ライフサイエンスコーパス: HCN channel

1 ated cyclic nucleotide-gated channels (Ih or HCN channels).

2 that has many similarities to the mammalian HCN channel.

3 . the primary cyclic nucleotide modulator of HCN channels.

4 inhibits the cyclic-nucleotide dependence of HCN channels.

5 and gating and voltage sensing in eukaryotic HCN channels.

6 clic nucleotide cCMP as another regulator of HCN channels.

7 rsed polarity gating, and cAMP regulation in HCN channels.

8 ed with the unique biophysical activities of HCN channels.

9 unopanned by an anti-Thy1 antibody activated HCN channels.

10 dimers instead of tetramers, as observed in HCN channels.

11 4 channel, as well as with other subtypes of HCN channels.

12 chanism for TRIP8b binding and regulation of HCN channels.

13 e, and bipolar cells appear to use homomeric HCN channels.

14 e closed state relative to the open state in HCN channels.

15 s, showing that CaN is a strong modulator of HCN channels.

16 many insights into cAMP-dependent gating in HCN channels.

17 with time lapse imaging of fluorophore-fused HCN channels.

18 o activity-dependent mechanisms mediated via HCN channels.

19 type 5b cells but that do not express these HCN channels.

20 al roles and biophysical behavior of CNG and HCN channels.

21 ith recent reports of native and recombinant HCN channels.

22 eolin was in accordance with the decrease in HCN channels.

23 of regulating the expression and function of HCN channels.

24 indicating that SHANK3 functions to organize HCN channels.

25 which hyperpolarizes the activation range of HCN channels.

26 or reducing the cAMP-dependent regulation of HCN channels.

27 perpolarization and cyclic nucleotide-gated (HCN) channel.

28 arization-activated cyclic nucleotide-gated (HCN) channels.

29 arization-activated cyclic nucleotide-gated (HCN) channels.

30 arization-activated cyclic nucleotide-gated (HCN) channels.

31 ation-activated cyclic nucleotide-modulated (HCN) channels.

32 arization-activated cyclic nucleotide-gated (HCN) channels.

33 GABAergic inhibition that was necessary for HCN channel activation.

34 zation-activated current (I(f), generated by HCN channels) activation from nonphysiological voltages

35 ays a fundamental role in the fine-tuning of HCN channel activity and is critical for the modulation

36 mechanisms underlying the dual regulation of HCN channel activity by cAMP/TRIP8b, we determined the N

37 hat the amplitude and properties of ensemble HCN channel activity were uniform in patches excised fro

38 KCNQ2/3 channel activity and a reduction in HCN channel activity.

39 Furthermore, the HCN channel agonist lamotrigine rescued the electrophysi

40 Similar to direct blockade of HCN channels, alpha(2)-NA receptor stimulation produced

41 Although HCN channels also limited the temporal summation of EPSP

42 Thus, do pre-synaptic HCN channels alter the rate of synaptic vesicle exocytos

43 w insights into the cAMP-dependent gating in HCN channel and the interpretation of protein allostery

44 Ultrastructurally, HCN channels and alpha2A-ARs were colocalized in dendrit

45 or mechanism underlying proper expression of HCN channels and I(h) in vivo, and suggest that targetin

46 ings establish cCMP as a gating regulator of HCN channels and indicate that this cyclic nucleotide ha

47 TRIP8b TPR domains both promotes binding to HCN channels and limits binding to type 1 peroxisomal ta

48 teracts with the carboxyl-terminal region of HCN channels and regulates their cell-surface expression

49 Our results uncover specific roles for HCN channels and their plasticity in phase-coding schema

50 ation-activated and nucleotide-gated cation (HCN) channels and establish their role in determining th

51 arization-activated cyclic nucleotide-gated (HCN) channels and plays a fundamental role in influencin

52 arization-activated Cyclic Nucleotide-gated (HCN) channels and strengthening the functional connectiv

53 arization-activated cyclic nucleotide-gated (HCN) channels, and contributes to depolarizing the affer

54 ide-binding domain and the C terminus of the HCN channel are critical for conferring specificity to T

55 ng, and computational modeling revealed that HCN channels are activated by GABA(A) receptor-mediated

