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Subthreshold changes

Subthreshold changes of voltage-dependent activation of the K V 7.2channel in neonatal epilepsy

Jessica Hunter,a,1Snezana Maljevic,b,1Anupama Shankar,a Anne Siegel,a Barbara Weissman,c Philip Holt,c Larry Olson,c Holger Lerche,b,?and Andrew Escayg a,?

Department of Human Genetics,Emory University,615Michael Street,Whitehead Building,Suite 301,Atlanta,Georgia 30322,USA

Departments of Neurology and Applied Physiology,University of Ulm,Zentrum Klinische Forschung,Helmholtzstr.8/1D-89081Ulm,Germany c

Department of Neurology,Emory University,615Michael Street,Whitehead Building,Suite 301,Atlanta,Georgia 30322,USA

Received 18March 2006;revised 9June 2006;accepted 20June 2006Available online 17August 2006

Benign familial neonatal convulsions (BFNC)is an epileptic disorder caused by dominant mutations in the genes KCNQ2and KCNQ3encoding the K +channels K V 7.2and K V 7.3.We identified two novel KCNQ2mutations in two BFNC families.One mutation predicted a truncated protein (S247X)that lacks the channel's pore region,the other resulted in the amino acid substitution S122L in the S2segment of K V 7.2.In comparison to wild-type (WT)K V 7.2,functional analysis of S122L mutant channels in Xenopus oocytes revealed a significant positive shift and increased slope of the activation curve leading to significant current reduction in the subthreshold range of an action potential (75%reduction at ?50mV).Our results establish an important role of the K V 7.2S2segment in voltage-dependent channel gating and demonstrate in a human disease that subthreshold voltages are likely to represent the physiologically relevant range for this K +channel to regulate neuronal firing.

Keywords:BFNC;Epilepsy;Ion channel;Genetics;Structure function analysis;V oltage clamp

Introduction

Benign familial neonatal convulsions (BFNC)is a rare idiopathic epilepsy of newborns with autosomal dominant inheritance.It is characterized by frequent unprovoked seizures that typically begin within the first days of life and spontaneously disappear within several weeks to months (Ronen et al.,1993).Seizures can be partial or manifest as generalized convulsions that

occur during wakefulness and sleep.Patients typically have a normal physical exam and long-term neurodevelopment,however,learning disabilities or delayed speech development have been observed in a few individuals (Ronen et al.,1993;Lerche et al.,2005).The early neonatal onset distinguishes BFNC from two other types of hereditary focal epilepsies of infancy,benign familial neonatal infantile convulsions (BFNIC)(Berkovic et al.,2004)and benign familial infantile convulsions (BFIC)(Vigevano et al.,1992).In addition to a later age of onset,BFNIC and BFIC are genetically distinct from BFNC.BFNIC is caused by mutations in a brain sodium channel,SCN2A (Heron et al.,2002)whereas the genetic defect that leads to BFIC is still unknown (reviewed by Lerche et al.,2005).

Genetic loci for BFNC were first mapped to human chromo-somes 20q13.3(Leppert et al.,1989)and 8q24(Lewis et al.,1993).Positional cloning led to the identification of causal mutations in KCNQ2on chromosome 20(Singh et al.,1998;Biervert et al.,1998)and KCNQ3on chromosome 8(Charlier et al.,1998).The KCNQ gene family encodes five voltage-gated K +channels,recently classified as K V 7.1–K V 7.5(Gutman et al.,2003),which are mainly expressed in cardiac muscle (K V 7.1),the central nervous system (K V 7.2–K V 7.5),the inner ear (K V 7.4)and skeletal muscle (K V 7.5)(Jentsch,2000).Mutations in four of the five genes are associated with inherited diseases.KCNQ1mutations lead to cardiac arrhythmia in long QT syndrome (Wang et al.,1996),KCNQ4mutations underlie congenital deafness (Kubisch et al.,1999),and mutations in KCNQ2or KCNQ3(proteins K V 7.2and K V 7.3)result in BFNC (Singh et al.,1998;Biervert et al.,1998;Charlier et al.,1998;Jentsch,2000;Lerche et al.,2005).

