Compartmental distribution of hyperpolarization-activated cyclic-nucleotide-gated channel 2 and hyperpolarization-activated cyclic-nucleotide-gated channel 4 in thalamic reticular and thalamocortical relay neurons

Abbas, Syed Y.; Ying, Shui‐Wang; Goldstein, Peter A.

doi:10.1016/j.neuroscience.2006.05.034

Cited by 51 publications

(51 citation statements)

References 54 publications

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“…For recordings of I h currents, an "I h isolation solution" was used, which contained the following (in mM): 114 NaCl, 26 NaHCO 3 , 15 KCl, 1.25 MgCl 2 , 2 CaCl 2 , 11 D-glucose, 0.001 tetrodotoxin (TTX), 1 BaCl 2 , 0.1 NiCl 2 , 0.04 D-(Ϫ)-2-amino-5-phosphonopentanoic acid (D-AP-5), and 0.02 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (Abbas et al, 2006;Rateau and Ropert, 2006). For recordings of I h currents and voltage responses, the pipette solution contained the following (in mM): 135 K ϩ -gluconate, 5 NaCl, 10 HEPES, 0.5 EGTA, 2 ATP-Mg 2ϩ , 0.3 GTP-Na ϩ , and 10 Na 2 -phosphocreatine, the pH adjusted to 7.3 with KOH.…”

Section: Methodsmentioning

confidence: 99%

“…Immunohistochemistry techniques for HCN channel labeling were modified from those described previously (Abbas et al, 2006). Briefly, wild-type (ϩ/ϩ) and HCN2 knock-out (Ϫ/Ϫ) mice of the same age (P28 -P35) were used.…”

Section: Methodsmentioning

confidence: 99%

“…Brain slices containing the RTN (and other structures) were sectioned at 20 m at a 45°angle using a vibrating microtome (Leica). After extensive rinsing in PBS (100 mM, pH 7.4) and permeabilization with 0.1% Triton X-100 in PBS for 15 min, freefloating brain slices from ϩ/ϩ and Ϫ/Ϫ mice were processed simultaneously for triple immunofluorescence labeling (Abbas et al, 2006). A blocking solution (10% donkey serum prepared in PBS) was used to minimize nonspecific binding before incubation of slices in a primary antibody.…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

“…Somatic I h in RTN neurons is small even at hyperpolarized membrane potentials (Abbas et al, 2006;Rateau and Ropert, 2006). We previously demonstrated that HCN2 is preferentially expressed in the dendritic spines of RTN neurons (Abbas et al, 2006). The small somatic I h recorded in these neurons may reflect current generation at sites distant from the soma (as in dendritic spines) and subsequent signal attenuation resulting from a large dendritic electrotonic length (Destexhe et al, 1996).…”

Section: Introductionmentioning

confidence: 98%

See 4 more Smart Citations

Dendritic HCN2 Channels Constrain Glutamate-Driven Excitability in Reticular Thalamic Neurons

Ying¹,

Fan²,

Abbas³

et al. 2007

J. Neurosci.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 98%

See 3 more Smart Citations

Dendritic HCN2 Channels Constrain Glutamate-Driven Excitability in Reticular Thalamic Neurons

Ying¹,

Fan²,

Abbas³

et al. 2007

J. Neurosci.

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Colocalization of hyperpolarization‐activated, cyclic nucleotide‐gated channel subunits in rat retinal ganglion cells

Stradleigh

Ogata

Partida

et al. 2011

J of Comparative Neurology

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The current-passing pore of mammalian hyperpolarization-activated, cyclic nucleotide-gated ("HCN") channels is formed by subunit isoforms denoted HCN1-4. In various brain areas, antibodies directed against multiple isoforms bind to single neurons and the current ("Ih") passed during hyperpolarizations differs from that of heterologously expressed homomeric channels. By contrast, retinal rod, cone, and bipolar cells appear to use homomeric HCN channels. Here, we assess the generality of this pattern by examining HCN1 and HCN4 immunoreactivity in rat retinal ganglion cells, measuring Ih in dissociated cells, and testing whether HCN1 and HCN4 protein coimmunoprecipitate. Nearly half of the ganglion cells in whole-mounted retinae bound antibodies against both isoforms. Consistent with colocalization and physical association, 8-bromo-cAMP shifted the voltage-sensitivity of Ih less than that of HCN4 channels and more than that of HCN1 channels, and HCN1 coimmunoprecipitated with HCN4 from membrane fraction proteins. Lastly, the immunopositive somata ranged in diameter from the smallest to the largest in rat retina, the dendrites of immunopositive cells arborized at various levels of the inner plexiform layer and over fields of different diameters, and Ih activated with similar kinetics and proportions of fast and slow components in small, medium, and large somata. These results show that different HCN subunits colocalize in single retinal ganglion cells, identify a subunit that can reconcile native Ih properties with the previously reported presence of HCN4 in these cells, and indicate that Ih is biophysically similar in morphologically diverse retinal ganglion cells and differs from Ih in rods, cones, and bipolar cells.

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Thalamocortical Circuit Controls Neuropathic Pain via Up-regulation of HCN2 in the Ventral Posterolateral Thalamus

et al. 2022

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The thalamocortical (TC) circuit is closely associated with pain processing. The hyperpolarization-activated cyclic nucleotide-gated (HCN) 2 channel is predominantly expressed in the ventral posterolateral thalamus (VPL) that has been shown to mediate neuropathic pain. However, the role of VPL HCN2 in modulating TC circuit activity is largely unknown. Here, by using optogenetics, neuronal tracing, electrophysiological recordings, and virus knockdown strategies, we showed that the activation of VPL TC neurons potentiates excitatory synaptic transmission to the hindlimb region of the primary somatosensory cortex (S1HL) as well as mechanical hypersensitivity following spared nerve injury (SNI)-induced neuropathic pain in mice. Either pharmacological blockade or virus knockdown of HCN2 (shRNA-Hcn2) in the VPL was sufficient to alleviate SNI-induced hyperalgesia. Moreover, shRNA-Hcn2 decreased the excitability of TC neurons and synaptic transmission of the VPL–S1HL circuit. Together, our studies provide a novel mechanism by which HCN2 enhances the excitability of the TC circuit to facilitate neuropathic pain.

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Compartmental distribution of hyperpolarization-activated cyclic-nucleotide-gated channel 2 and hyperpolarization-activated cyclic-nucleotide-gated channel 4 in thalamic reticular and thalamocortical relay neurons

Cited by 51 publications

References 54 publications

Dendritic HCN2 Channels Constrain Glutamate-Driven Excitability in Reticular Thalamic Neurons

Dendritic HCN2 Channels Constrain Glutamate-Driven Excitability in Reticular Thalamic Neurons

Colocalization of hyperpolarization‐activated, cyclic nucleotide‐gated channel subunits in rat retinal ganglion cells

Thalamocortical Circuit Controls Neuropathic Pain via Up-regulation of HCN2 in the Ventral Posterolateral Thalamus

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