumi; Wang, Zhi Ming; Jeong, Hyo Jin; Higashi, Hideho; Murayama, Nobuki; Akaike, Norio

doi:10.1016/j.brainres.2006.09.097

Cited by 21 publications

(13 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly, the probability of GABA release onto neurons of the central amygdala is enhanced by iberiotoxin and paxilline, as reflected by increased amplitude of evoked IPSCs and increased frequency of miniature IPSCs (Li, Madison, & Moore, 2014). Iberiotoxin also augments glycine release in the spinal cord (Shoudai et al, 2007). In addition, BK channel activity mediates the inhibitory influence of presynaptic α1-adrenoreceptors on GABA release onto ventral tegmental area dopaminergic neurons (Velasquez-Martinez, Vazquez-Torres, Rojas, Sanabria, & Jimenez-Rivera, 2015).…”

Section: Role Of Bk Channels In Cns Cellular Physiologymentioning

confidence: 99%

BK Channels in the Central Nervous System

Contet

Goulding

Kuljis

et al. 2016

International Review of Neurobiology

129

170

View full text Add to dashboard Cite

Large conductance Ca2+- and voltage-activated K+ (BK) channels are widely distributed in the postnatal central nervous system (CNS). BK channels play a pleiotropic role in regulating the activity of brain and spinal cord neural circuits by providing a negative feedback mechanism for local increases in intracellular Ca2+ concentrations. In neurons, they regulate the timing and duration of K+ influx such that they can either increase or decrease firing depending on the cellular context, and they can suppress neurotransmitter release from presynaptic terminals. In addition, BK channels located in astrocytes and arterial myocytes modulate cerebral blood flow. Not surprisingly, both loss and gain of BK channel function have been associated with CNS disorders such as epilepsy, ataxia, mental retardation, and chronic pain. On the other hand, the neuroprotective role played by BK channels in a number of pathological situations could potentially be leveraged to correct neurological dysfunction.

show abstract

Section: Role Of Bk Channels In Cns Cellular Physiologymentioning

confidence: 99%

BK Channels in the Central Nervous System

Contet

Goulding

Kuljis

et al. 2016

International Review of Neurobiology

129

170

View full text Add to dashboard Cite

show abstract

“…Extrapolating from our data in the nodose soma, where the C-fiber population (but not A-or Ah-type neurons) responds to MgTx with an increase in the duration of the action potential, we propose that the responding NTS neurons are innervated by C-type fibers and that the increase in the duration of the presynaptic action potential in the presence of MgTx augments transmitter release, leading to an increased amplitude of the synaptic potential (Wheeler et al 1996;Raffaelli et al 2004;Stephens and Mochida 2005). A role for Kv1.3 in transmitter release has been reported in other neuronal studies (OhnoShosaku et al 1996;Shoudai et al 2007;Doczi et al 2008). Our data suggest that Kv1.3 in presynaptic terminals, presumably from C-type fibers, plays a significant role in modulating neurotransmitter release at the NTS.…”

Section: Discussionmentioning

confidence: 82%

“…Kv1.3 has been reported to be targeted primarily to axons (Veh et al 1995;Rivera et al 2005) and to be involved in the regulation of transmitter release (Ohno-Shosaku 1996, Shoudai et al 2007Doczi et al 2008). A recent study (Gazula et al 2010) has identified Kv1.3 in presynaptic terminals in the calyx of Held.…”

mentioning

confidence: 95%

Kv1.3 channels regulate synaptic transmission in the nucleus of solitary tract

Ramirez‐Navarro

Glazebrook

Kane-Sutton

et al. 2011

Journal of Neurophysiology

View full text Add to dashboard Cite

The voltage-gated K(+) channel Kv1.3 has been reported to regulate transmitter release in select central and peripheral neurons. In this study, we evaluated its role at the synapse between visceral sensory afferents and secondary neurons in the nucleus of the solitary tract (NTS). We identified mRNA and protein for Kv1.3 in rat nodose ganglia using RT-PCR and Western blot analysis. In immunohistochemical experiments, anti-Kv1.3 immunoreactivity was very strong in internal organelles in the soma of nodose neurons with a weaker distribution near the plasma membrane. Anti-Kv1.3 was also identified in the axonal branches that project centrally, including their presynaptic terminals in the medial and commissural NTS. In current-clamp experiments, margatoxin (MgTx), a high-affinity blocker of Kv1.3, produced an increase in action potential duration in C-type but not A- or Ah-type neurons. To evaluate the role of Kv1.3 at the presynaptic terminal, we examined the effect of MgTx on tract evoked monosynaptic excitatory postsynaptic currents (EPSCs) in brain slices of the NTS. MgTx increased the amplitude of evoked EPSCs in a subset of neurons, with the major increase occurring during the first stimuli in a 20-Hz train. These data, together with the results from somal recordings, support the hypothesis that Kv1.3 regulates the duration of the action potential in the presynaptic terminal of C fibers, limiting transmitter release to the postsynaptic cell.

show abstract

“…The channel requires relatively high Ca i 2+ concentrations and depolarization to activate and may contribute little to the resting membrane potential but seems more important for balancing local calcium signaling in smooth muscle, determining action potential duration and presynaptic neurotransmitter release. Pharmacological inhibition of BK channel is known to induce vasoconstriction [2], increased firing rate in some neurons [17,38] but decreased firing rate in others [10], action potential broadening [20], loss of spike frequency adaptation [18], and neuronal bursting [42]. This diversity of observations suggests that BK channels play different roles in parts of the nervous system and in various cellular compartments of neurons.…”

Section: Introductionmentioning

confidence: 96%

Neuronal fast activating and meningeal silent modulatory BK channel splice variants cloned from rat

Poulsen

Jansen‐Olesen

Olesen

et al. 2010

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

The big conductance calcium-activated K(+) channel (BK) is involved in regulating neuron and smooth muscle cell excitability. Functional diversity of BK is generated by alpha-subunit splice variation and co-expression with beta subunits. Here, we present six different splice combinations cloned from rat brain or cerebral vascular/meningeal tissues, of which at least three variants were previously uncharacterized (X1, X2(92), and X2(188)). An additional variant was identified by polymerase chain reaction but not cloned. Expression in Xenopus oocytes showed that the brain-specific X1 variant displays reduced current, faster activation, and less voltage sensitivity than the insert-less Zero variant. Other cloned variants Strex and Slo27,3 showed slower activation than Zero. The X1 variant contains sequence inserts in the S1-S2 extracellular loop (8 aa), between intracellular domains RCK1 and RCK2 (4 aa at SS1) and upstream of the calcium "bowl" (27 aa at SS4). Two other truncated variants, X2(92) and X2(188), lacking the intracellular C-terminal (stop downstream of S6), were cloned from cerebral vascular/meningeal tissue. They appear non-functional as no current expression was observed, but the X2(92) appeared to slow the activation of the Zero variant when co-expressed. Positive protein expression of X2(92) was observed in oocytes by immunoblotting and fluorescence using a yellow fluorescent protein-tagged construct. The functional characteristics of the X1 variant may be important for a subpopulation of BK channels in the brain, while the "silent" truncated variants X2(92) and X2(188) may play a role as modulators of other BK channel variants in a way similar to well known beta subunits.

show abstract

Effects of various K+ channel blockers on spontaneous glycine release at rat spinal neurons

Cited by 21 publications

References 56 publications

BK Channels in the Central Nervous System

BK Channels in the Central Nervous System

Kv1.3 channels regulate synaptic transmission in the nucleus of solitary tract

Neuronal fast activating and meningeal silent modulatory BK channel splice variants cloned from rat

Contact Info

Product

Resources

About