56 Whereas HCN channels are activated by voltage and CNG channels a

57 HCN channels are actively trafficked to dendrites by bin

58 Neuronal HCN channels are also regulated by tetratricopeptide rep

59 Here, we demonstrate that HCN channels are developmentally precocious in OSNs and

60 In conclusion, HCN channels are expressed in multiple neuronal subcellu

61 HCN channels are found in many neurons in the retina, bu

62 If HCN channels are held open for prolonged times (>50 ms),

63 motor neurons, and therefore tested whether HCN channels are involved in simple forms of learning of

64 These studies show that HCN channels are key regulators of synaptic integration

65 Intriguingly, HCN channels are present in certain cortical axons and s

66 ts of hyperpolarizing currents, we show that HCN channels are present in the plasma membrane and in t

67 ties and subcellular distribution pattern of HCN channels are therefore tuned to regulate the interac

68 arization-activated cyclic-nucleotide-gated (HCN) channels are activated by hyperpolarizations that c

69 n-activated, cyclic nucleotide-gated cation (HCN) channels are critical regulators of neuronal excita

70 perpolarization and cyclic-nucleotide-gated (HCN) channels are expressed in the AIS and decrease spik

71 arization-activated cyclic nucleotide-gated (HCN) channels are expressed in the brain and heart and a

72 ation-activated cyclic nucleotide-modulated (HCN) channels are pacemaker channels whose currents cont

73 arization-activated cyclic nucleotide-gated (HCN) channels are pacemakers in cardiac myocytes and neu

74 arization-activated cyclic nucleotide-gated (HCN) channels are subthreshold activated voltage-gated i

75 arization-activated cyclic nucleotide-gated (HCN) channels are subthreshold, voltage-gated ion channe

76 ation-activated cyclic nucleotide-modulated (HCN) channels are tetrameric proteins that evoke electri

77 arization-activated cyclic-nucleotide-gated (HCN) channels are tetramers that evoke rhythmic electric

78 Our results highlight KCNQ2/3 and HCN channels as potential targets for designing novel th

79 TRIP8b knockout mice lacking functional HCN channels as well as both HCN1 and HCN2 knockout mice

80 hyperpolarization-activated cAMP-regulated (HCN) channel as a model system to study the intersubunit

81 rpolarization-activated cation-nonselective (HCN) channels as an active mechanism to counteract locat

82 arization activated cyclic nucleotide-gated (HCN) channels as blockade with ZD7288 eliminated directi

83 r stress weakens PFC function via opening of HCN channels at network synapses.

84 of Ih activation that causes the opening of HCN channels at rest, thereby increasing VSN excitabilit

85 , we generated a knock-out mouse lacking the HCN channel auxiliary subunit, tetratricopeptide repeat-

86 Knockout (KO) of the brain-specific HCN-channel auxiliary subunit tetratricopeptide repeat-c

87 arization-activated cyclic nucleotide-gated (HCN) channels belong to the superfamily of voltage-gated

88 red that hyperpolarization-activated cation (HCN) channel block with the specific anatagonist ZD7288

89 Behaviorally, acute HCN channel blockade by local injection of ZD7288 in the

90 r alpha2A-AR stimulation, cAMP inhibition or HCN channel blockade enhanced spatially tuned delay-rela

91 C impaired working memory performance, while HCN channel blockade in PFC prevented this impairment in

92 n increased HCN channel current, while local HCN channel blockade in primate PFC protected task-relat

93 augmented by transfection or blocked with an HCN channel blocker (ZD7288), show modulated fusion pore

94 ed whether septal infusions of the selective HCN channel blocker ZD7288 would impair performance on t

95 These effects were unchanged by the Ca2+ and HCN channel blockers mibefradil and ZD7288, respectively

96 odification of this activity during block of HCN channels, both reflect altered frequency distributio

97 dependence of I(h), the current produced by HCN channels, but did not affect the loss of HCN channel

98 tion-activated, cyclic nucleotide-regulated (HCN) channels, but does not alter gating of the plant hy

99 Our results show that blockade of HCN channels by ZD7288 decreases MNC firing rate with si

100 hyperpolarization-activated cAMP-regulated (HCN) channel by simultaneously recording channel opening

101 Cyclic AMP binds to the HCN channel C terminus and variably stabilizes its open

102 on, and suggest that potassium ion action on HCN channels can modulate neurotransmission, preserving

103 putational model confirms that activation of HCN channels can override a preference for centripetal s

104 e cAMP-induced conformational changes in the HCN channel CNBD.

105 ional changes induced by cAMP binding to the HCN channel CNBD.

