ライフサイエンスコーパス: AHP

1 AHP current did not have time to decay between action po

2 AHP dUTP is a versatile clickable nucleotide with potent

3 AHP expression appears unaffected by Mn(II), yet the lar

4 AHP is blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (

5 AHP is blocked by Li+o substitution for Na+o and by ouab

6 AHP is seen in dissociated horizontal cells (HCs) and hy

7 AHP never occurs in depolarizing, or ON type, bipolar ce

8 AHP occurs only in neurons that are depolarized by gluta

9 AHPs triggered with theta-burst firing every 30 s were p

10 osteric 4-(aminomethyl)-1-hydroxypyrazole (4-AHP) analogues of muscimol, a GABA(A) receptor agonist,

11 The unsubstituted 4-AHP analogue (2a) (EC(50) 19 muM, R(max) 69%) was a mode

12 A slowly accumulating AHP current, also insensitive to apamin, was extremely s

13 examined how changes in PIP2 levels affected AHPs, somatic [Ca(2+) ]i , and whole cell Ca(2+) current

14 is terminated by an afterhyperpolarization (AHP) that displays two main components; the medium AHP (

15 ce and absence of an afterhyperpolarization (AHP).

16 Medians of AP and afterhyperpolarization (AHP) durations and AP overshoots were significantly grea

17 es in the post-burst afterhyperpolarization (AHP) and spike-frequency accommodation, is altered durin

18 enhanced post-burst afterhyperpolarization (AHP), in CA1 hippocampal pyramidal neurons.

19 ut not the decreased afterhyperpolarization (AHP) durations (C, Adelta, and Aalpha/beta).

20 ng, sodium-dependent afterhyperpolarization (AHP) following bursts of action potentials that was medi

21 the Ca2+ -dependent afterhyperpolarization (AHP) following spike trains is significantly larger duri

22 to the long lasting afterhyperpolarization (AHP) that follows an action potential in many central ne

23 of the long-lasting afterhyperpolarization (AHP) that follows individual theta bursts.

24 ad larger and longer afterhyperpolarization (AHP) as well as slower frequency-responses to depolarizi

25 pendent, K+-mediated afterhyperpolarization (AHP) is related to cognitive decline.

26 BK channel mediated afterhyperpolarization (AHP), repetitive spiking is maintained, through the incr

27 the slow and medium afterhyperpolarization (AHP) currents (I(sAHP), I(mAHP)).

28 owed by a monophasic afterhyperpolarization (AHP).

29 on, the amplitude of afterhyperpolarization (AHP) and the pattern of AP firing; SLO-2 is also importa

30 ion of the postburst afterhyperpolarization (AHP) have been repeatedly demonstrated in multiple brain

31 ons of the postburst afterhyperpolarization (AHP) in hippocampal pyramidal neurons have been shown ex

32 ion in the postburst afterhyperpolarization (AHP).

33 del with a postspike afterhyperpolarization (AHP), but absent from those calculated from the discharg

34 Action potential afterhyperpolarization (AHP) enhances precision of firing by ensuring that the i

35 lowed by a prolonged afterhyperpolarization (AHP) that influences firing frequency and affects neuron

36 possess a prominent afterhyperpolarization (AHP) that contributes to spike patterning.

37 a slowly recovering afterhyperpolarization (AHP), but, unlike in cortical cells, this AHP is not pri

38 of the motoneurone's afterhyperpolarization (AHP) and the variability in its spike discharge.

39 the apamin-sensitive afterhyperpolarization (AHP) in rat superior cervical ganglion (SCG) neurones.

40 with increased slow afterhyperpolarization (AHP) potential, whereas vulnerability was associated wit

41 rges and of the slow afterhyperpolarization (AHP) that follows, as occur in vivo with contrast adapta

42 a depression of the afterhyperpolarization (AHP) and an increase in frequency of evoked and spontane

43 ngs, we examined the afterhyperpolarization (AHP) in CA1 pyramidal cells in hippocampal slices from y

44 The afterhyperpolarization (AHP) that follows each spike, however, decays relatively

45 currents that cause afterhyperpolarizations (AHPs) and afterdepolarizations (ADPs).

46 y calcium-dependent afterhyperpolarizations (AHPs) following a train of action potentials that are cr

47 KEY POINTS: Afterhyperpolarizations (AHPs) generated by repetitive action potentials in supra

48 r lasting postburst afterhyperpolarizations (AHPs) and greater spike frequency adaptation (accommodat

49 e rise to prominent afterhyperpolarizations (AHPs).