K V 7proteins share a predicted topologic arrangement of voltage-gated potassium channels with an intracellular amino terminus,six transmembrane segments (S1–S6),a pore loop (P-loop)between S5and S6that forms the selectivity filter of the channel,a positively charged voltage-sensing S4segment and a large intracellular carboxy terminus (C-terminus).All K V 7subunits assemble into functional homomeric potassium channels,whereas K V 7.2,K V 7.4and K V 7.5can also form

functional

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Neurobiology of Disease 24(2006)194–201

?Corresponding authors.A.Escayg is to be contacted at fax:+14047273949.H.Lerche,fax:+497311771202.

E-mail addresses:holger.lerche@uni-ulm.de (H.Lerche),aescayg@https://www.sodocs.net/doc/5a6998928.html, (A.Escayg).1

Contributed equally to this study.

heteromeric channels with K V 7.3(Jentsch,2000).K V 7.2–K V 7.5and especially heteromeric K V 7.2/K V 7.3channels,give rise to the M-current,a slowly activating and deactivating potassium current which can be suppressed by the activation of muscarinic acetylcholine receptors (Brown and Adams,1980).Since K V 7/M-type K +channels are active at potentials around the threshold of action potential firing,they regulate neuronal excitability by impeding repetitive spike firing of neurons in response to persistent depolarizing inputs,a mechanism known as “spike-frequency adaptation ”(Brown and Adams,1980;Wang et al.,1998;Rogawski,2000).

The majority of identified BFNC mutations occur in KCNQ2(Fig.2A).All missense mutations reported to date have been distributed in the S4segment,the pore region or the C-terminus (Lerche et al.,2005).Functional analyses of several BFNC mutations have demonstrated a reduction in the maximum potassium current,suggesting a mechanism of haploinsufficiency (Singh et al.,1998;Biervert et al.,1998;Schroeder et al.,1998;Yang et al.,1998;Lerche et al.,1999).Pore mutations probably reduce K +current by affecting ion channel conductance,whereas the C-terminal mutations may affect the assembly of K V 7subunits (Lerche et al.,2005;Schwake et al.,2003;Maljevic et al.,2003).Though not frequently observed in typical BFNC,dominant negative effects or alterations in channel gating have been reported in patients with BFNC and epileptic encephalo-pathy or myokymia (Dedek et al.,2001;Singh et al.,2003;Borgatti et al.,2004).

In this study,we examined two BFNC families.Molecular genetic analysis revealed novel KCNQ2mutations in all affected members of both families.The mutation in Family 1,S247X,will truncate the channel in the fifth transmembrane segment predicting a non-functional protein.The mutation in Family 2,S122L,is located in the S2segment in which point mutations have not been previously described.Biophysical analysis of this mutation provided evidence for an important function of the K V 7.2S2segment in voltage-sensing,and for the physiological relevance of

this ion channel in the regulation of neuronal firing properties in the subthreshold range of an action potential.Subjects and methods Subjects

Two families with clinical presentations consistent with BNFC were enrolled from the Emory University Epilepsy Clinic.Medical records and neurological examination results were obtained for both probands and for one additional member of Family 2(III-2,Fig.1B).All available family members were interviewed in person or by telephone,and epilepsy histories were documented and corroborated by other family members.Medical records including magnetic resonance imaging (MRI),cranial CT scan and electroencephalography (EEG)were reviewed by a board certified neurologist and neuroradiologist.All participants signed Emory University Institutional Review Board approved informed consent forms.