106 HCN channels contain a K(+) channel selectivity filter-f

107 urrent in the motor neurons, suggesting that HCN channels contribute to conditioning through this pat

108 KEY POINTS: The present study tested whether HCN channels contribute to the organization of motor cor

109 The present study tested whether HCN channels contribute to the organization of motor cor

110 rization-activated, cyclic nucleotide-gated (HCN) channels contribute to cationic Ih current in neuro

111 activated cation current (I(h)), mediated by HCN channels, contributes to intrinsic neuronal properti

112 arization-activated cyclic nucleotide-gated (HCN) channels, contributes to the initiation and regulat

113 -photon glutamate uncaging demonstrated that HCN channels control the amplitude and duration of synap

114 demonstrated that D1R stimulation increased HCN channel current, while local HCN channel blockade in

115 n vitro recordings tested for D1R actions on HCN channel current, while recordings in monkeys perform

116 a dynamic interaction among Kir2, Kleak, and HCN channel currents in shaping membrane potential and t

117 on-activated cyclic nucleotide-gated cation (HCN) channel currents have been identified in various pe

118 and somatic recording sites, the blockade of HCN channels decreased excitability.

119 evealed that the pharmacological blockade of HCN channels decreased voltage compartmentalization and

120 Increases in HCN channel density or in input variance increased the S

121 tent activator of vomeronasal Ih and suggest HCN channel-dependent vomeronasal gain control of social

122 ation-activated and cyclic nucleotide-gated (HCN) channels, determined the size and time course of th

123 arization-activated cyclic nucleotide-gated (HCN) channels directly bind cAMP through their cytoplasm

124 Notably, cCMP is a partial agonist of HCN channels, displaying an efficacy of approximately 0.

125 These results suggest two mechanisms of HCN channel downregulation after SE, one dependent on an

126 dels, thereby establishing the importance of HCN channel dysfunction in NF1.

127 tential were examined: ZD-7288, a blocker of HCN channels; EAA-090, an NMDA antagonist; and WAY-13298

128 Similar to CNG and HCN channels, EAG and ERG channels contain a cyclic nucl

129 arization-activated cyclic nucleotide-gated (HCN) channels enhanced presynaptic Na(+) concentration a

130 Inhibition of pre-synaptic HCN channels enhances miniature excitatory post-synaptic

131 njured epileptic cortex underwent changes in HCN channel expression and became hyperexcitable.

132 e regulatory networks and pathways governing HCN channel expression and function in the brain are lar

133 hat presynaptic, but not dendritic, cortical HCN channel expression and function is comparable in adu

134 describe a novel developmental plasticity of HCN channel expression in axonal and presynaptic compart

135 HCN channels, but did not affect the loss of HCN channel expression.

136 the affective aspects of pain, exhibits high HCN channel expression.

137 HCN channels expression were decreased at the mRNA and p

138 The two other members of the HCN channel family, HCN1 and HCN3, are not sensitive to

139 the activation curves of two members of the HCN channel family, HCN2 and HCN4, to more depolarized v

140 Within the HCN channel family, KCTD3 specifically binds to HCN3 and

141 In doing so, HCN channels form the first of several systems in the re

142 ablishes the pacemaking driven by sodium and HCN channels found in juvenile SN.

143 They are able to restore HCN channel function and reduce behavioral hypersensitiv

144 ; conversely, pharmacological enhancement of HCN channel function decreased spontaneous IPSC frequenc

145 gulate excitability in neurons, and blocking HCN channel function has been proposed as a novel antide

146 and progressive downregulation of dendritic HCN channel function increases neuronal excitability and

147 processes that are critically dependent upon HCN channel function may be distinctly influenced.

148 we showed a critical role RPTPalpha plays in HCN channel function via tyrosine dephosphorylation.

149 ke dendritic channels, wild-type presynaptic HCN channel function was persistently decreased followin

150 axis in mPFC neurons underlie alterations to HCN channel function, which can influence descending inh

151 n important step toward the understanding of HCN channel function.

152 s hyperpolarization-dependent opening of the HCN channel gate; cAMP binding relieves this autoinhibit

153 antoro et al. and Zolles et al.) report that HCN channel gating and expression are controlled by Trip

154 Our findings illuminate the mechanism of HCN channel gating and provide a framework that will fac

155 first found that CaN inhibition upregulated HCN channel gating and reduced neuronal excitability und

156 spontaneous seizures cause downregulation of HCN channel gating are yet unknown.

