Roles of A-type potassium currents in tuning spike frequency and integrating synaptic transmission in noradrenergic neurons of the A7 catecholamine cell group in rats

Min, Ming‐Yuan; Wu, Yu-Wei; Shih, Pei‐Yu; Lu, Hsin-Wei; Hsu, C-H; Li, M J; Yang, He

doi:10.1016/j.neuroscience.2010.03.063

Cited by 13 publications

(18 citation statements)

References 53 publications

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“…All data shown hereafter were obtained from neurons showing DBH immunoreactivity ( Fig. 1, C-E), which also exhibited previously reported physiological properties of NAergic A7 neurons, including not showing voltage sag and rebound APs on injection of a hyperpolarizing current pulse and showing a prominent voltagedependent delay in initiation of the first AP on injection of depolarizing current pulses (Min et al 2008b(Min et al , 2009(Min et al , 2010.…”

Section: Naergic A7 Neurons Express Functional Gaba B Receptorssupporting

confidence: 71%

“…Slices were transferred to an immersion-type recording chamber mounted on an upright microscope (BX51WI; Olympus Optical, Tokyo, Japan) and continuously perfused with oxygenated ACSF at 2-3 ml/min. Neurons were viewed using Nomarski optics; those located ϳ200 m rostral to the anterior border of Mo5 and having a large cell body (diameter ϳ20 -25 m) were considered NAergic A7 neurons (Min et al 2008b(Min et al , 2009(Min et al , 2010 and used for recordings (Fig. 1, A and B).…”

Section: Methodsmentioning

confidence: 99%

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GABA_B receptor-mediated tonic inhibition of noradrenergic A7 neurons in the rat

Wu¹,

Wang²,

Cy³

et al. 2011

Journal of Neurophysiology

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Noradrenergic (NAergic) A7 neurons that project axonal terminals to the dorsal horn of the spinal cord to modulate nociceptive signaling are suggested to receive tonic inhibition from local GABAergic interneurons, which are under the regulation of descending analgesic pathways. In support of this argument, we presently report GABA(B) receptor (GABA(B)R)-mediated tonic inhibition of NAergic A7 neurons. Bath application of baclofen induced an outward current (I(Bac)) in NAergic A7 neurons that was blocked by CGP 54626, a GABA(B)R blocker. The I(Bac) was reversed at about -99 mV, displayed inward rectification, and was blocked by Ba(2+) or Tertipian-Q, showing it was mediated by G protein-activated inward-rectifying K(+) (GIRK) channels. Single-cell RT-PCR results suggested that GIRK1/3 heterotetramers might dominate functional GIRK channels in NAergic A7 neurons. Under conditions in which GABA(A) and glycine receptors were blocked, bath application of GABA inhibited the spontaneous firing of NAergic A7 neurons in a dose-dependent manner. Interestingly, CGP 54626 application not only blocked the effect of GABA but also increased the firing rate to 126.9% of the control level, showing that GABA(B)Rs were constitutively active at an ambient GABA concentration of 2.8 μM and inhibited NAergic A7 neurons. GABA(B)Rs were also found at presynaptic excitatory and inhibitory axonal terminals in the A7 area. Pharmacological activation of these GABA(B)Rs inhibited the release of neurotransmitters. No physiological role was found for GABA(B)Rs on excitatory terminals, whereas those on the inhibitory terminals were found to exert autoregulatory control of GABA release.

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Section: Naergic A7 Neurons Express Functional Gaba B Receptorssupporting

confidence: 71%

Section: Methodsmentioning

confidence: 99%

GABA_B receptor-mediated tonic inhibition of noradrenergic A7 neurons in the rat

Wu¹,

Wang²,

Cy³

et al. 2011

Journal of Neurophysiology

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“…As the degree of 4-AP-sensitivity already indicated the contribution of K V 4 channels, we used the K V 4-specific blocker HpTx2 in the following [13,31,41]. In the presence of TEA (10 mM), the amplitude of the early current peak decreased with increasing concentrations of HpTx2 (Fig.…”

Section: Pharmacological Properties Of I a In Intralaminar Tc Neuronsmentioning

confidence: 99%

“…In intralaminar TC neurons, less than 10% of I A was sensitive to these toxins, although the high selectivity of BDS toxins for K V 3.4 channels has been questioned recently [51]. (4) Based on the strong reduction of I A by HpTx2 [13,31,41], quantitative PCR, and immunohistochemical staining, our findings corroborate the view that more dendritic K V 4.2 and more somatic K V 4.3, but not K V 4.1, constitute I A in intralaminar TC neurons. It has been noticed before that K V 4.1 reveals very low expression in most brain areas, including the thalamus [42].…”