Family 1is a four-generation family of Ashkenazi Jewish ancestry (Fig.1A).Five affected members were identified.At 5days of age the proband (IV-1)exhibited two episodes of abnormal movements described as rhythmic bicycling of legs and arms with the second episode associated with cyanosis and apnea.Her interictal EEG was abnormal during waking and sleep showing frequent central sharp waves or spikes on both sides,and rare right temporal sharp waves.Sleep demonstrated 2-to 3-s periods of amplitude attenuation and mixed frequency activity consistent with a trace alternans pattern.A normal MRI was obtained.No further seizures were registered after starting treatment with phenobarbital.Three of the remaining four affected family members,III-2,III-3,and III-4also had seizure onset on days 5–6of life.Seizure semiology in these three individuals was described as whole body twitching by their mother.In III-2,III-3and III-4seizures resolved at 6months of age on medication.Whereas phenobarbital was effective in

III-2

Fig.1.Cosegregation of KCNQ2mutations with disease in two BFNC families.(A)Family 1with fourteen individuals from four generations.DNA was obtained from one unaffected and five affected family members.Bfa I digestion of the 221bp exon 5PCR product resulted in the generation of two fragments,84bp and 137bp,from the mutant allele in the affected family members.(B)Family 2with seven individuals from three generations.DNA was obtained from three unaffected and three affected family members.Sac I digestion of the wild-type 417bp exon 2PCR product resulted in the generation of three fragments,228bp,123bp and 66bp.The c.365C>T nucleotide substitution in the mutant allele resulted in the loss of one Sac I site leading to the appearance of an additional 351bp fragment (arrow)in the affected individuals II-2,III-1and III-2.MW,100bp molecular weight marker.Open symbols,unaffected individuals;filled symbols,affected individuals.

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and III-4,further seizures occurring at a frequency of one per hour in III-3required treatment with both phenobarbital and phenytoin.III-3also had1febrile seizure(fever40.5°C)at3 years of age.II-3was told about her neonatal seizures from family members and no further medical history was available for this individual.

Family2is a three-generation Caucasian family(Fig.1B). The proband(III-2)presented with epileptic seizures starting on postnatal day1.His typical seizures involved his head and eyes turning to either the left or right with smacking of his lips and arching of his back.Tonic–clonic convulsions were also observed.Treatment with phenobarbital resulted in the cessation of seizures at11weeks.For III-1,seizures with tonic arm flexions and tonic–clonic convulsions started12h after birth. He was treated with phenobarbital but continued to seize so that carbamazepine was first added.He was then switched unsuccessfully to levetiracetam.His seizures at this time were described as small,symmetric,rapid clonic movements of all four limbs for30s.He became seizure free upon treatment with a higher dosage of carbamazepine(20mg tid)at6weeks of age.III-1also had two febrile seizures at2and7months of age.Both had normal interictal EEGs.Cranial CT scan for III-2 and MRI for III-1were normal.II-2experienced numerous seizures from birth to7years of age.His seizures were described as crying with eyes rolling back,shaking,then drooling and sleeping for several hours.His therapy included phenobarbital and phenytoin which resolved initial seizures,though he continued to have infrequent seizures until age6.The cessation of medications at the age of7was followed by one seizure, however,therapy was not restarted and he has remained seizure free until the present time(currently26years of age).II-1is unaffected.

Mutation analysis

Blood samples were obtained from6members of each family and DNA was extracted by standard methods.The coding regions and exon–intron boundaries of KCNQ2and KCNQ3were PCR amplified from genomic DNA from the probands of both families using previously published PCR primers(Singh et al.,2003).Gel purified products were sequenced on an ABI3100automated sequencer.Patient sequences were compared to published sequences for KCNQ2(GenBank,NM_172107)and KCNQ3 (GenBank,NM_004519).Putative mutations in the probands were confirmed by sequence analysis of the other affected family members.

The c.740C>A nucleotide substitution in exon5of KCNQ2 identified in Family1created a Bfa I restriction site.Exon5was amplified by PCR and the product was digested with Bfa I.The digestion products were visualized on a4%agarose gel(Amresco Agarose SFR,Rockland,ME)with ethidium bromide staining.A 221bp band was obtained for the wild-type allele and137bp and 84bp bands were obtained for the mutant allele.