157 ance of proximal C terminus in modulation of HCN channel gating by diverse agents, and advance neuron

158 cuculline at 35-37 degrees C) reproduced the HCN channel gating change seen in vivo.

159 al of these phosphorylation changes restored HCN channel gating downregulation and neuronal hyperexci

160 Decoupling of HCN channel gating from cAMP and internal protons reveal

161 ther the seizure-dependent downregulation of HCN channel gating was due to altered phosphorylation si

162 itro seizure-induced hyperpolarized shift in HCN channel gating, and the shift was fully reversed by

163 compete for binding the HCN CNBD to control HCN channel gating, kinetics, and trafficking.

164 pilepsy contributes to the downregulation of HCN channel gating, which consequently produces neuronal

165 The leucine zipper is essential for HCN channel gating.

166 d thus provides a model of how cAMP controls HCN channel gating.

167 ation-activated cyclic-nucleotide-modulated (HCN) channel gene family, is known to be functionally im

168 arization-activated cyclic nucleotide-gated (HCN) channels generate a pacemaking current, I(h), which

169 The HCN channels generated an excitatory inward current (I(h

170 Here we examined a role for HCN channels, given their ability to alter synaptic inte

171 arization-activated cyclic nucleotide-gated (HCN) channels (h channels) are the molecular basis for t

172 The unitary neuronal HCN channels had voltage-dependent latencies to first ch

173 To date, HCN channels have been considered to be animal-specific.

174 While native HCN channels have been studied at the macroscopic level,

175 sical characteristics of individual neuronal HCN channels have not been described.

176 multiple actions of anesthetics on neuronal HCN channels, highlight the importance of proximal C ter

177 Here, we demonstrate the presence of an HCN channel homolog (SroHCN) in the choanoflagellate pro

178 arization-activated cyclic nucleotide-gated (HCN) channels, I(h), in hippocampal maturation and speci

179 -electron microscopy structures of the human HCN channel in the absence and presence of cAMP at 3.5 A

180 s modulate neuronal Ih and the corresponding HCN channels in a subunit-specific and cAMP-dependent ma

181 usly described depolarizing influence of the HCN channels in baroreceptor neurons and their terminals

182 Inhibition of HCN channels in dissociated OSNs significantly reduced n

183 rrent knowledge of dysregulation of I(h) and HCN channels in epilepsy in light of the multifaceted fu

184 Acute pharmacological inhibition of HCN channels in forelimb motor cortex decreases reaching

185 sults indicate that the loss of caveolae and HCN channels in ICCs-DM is important in the pathogenesis

186 to the substantial dendritic localization of HCN channels in many types of neurons.

187 Recent studies have implicated HCN channels in neuropathological conditions including e

188 sruption of the normal expression pattern of HCN channels in pyramidal neuron dendrites.

189 Somato-dendritic HCN channels in pyramidal neurons modulate spike firing

190 We also analyze the properties of HCN channels in salamander rods and cones, from the biop

191 Together the data demonstrate that HCN channels in STN neurons selectively counteract GABA(

192 rthermore, the control of spike threshold by HCN channels in the AIS can be altered through serotoner

193 vioral pharmacology revealed that functional Hcn channels in the basolateral amygdala are necessary f

194 sing behavioral pharmacology, revealing that Hcn channels in the basolateral amygdala are required fo

195 rgic system and strengthen the importance of HCN channels in the control of hydroelectrolyte homeosta

196 nd distributed impact of the high density of HCN channels in the distal apical dendritic arbor.

197 s, we examined the expression of isoforms of HCN channels in the L6-S1 spinal cord and bladder affere

198 ts appear to be the first demonstration that HCN channels in the medial septum influence memory.

199 obability, in a manner distinct from that of HCN channels in the soma and dendrites.

200 arization-activated cyclic-nucleotide-gated (HCN) channels in altering hippocampal theta-frequency LF

201 rties of hyperpolarization-activated cation (HCN) channels in CA1 hippocampal pyramidal neurons in co

202 arization-activated cyclic nucleotide-gated (HCN) channels in human SAN has only been investigated at

203 arization-activated cyclic nucleotide-gated (HCN) channels in ICCs-DM were responsible for the detrus

204 cyclic nucleotide-gated nonselective cation (HCN) channels in rat layer 5B pyramidal neurons.