50 approximately 20 s) afterhyperpolarizations (AHPs) that were insensitive to blockade of voltage-gated

51 Slow afterhyperpolarizations (AHPs) follow action potentials in a subset of vagal C af

52 s underwent strabismus surgery to correct an AHP and/or improve ocular alignment.

53 These cells commonly respond with only an AHP component.

54 ted from the discharge of a model without an AHP.

55 orrelated with BLA neuronal excitability and AHP.

56 AP overshoots and AHP durations were similar in nociceptors of all CV grou

57 associated with a reduction in rheobase and AHP.

58 ability were related to the altered ADPs and AHPs.

59 ations, but did possess a prolonged biphasic AHP.

60 neous action potentials followed by biphasic AHPs.

61 P current (I(AHP)) was insufficient to block AHP plasticity, suggesting that plasticity is manifested

62 Inhibition of both AHP components by L-type Ca(2+) channel antagonists was

63 amplicon with all 335 thymidines replaced by AHP dU was shown to be a perfect copy of the template fr

64 hat adult hippocampal stem/progenitor cells (AHPs) express receptors and signalling components for Wn

65 equently, the levels of IgG anti-dsDNA, CR1, AHP, or C3b on both erythrocytes and U937 cells were mea

66 result in accumulation of calcium-dependent AHP current.

67 erically undemanding azide analogue of dTTP (AHP dUTP) with an alkyl chain and ethynyl attachment to

68 ned that an apamin-sensitive medium-duration AHP (mAHP) and an apamin-insensitive slow AHP (sAHP) wer

69 ications for the potential use of endogenous AHPs in neurological disease.

70 Because enhanced AHP in aging neurons has been hypothesized to be seconda

71 enhanced sI(AHP) contributes to the enhanced AHP in aging.

72 onses/no. of stimuli) by using the estimated AHP to create a fixed threshold 'daughter' model MN to m

73 Cells with exclusively AHP responses are tonically depolarized.

74 AHP became faster and shallower, and a fast AHP emerged.

75 We therefore suggest that the large, fast AHP is a key feature of BD and a main contributor to the

76 er a burst of action potentials and the fast AHP (fAHP) after individual action potentials.

77 through BK channels, contributes to the fast AHP and appears to offset the DAP; this current is sensi

78 ng, we isolated T-DNA insertions in the five AHP genes that are predicted to encode functional HPts a

79 assays, indicating both a positive role for AHPs in cytokinin signaling and functional overlap among

80 In contrast with the other four AHPs, AHP4 may play a negative role in some cytokinin re

81 of Wnt signalling reduces neurogenesis from AHPs in vitro and abolishes neurogenesis almost complete

82 is sufficient to increase neurogenesis from AHPs in vitro and in vivo.

83 decay times (24.67 vs. 11.02 ms) and greater AHP amplitudes (3.27 vs. 1.56 mV) than MNs lacking SK3-i

84 Fewer patients in the FRMD7 group had AHPs, their amplitude of nystagmus being lower in primar

85 ies propose that anosognosia for hemiplegia (AHP) results from specific impairments in motor planning

86 ium (SK2) channels, also reduced hippocampal AHPs and closely reproduced the effects of BDNF on theta

87 However AHP is not blocked by nifedipine and is insensitive to [

88 ne (3AT) and 4-amino-3-hydroxyphenylalanine (AHP), markers for 2-CysDopa and 5-CysDopa, respectively,

89 contributing to the after-hyperpolarisation (AHP) and spike repolarisation; a slower prolonged Ba(2+)

90 rst, the model MN's after-hyperpolarisation (AHP) was deduced from its interval histogram for tonic f

91 nels mediate medium after-hyperpolarization (AHP) conductances in neurons throughout the central nerv

92 nd amplitude of the after-hyperpolarization (AHP), without affecting the pre- and postsynaptic membra

93 share a large, fast after-hyperpolarization (AHP).

94 e potential, termed after-hyperpolarization (AHP).

95 s and long-lasting after-hyperpolarizations (AHPs), mediated by calcium-activated, cyclic AMP-sensiti

96 Two prominent after-hyperpolarizations (AHPs), one of medium duration that was apamin-sensitive

97 ed fast and medium after-hyperpolarizations (AHPs); (iv) strongly enhanced burst firing and increased

98 hannels that underlie after hyperpolarizing (AHP) currents and contribute to the shaping of the firin

99 of the Ca(2+)-activated potassium current (I(AHP)) and potentiation of the NMDA receptor.