Section: Expression Profile Of K V Channel Subunits Producing Transiementioning

confidence: 99%

A-type K+ currents in intralaminar thalamocortical relay neurons

Kanyshkova

Broicher

Meuth

et al. 2011

Pflugers Arch - Eur J Physiol

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Transient A-type K+ currents (I(A)) are known to influence the firing pattern of a number of thalamic cell types, but have not been investigated in intralaminar thalamocortical (TC) relay neurons yet. We therefore combined whole-cell patch-clamp techniques, PCR analysis, and immunohistochemistry to investigate the voltage-dependent and pharmacological properties of I(A) and to determine its molecular basis in TC neurons from the centrolateral, paracentral, and centromedial thalamic nuclei. I(A) revealed half-maximal (V (h)) activation and inactivation at about -17 and -67 mV, respectively. At a concentration of 5-10 mM 4-aminopyridine (4-AP) completely blocked I(A). Furthermore, I(A) was nearly unaffected by two sea anemone toxins (blood depressing substances 1 and 2, BDS1 and BDS2; 6-8% block at a concentration of 1 μM) but strongly sensitive to the K(V)4 channel blocker Heteropoda venatoria toxin 2 (HpTx2; about 45% block at a concentration of 5 μM). PCR screening revealed the expression of K(V)4.1-4.3, with strongest expression for K(V)4.2 and weak expression for K(V)4.1. Accordingly K(V)4.1 was not detected in immunohistochemical staining. Furthermore, K(V)4.2 and K(V)4.3 revealed mainly dendritic and somatic staining, respectively. Together with current clamp recordings, these findings point to a scenario where the fast transient I(A) in intralaminar TC neurons has a depolarized threshold at potentials negative to -50 mV, is substantially generated by K(V)4.2 and K(V)4.3 channels, allows prominent burst firing at hyperpolarized potentials, prevents the generation of high-threshold potentials, generates a delayed onset of firing at more depolarized potentials, and allows fast tonic firing.

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“…Synaptic terminals that contain dopamine-β-hydroxylase appear to form synapses both with identified spinothalamic tract neurons (Westlund et al, 1990), and with unidentified dorsal horn neurons (Hagihira et al, 1990; Doyle and Maxwell, 1991a; Doyle and Maxwell, 1991b). Behavioral studies have shown that stimulating the A7 area using electrical or chemical applications produces nociceptive modulation (Yeomans et al, 1992; Yeomans, 1992; Holden et al, 1999; Nuseir et al, 1999; Nuseir and Proudfit, 2000; Holden and Naleway, 2001; Min et al, 2008; Bajic and Commons, 2010; Min et al, 2010). …”

Section: Introductionmentioning

confidence: 99%

The posterior hypothalamus exerts opposing effects on nociception via the A7 catecholamine cell group in rats

et al. 2012

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Stimulation of the posterior hypothalamic area (PH) produces antinociception in rats and humans, but the precise mechanisms are unknown. The PH forms anatomical connections with the parabrachial area, which contains the pontine A7 catecholamine cell group, a group of spinally projecting noradrenergic neurons known to produce antinociception in the dorsal horn. The aim of the present study was to determine whether PH-induced antinociception is mediated in part through connections with the A7 cell group in female Sprague-Dawley rats, as measured by the tail flick and foot withdrawal latency. Stimulation of the PH with the cholinergic agonist carbachol (125 nmol) produced antinociception that was blocked by pretreatment with atropine sulfate. Intrathecal injection of the α2-adrenoceptor antagonist yohimbine reversed PH-induced antinociception, but the α1-adrenoceptor antagonist WB4101 facilitated antinociception. Intrathecal injection of normal saline had no effect. In a separate experiment, cobalt chloride, which reversibly arrests synaptic activity, was microinjected into the A7 cell group and blocked PH-induced antinociception. These findings provide evidence that the PH modulates nociception in part through connections with the A7 catecholamine cell group through opposing effects. Antinociception occurs from actions at α2-adrenoceptors in the dorsal horn, while concurrent hyperalgesia occurs from actions of norepinephrine at α1-adrenoceptors. This hyperalgesic response likely attenuates antinociception from PH stimulation.

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Roles of A-type potassium currents in tuning spike frequency and integrating synaptic transmission in noradrenergic neurons of the A7 catecholamine cell group in rats

Cited by 13 publications

References 53 publications

GABA_B receptor-mediated tonic inhibition of noradrenergic A7 neurons in the rat

GABA_B receptor-mediated tonic inhibition of noradrenergic A7 neurons in the rat

A-type K+ currents in intralaminar thalamocortical relay neurons

The posterior hypothalamus exerts opposing effects on nociception via the A7 catecholamine cell group in rats

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Roles of A-type potassium currents in tuning spike frequency and integrating synaptic transmission in noradrenergic neurons of the A7 catecholamine cell group in rats

Cited by 13 publications

References 53 publications

GABAB receptor-mediated tonic inhibition of noradrenergic A7 neurons in the rat

GABAB receptor-mediated tonic inhibition of noradrenergic A7 neurons in the rat

A-type K+ currents in intralaminar thalamocortical relay neurons

The posterior hypothalamus exerts opposing effects on nociception via the A7 catecholamine cell group in rats

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Product

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GABA_B receptor-mediated tonic inhibition of noradrenergic A7 neurons in the rat

GABA_B receptor-mediated tonic inhibition of noradrenergic A7 neurons in the rat