205 ation-activated cyclic nucleotide-regulated (HCN) channels in the brain associate with their auxiliar

206 immunoelectron microscopy localized D1R and HCN channels, in vitro recordings tested for D1R actions

207 es sequence similarity to eukaryotic CNG and HCN channels-in the presence of a saturating concentrati

208 We show that in rods and cones, HCN channels increase the natural frequency response of

209 The subcellular distribution pattern of the HCN channels influences the effects that they exert on t

210 HCN channels inhibited glutamate synaptic release by sup

211 In medium-sized bladder neurons, a selective HCN channel inhibitor, ZD7288, dose-dependently inhibite

212 forming a working memory task tested for D1R-HCN channel interactions in vivo.

213 ng intra-PFC infusions of drugs examined D1R-HCN channel interactions on working memory performance.

214 theta phase of the LFP, and the insertion of HCN channels introduced large lags in this spike phase a

215 Thus, we conclude that the leucine zipper of HCN channels is a major determinant for hyperpolarizatio

216 izure-dependent plasticity of these cortical HCN channels is not conditional upon TRIP8b.

217 ucleotide-modulated channels such as CNG and HCN channels is promoted by ligand-induced conformationa

218 A unique property of HCN channels is their small single-channel current, whic

219 tion-activated, cyclic nucleotide-regulated (HCN) channel is activated by membrane hyperpolarization.

220 arization-activated cyclic nucleotide-gated (HCN) channels is facilitated in vivo by direct binding o

221 rization-activated, cyclic nucleotide-gated (HCN) channels is formed by subunit isoforms denoted HCN1

222 ating of hyperpolarization-activated cation (HCN) channels is potentiated by direct binding of cAMP t

223 However, structures of other mammalian HCN channel isoforms have been lacking.

224 ation-activated and cyclic nucleotide-gated (HCN) channel isoforms HCN1, HCN2, and HCN4 were localize

225 bunit contacts in allosteric coupling in the HCN channel, it also illustrates an effective strategy f

226 Superposition of HCN channel labeling with VGLUT1 staining confirmed the

227 umber of caveolae to enhance the function of HCN channels may represent a viable target for the pharm

228 arization-activated cyclic nucleotide-gated (HCN) channels mediate the hyperpolarization-activated cu

229 Previously, we showed that loss of HCN channel-mediated current (I(h)) occurred in the dend

230 Loss of HCN channel-mediated current (Ih ), particularly that me

231 creased intrinsic excitability and decreased HCN channel-mediated IH currents.

232 arization-activated cyclic nucleotide-gated (HCN) channel-mediated current (Ih) in CA1 hippocampal py

233 microscopy confirmed D1R colocalization with HCN channels near excitatory-like synapses on dendritic

234 Our conclusions on the impact of HCN channels on LFPs and spike phase were invariant to c

235 properties was attributable to reduction of HCN channels on the neuronal surface, and there was a st

236 HCN channels open in response to hyperpolarizing voltage

237 de binding has been shown to promote CNG and HCN channel opening, the precise mechanism underlying ga

238 arization-activated cyclic nucleotide-gated (HCN) channels, particularly that of the HCN1 isoform, ar

239 of Neuron, Santello and Nevian (2015) report HCN channel plasticity and increased temporal summation

240 chanism underlying seizure-induced dendritic HCN channel plasticity.

241 Thus, HCN channels play a critical role in the separation of o

242 Specifically, they suggest that septal HCN channels play a permissive role in spatial working m

243 is accomplished in these neurons and whether HCN channels play a role.

244 Hyperpolarization-activated cAMP-regulated (HCN) channels play important physiological roles in both

245 rization-activated, cyclic nucleotide-gated (HCN) channels play in this nociceptive sensitization usi

246 arization-activated cyclic nucleotide-gated (HCN) channels play key roles in intrinsic excitability a

247 dal neurons, the subcellular localization of HCN channels plays a critical functional role, yet mecha

248 arization-activated cyclic nucleotide-gated (HCN) channels plays an important role in pain by facilit

249 nteracts directly with two distinct sites of HCN channel pore-forming subunits to control channel tra

250 However, systemic blockade of HCN channels produces cardiac effects that limit this ap

251 ism of decreased tyrosine phosphorylation on HCN channel properties.