100 onditions, calcium-activated K(+) current (I(AHP)) improved efficient spike-rate coding at the expens

101 ckade of the apamin-sensitive AHP current (I(AHP)) was insufficient to block AHP plasticity, suggesti

102 o the distinct activation requirements for I(AHP) and I(M), which in turn dictate whether those curre

103 mical systems analysis, we demonstrate how I(AHP) minimizes perturbation of the interspike interval c

104 The reduction of I(AHP) was occluded by previous blockade of calcium-activa

105 d on their distinct activation properties, I(AHP) implements noise shaping that improves spike-rate c

106 polarization amplitudes (ADP), and reduced I(AHP) and enhanced I(ADP).

107 stration that altered awareness of action in AHP reflects a dominance of motor intention prior to act

108 bserved non-veridical awareness of action in AHP.

109 spontaneous activity but not in decreases in AHP duration and (2) suggest clinical advantages of redu

110 KGluc, repetitive theta-burst firing induced AHP plasticity that mimics learning-related reduction in

111 Place-cell-train-induced AHPs were blocked by ouabain or removal of extracellular

112 PIP2 appears to influence AHPs in OT neurons by reducing Ca(2+) influx during spik

113 ng was governed by a fast apamin-insensitive AHP current that did not accumulate, but rather showed d

114 uced findings, we propose that the intrinsic AHP level might determine the degree of synaptic plastic

115 re hyperpolarized potentials and have larger AHPs than young neurons.

116 ce cell train" generated small, long-lasting AHPs capable of reducing neuronal excitability for many

117 mmunoreactivity exhibit significantly longer AHP half-decay times (24.67 vs. 11.02 ms) and greater AH

118 ed from discharge statistics to the measured AHP trajectory of the motoneurone.

119 mechanism (reduction in SK channel-mediated AHP) that led to the learning-induced increased intrinsi

120 ationships between SK3 expression and medium AHP properties.

121 ability was associated with decreased medium AHP.

122 influenced by the SK channel-mediated medium AHP (mAHP), because the SK blocker apamin reduced the sh

123 l cord may contribute to the range of medium AHP durations across specific MN functional types and ma

124 currents generate an apamin-sensitive medium AHP (mAHP) after each AP; and bursts of APs generate lon

125 hat displays two main components; the medium AHP (I(mAHP)), lasting a few hundred milliseconds and th

126 threshold hyperpolarized 6.7 mV, the medium AHP became faster and shallower, and a fast AHP emerged.

127 distinguishable currents known as the medium AHP current (I(mAHP)) and the slow AHP current (I(sAHP))

128 erformance-related differences in the medium AHP.

129 ccessful, while ET in a patient with a minor AHP was corrected by performing a bimedial recession.

130 anipulations of PIP2 levels did not modulate AHPs by influencing Ca(2+) release from IP3 -triggered C

131 ctivation of GluR6-containing KARs modulates AHP amplitude, and influences the firing frequency of py

132 d depolarisations and only a fast monophasic AHP.

133 However, no AHP plasticity was observed using KMeth.

134 hannels results in the generation of a novel AHP not seen in wild-type Purkinje neurons that also acc

135 ) and adaptive hierarchically penalized NSC (AHP-NSC), with two different penalty functions for micro

136 these to the time course and accumulation of AHP currents using whole-cell and perforated patch recor

137 Outcome measures included amount of AHP and deviation at last follow-up.

138 thalmological papers, as a possible cause of AHP.

139 membrane properties, and on the induction of AHP plasticity in CA1 pyramidal neurons from rat hippoca

140 On average, a reduction of AHP of 1.3 degrees /mm was achieved by predominantly per

141 current models indicating relocalization of AHP protein into the nucleus in response to cytokinin ar

142 Studies of AHP plasticity require stable long-term recordings, whic

143 Transfer of AHP-anti-dsDNA ICs from erythrocyte CR1 to model phagocy

144 regulates differentiation and maturation of AHPs non-cell-autonomously via SCG2.

145 or IP3 availability, i.e. PIP2 modulation of AHPs is not likely to involve downstream Ca(2+) release

146 To assess the role of AHPs in cytokinin signaling, we isolated T-DNA insertion

147 We examined the effects of cytokinin on AHP subcellular localization in Arabidopsis and, contrar

148 e trains in OT neurons, but had no effect on AHPs evoked by uncaging intracellular Ca(2+) .