252 s in motivation and attention states, axonal HCN channels provide a mechanism to translate these sign

253 chanism may provide a general means by which HCN channels regulate dendritic excitability.

254 ents a previously unknown mechanism by which HCN channels regulate synaptic strength and thereby neur

255 arization-activated cyclic nucleotide-gated (HCN) channels regulate excitability in neurons, and bloc

256 arization-activated cyclic nucleotide-gated (HCN) channels regulate neuronal excitability, pacemaking

257 is cyclic nucleotide has to be considered in HCN channel-regulated processes.

258 erisomatic Ih in dorsal CA1 neurons and that HCN channels represent a potential target for the treatm

259 retina to estimate the conductance of single HCN channels, revealing a conductance of approximately 6

260 Finally, the presence of HCN channels set the STA characteristic frequency in the

261 studies of strong open-state trapping in an HCN channel showing that the well-established autoinhibi

262 Experimental reductions in HCN channel signalling increase the representation of co

263 ding pocket and exerts regulatory effects on HCN channels similar to those imposed by cAMP.

264 at a GPI-anchored protein associates with an HCN channel subunit protein.

265 ation-activated and cyclic nucleotide-gated (HCN) channel subunits HCN1, HCN2, and HCN4 in the MSO, b

266 arization-activated cyclic nucleotide-gated (HCN) channel subunits, HCN1 and HCN2.

267 arization-activated cyclic nucleotide-gated (HCN) channels that contributes to the substantial dendri

268 arization-activated cyclic nucleotide-gated (HCN) channels that underlie the h-current (Ih), a key re

269 In both ELK and HCN channels the C-linker is the site of virtually all o

270 o depolarize, leading to the deactivation of HCN channels, the initiation of regular spiking (4-5 Hz)

271 In the absence of HCN channels, the STA exhibited weak delta frequency sel

272 arization-activated cyclic nucleotide-gated (HCN) channels, the STA characteristic frequency strongly

273 been shown to facilitate opening of CNG and HCN channels, their effect on EAG and ERG channels is le

274 Despite the physiological importance of HCN channels, their elementary functional properties are

275 ever, in STN neurons, which strongly express HCN channels, their roles remain relatively obscure.

276 ation-activated cyclic-nucleotide-modulated (HCN) channels, there are marked differences.

277 HCN channels, though, are also located in certain mature

278 common biophysical models, allowing CNG and HCN channels to be viewed as a single genre.

279 functional role, yet mechanisms controlling HCN channel trafficking are not fully understood.

280 Here we studied the dynamics of HCN channel trafficking in hippocampal neurons using dis

281 HCN channel trafficking to dendrites is regulated by the

282 e is known about the mechanisms that control HCN channel trafficking to subcellular compartments or t

283 ampus was sufficient to reverse the impaired HCN-channel trafficking and antidepressant-like behavior

284 a mutated version of TRIP8b further impaired HCN-channel trafficking and increased the antidepressant

285 ined the structural basis of TRIP8b-mediated HCN-channel trafficking and its relationship with antide

286 nding to the carboxyl-terminal tripeptide of HCN channels, TRIP8b also binds directly to the cyclic n

287 are held open for prolonged times (>50 ms), HCN channels undergo a mode shift, which in sea urchin (

288 We further investigated whether presynaptic HCN channels undergo seizure-dependent plasticity.

289 arization-activated cyclic nucleotide-gated (HCN) channels underlie the control of rhythmic activity

290 and DCP rats, but the sensitivity of FSK on HCN channels was clearly down-regulated in DCP rats.

291 pacitance measurements of lactotrophs, where HCN channels were either augmented by transfection or bl

292 d that these compartment-specific actions of HCN channels were heavily influenced by the local and di

293 Our results showed that dendritic HCN channels were significantly downregulated at an acut

294 les with HCN4 to form functional heteromeric HCN channels, which activate faster than homomeric HCN2

295 local cation concentration, mediated through HCN channels, which are located on or near secretory ves

296 est that HCN-2 is the predominant subtype of HCN channels, which can control neuronal excitability, i

297 o a short-term, activity-dependent memory in HCN channels, which has been shown previously to be impo

298 arization-activated cyclic nucleotide-gated (HCN) channels, which are activated by cAMP, are involved

299 ation-activated cyclic nucleotide-regulated (HCN) channels, which generate the I(h) current, mediate

300 ve lead in the impedance phase introduced by HCN channels without altering neuronal excitability and