149 HW: 3.9 +/- 0.7 ms) spike AHPs with only one AHP minimum (TTP: 0.9 +/- 0.1 ms).

150 associated to a new onset of sudden, painful AHP with normal ocular exam).

151 We show that animal haem peroxidases (AHPs) located on the outer membrane and within the secre

152 e and that of histidine phosphotransferases (AHPs) in guard cell signalling remain to be fully elucid

153 n maintaining the learning-related postburst AHP reduction observed in CA1 pyramidal neurons.

154 tically significant differences in postburst AHPs or accommodation, indicating that similar levels of

155 s from both age groups had reduced postburst AHPs and reduced accommodation.

156 Anomalous head posture (AHP) or torticollis is a relatively common condition in

157 adopt a significant anomalous head posture (AHP) towards the fixing eye in order to dampen the nysta

158 The presence of anomalous head posture (AHP) was significantly higher in the non-FRMD7 group (P

159 ing, reduced afterhyperpolarizing potential (AHP) and increased slow afterdepolarization amplitudes (

160 tude of the after-hyperpolarizing potential (AHP) following a train of spikes and the underlying apam

161 uction of afterhyperpolarization potentials (AHPs) in hippocampal CA1 cells, suggesting a direct role

162 iferating adult hippocampal stem/progenitor (AHP) progeny and lead to the exclusive generation of cel

163 maturation of adult hippocampal progenitors (AHPs).

164 thaliana histidine phosphotransfer proteins (AHPs) are similar to bacterial and yeast histidine phosp

165 bidopsis histidine phosphotransfer proteins (AHPs), which have been suggested to translocate to the n

166 entiation and affected the maturation of rat AHPs.

167 Rather, AHPs actively maintain a consistent nuclear/cytosolic di

168 reover, our results suggest that the reduced AHP is related to a down-regulation of SK2/SK3 channel s

169 alcium-activated potassium channels regulate AHP and excitability in neurons.

170 Pyramidal cells of layer V exhibit robust AHP currents composed of two kinetically and pharmacolog

171 hat the longest component of the GP neuron's AHP is blocked by apamin, a selective antagonist of calc

172 e prolonged discharge was a slow (12-75 sec) AHP that was associated with an increase in membrane con

173 Apamin-sensitive AHP (SK) current was measured by subtraction of tail cur

174 Blockade of the apamin-sensitive AHP current (I(AHP)) was insufficient to block AHP plast

175 nant SK2 channels, neuronal apamin-sensitive AHP currents, and the excitability of CA1 neurons.

176 ion in SK channel-mediated, apamin-sensitive AHP is a critical contributing mechanism.

177 ward calcium-activated potassium current (sI(AHP)), a major constituent of the AHP, also facilitate l

178 the apamin-insensitive slow AHP current (sI(AHP)).

179 Thus, an enhanced sI(AHP) contributes to the enhanced AHP in aging.

180 ng neurons were found to have an enhanced sI(AHP,) the amplitude of which was significantly correlate

181 n in young neurons; however, the residual sI(AHP) was still significantly larger in aging neurons tha

182 ning, suggest that the enhancement of the sI(AHP) in aging is a mechanism that contributes to age-rel

183 quantitatively greater reductions in the sI(AHP) in aging neurons than in young neurons; however, th

184 pe Ca2+ channels, we further examined the sI(AHP) in the presence of an L-type Ca2+ channel blocker,

185 facilitate learning in aging animals, the sI(AHP) was pharmacologically isolated and characterized.

186 c and voltage-dependent properties of the sI(AHP).

187 In typical patients who adopt a significant AHP accompanied by a large ET, we suggest an initial com

188 ppocampal pyramidal cells reveal that a slow AHP is reduced by blocking different components of the C

189 afterdepolarizing potential (ADP), and slow AHP (sAHP) that was attributable to calcium influx via h

190 in robustly blocked both the medium and slow AHP currents (ImAHP and IsAHP ) of OT, but not VP neuron

191 of PIP2 levels affected both medium and slow AHP currents in oxytocin (OT) neurons of the supraoptic

192 the modulation of a potassium current (slow AHP current, I(sAHP)) known to be targeted by multiple t

193 on AHP (mAHP) and an apamin-insensitive slow AHP (sAHP) were specifically increased in OT neurons.

194 rough changes in the apamin-insensitive slow AHP current (sI(AHP)).

195 d concurrently with progressive loss of slow AHP tail current (IsAHP) evoked by brief depolarizations

196 ting a few hundred milliseconds and the slow AHP (I(sAHP)), that has a duration of several seconds.

197 The slow AHP (sAHP) recorded from learning-impaired aged rats (AI

198 ol 4,5-bisphosphate (PIP2 ) enabled the slow AHP component (sAHP) in cortical pyramidal neurons.

199 he medium AHP current (I(mAHP)) and the slow AHP current (I(sAHP)).

200 resence of apamin and tetrodotoxin, the slow AHP was strongly reduced by 5-HT, and fully abolished by

201 t, reductions of [Na(+)](o) reduced the slow AHP, even in the presence of pronounced Ca(2+) spikes.

202 activated K+ channels that underlie the slow AHP, without the predicted elevation of bulk [Ca2+]i.

203 Ca(2+) conductances did not reduce the slow AHP.

204 vagal neuronal excitability by blocking slow AHPs and to determine the adenosine receptor subtype med

205 Adenosine inhibits slow AHPs in vagal afferent neurons.

206 During adenosine (10 micromol/L), slow AHPs were suppressed and action potential response rate

207 and bursts of APs generate long-lasting slow AHPs (sAHPs) attributable to apamin-insensitive currents

208 I(K(Ca)) and consequent suppression of slow AHPs, or (2) A(2)-receptor-mediated elevation of cAMP di

209 elevation of cAMP directly suppressing slow AHPs.

210 adult rabbit nodose ganglion cells with slow AHPs in current-clamp mode.

211 t, we show that in this Roseobacter species, AHPs mediate Mn(II) oxidation not through a direct react

212 Spike AHP currents were measured in voltage clamp as tail curr

213 ion potential afterhyperpolarisations (spike AHPs) of CA1 interneurones were investigated in 25 baske

214 nged with GABA(A) receptor modulators, spike AHPs in basket and bistratified cells were enhanced by z

215 ety showed narrow (HW: 3.9 +/- 0.7 ms) spike AHPs with only one AHP minimum (TTP: 0.9 +/- 0.1 ms).

216 The spike AHPs of three axo-axonic cells tested showed no sensitiv

217 The spike AHPs showed two minima in all regular-spiking (5), burst

218 d time courses resembling those of the spike AHPs.

219 pus autaptic connections contribute to spike AHPs in many interneurones.

220 Interneurones with spike AHPs affected by the GABA(A) receptor ligands exhibited

221 ghlighting two consistent findings: (i) that AHP and accommodation are reduced in pyramidal neurons f

222 mals that have learned a task; and (ii) that AHP and accommodation are enhanced in pyramidal neurons

223 pense of newborn neurons, demonstrating that AHPs in the adult mouse brain are not irrevocably specif

224 These data indicate that AHPs have substantial plasticity, which might have impor

225 Finally, we present data indicating that AHPs maintain a nuclear/cytosolic distribution by balanc

226 The AHP is also reduced by many neuromodulators, such as nor

227 The AHP is supported by at least three subtypes of K(Ca) cha

228 The AHP measured immediately after establishing whole-cell r

229 The AHP width at half-amplitude (HW) was 12.5 +/- 5.7 ms in

230 R code for the ALP-NSC and the AHP-NSC algorithms are available from authors upon reque

231 However, because the AHP is measured following completion of training, it is

232 us studies showing a correlation between the AHP and learning, suggest that the enhancement of the sI

233 influence of prior discharge mediated by the AHP, and it increases in amplitude when AHP amplitude is

234 e accuracy of this estimate by comparing the AHP trajectory predicted from discharge statistics to th

235 Correspondingly, the AHP time course was similar to the decay of activity-ind

236 t the death rate can be used to estimate the AHP trajectory.

237 In general, the AHP in KMeth was comparable to the AHP measured in the p

238 restores membrane potential, generating the AHP response.

239 Furthermore, it seems that reductions in the AHP must occur before learning if young and aging subjec

240 imarily due to a significant decrease in the AHP that in turn resulted in a reduction in the fraction

241 hat mimics learning-related reduction in the AHP.

242 activity is not involved in maintaining the AHP reduction at this point after learning.

243 PKA activity is involved in maintaining the AHP reduction measured ex vivo after successful learning

244 ificantly correlated to the amplitude of the AHP (r = 0.63; p < 0.001).

245 ntracellular solutions on measurement of the AHP and basic membrane properties, and on the induction

246 Examination of the AHP demonstrated that the amplitude was significantly re

247 g from sharp electrodes that the size of the AHP following spike trains increased in OT, but not VP n

248 The Ca2+-dependent components of the AHP have been attributed to the activity of small conduc

249 e results indicate that the amplitude of the AHP in hippocampal pyramidal cells from aged animals is

250 The pivotal role of the AHP in regulating spike patterning indicates that burst

251 e sought to determine which component of the AHP is enhanced, and whether the enhancement could be re

252 te that activity-dependent plasticity of the AHP occurs with physiologically relevant stimuli in KGlu

253 t affect the subcellular localization of the AHP proteins.

254 of them underlie the medium component of the AHP that regulates interspike interval and plays an impo

255 Ca(2+) rises showed that mGluR block of the AHP was not mediated by alterations of action potential-

256 se from direct or indirect modulation of the AHP without requiring phasic synaptic input.

257 , thereby providing the time constant of the AHP's decay of conductance.

258 urrent (sI(AHP)), a major constituent of the AHP, also facilitate learning in aging animals, the sI(A

259 ved phosphoacceptor histidine residue of the AHP, as well as disruption of multiple cytokinin signali

260 ufficient depolarization, enhancement of the AHP, or sustained Na+ channel inactivation.

261 obscures activity-dependent reduction of the AHP.

262 ent, and possibly other constituents, of the AHP.

263 involved in rate-dependent regulation of the AHP.

264 consistent with circadian modulation of the AHP.

265 in a marked reduction or elimination of the AHP.

266 he effect of environmental enrichment on the AHP amplitude.

267 inhibited transmission, and also reduced the AHP amplitude.

268 actam V (0.2 muM), significantly reduced the AHP in CA1 neurons from both control and trained rats, i

269 hat activates PKA, significantly reduced the AHP in CA1 neurons from control animals, but not from ra

270 in slice preparation, we have found that the AHP has a shorter duration in cells firing at higher fre

271 ramidal neurons, the current ascribed to the AHP (IAHP) has three kinetic components.

272 by flumazenil (-31 +/- 13 %, relative to the AHP HW during exposure to zolpidem, 3:4).

273 eral, the AHP in KMeth was comparable to the AHP measured in the perforated-patch configuration.

274 nally, we found calcium contributions to the AHP to be temperature dependent: prominent at room tempe

275 ominantly L- and R-type currents trigger the AHP.

276 -threshold' measure which underestimated the AHP's absolute size but had the same time course, thereb

277 To identify the current(s) underlying the AHP altered in aging neurons, whole-cell voltage-clamp r

278 to the time in question rather than upon the AHP per se; the survivors' mean is more hyperpolarised b

279 etion of training, it is unclear whether the AHP amplitude is strictly dependent on biological aging

280 n signaling and functional overlap among the AHPs.

281 urrents underlying AP repolarization and the AHPs.

282 abidopsis and, contrary to expectations, the AHPs maintained a constant nuclear/cytosolic distributio

283 These data indicate that most of the AHPs are redundant, positive regulators of cytokinin sig

284 ones via 5-HT2 receptors, by suppressing the AHPs associated with two distinct calcium-activated pota

285 -dependent potassium currents underlying the AHPs, thereby creating mechanisms for control of the spo

286 These AHPs, rather than a depletion of neurotransmitters (as w

287 dative-peroxidative enzymatic cycle by these AHPs that leads to Mn oxide formation by this organism.

288 ttle is known about PIP2 's control of these AHPs.

289 This AHP is probably underlain by a small-conductance, CA2+-d

290 This AHP persisted for multiple seconds following volleys of

291 n (AHP), but, unlike in cortical cells, this AHP is not primarily driven by an intrinsic cellular pro

292 The estimated 'distance-to-threshold' AHP did not, however, give an accurate measure of the re

293 the differentiation of neighboring wild-type AHPs, suggesting that REST may play a non-cell-autonomou

294 the AHP, and it increases in amplitude when AHP amplitude is increased by pharmacological manipulati

295 ery 30 s were progressively reduced, whereas AHPs elicited every 150 s were stable.

296 Cells with AHP expressed greater density of sodium currents.

297 motor planning in awareness in patients with AHP: Four hemiplegic patients with and four without anos

298 tion had a selective effect on patients with AHP; they were more likely than controls (U = 16, P < 0.

299 Replacement of thymidine with AHP dU increases duplex stability, accounting in part fo

300 By contrast, patients without AHP were not influenced by these manipulations, and did