The c.365C>T nucleotide substitution in exon2of KCNQ2 identified in Family2eliminated a Sac I restriction site.Exon2 was amplified by PCR and the product was digested with Sac I. The digestion products were visualized as described above.Sac I digestion of the wild-type417bp exon2PCR product resulted in the generation of three fragments,228bp,123bp and66bp. Digestion of the mutant allele resulted in the generation of two fragments,351bp and66bp.Mutagenesis and RNA preparation

Site directed mutagenesis was used to introduce the c.365C>T substitution into the KCNQ2cDNA cloned in the pTLN vector, kindly provided by Prof.Thomas J.Jentsch,Zentrum für Molekulare Neurobiologie Hamburg(ZMNH),Germany.Insertion of the mutation was verified by automated sequencing.Plasmids carrying the WT or the mutant cDNA were linearized by restriction enzyme digestion using either Mlu I(KCNQ2)or Hpa I(KCNQ3). Linearized plasmids served as templates for in vitro transcription using the Ambion SP6mMessagemMachine kit.

Oocyte preparation and injection

Procedures were performed as described previously(Lerche et al.,1999).Briefly,Xenopus laevis frogs were anesthetized with 0.1%tricain(Sigma,Deisenhofen,Germany),pieces of ovary were surgically removed,oocytes were defolliculated using collagenase (2mg/ml of type CLS III collagenase,Biochrom KG,Berlin, Germany)in OR-2solution(in mM:82.5NaCl,2.5KCl,1MgCl2, 5HEPES,pH7.6)and stored at18°C in frog Ringer solution(in mM:115NaCl, 2.5KCl, 1.8CaCl2and10Hepes,pH7.4) supplemented with50μg/ml gentamicin(Biochrom KG,Berlin, Germany).10–20ng of diluted cRNA was injected into each oocyte.To study WT vs.mutant channels,the same molar concentrations were injected on the same day into the same batch of oocytes and measured in parallel at days2–5after injection.All results were reproduced with at least two different batches of oocytes and cRNA.

Electrophysiology

Potassium currents were recorded using a standard two microelectrode voltage clamp technique with a Turbo TEC01C amplifier(npi electronic GmbH,Tamm,Germany)and pClamp6.02data acquisition(Axon instruments,Foster City,CA, USA)as previously described(Lerche et al.,1999).The bathing solution was frog Ringer solution(see above).When filled with 3M KCl,electrodes had a resistance of0.3to1MΩ.Currents were sampled at1kHz and low-pass filtered at0.3kHz.Oocytes were held at?80mV and depolarized in10-mV steps.Tail currents were recorded at?30mV and analyzed to generate conductance–voltage plots.Data were analyzed with a combination of pClamp(Axon Instruments Inc.,Foster City,CA),Excel(Microsoft,Redmond, WA)and Origin(OriginLab Corporation,Northampton,MA) software.For statistic evaluation,Student's t-test was applied (p<0.05).All data are shown as mean±SEM.

Results

Molecular genetic analysis

A heterozygous C→A transversion(c.740C>A)in KCNQ2 exon5was identified in the proband(IV-1)of Family1(Fig.1A). This substitution results in the premature termination mutation S247X that will give rise to a truncated protein which lacks essential domains required for channel function including the pore with the selectivity filter,the sixth transmembrane segment containing the activation gate,and the C-terminus(Fig.2A).The c.740C>A substitution creates a Bfa I restriction site.Bfa I restriction digestion of exon5PCR products from the five affected

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family members showed a digestion pattern consistent with the introduction of a Bfa I restriction site in the mutant allele.The wild-type restriction pattern was observed on the analysis of an unaffected family member (II-2)(Fig.1A).These results were confirmed by direct sequence analysis of the six family members.The S247X mutation was not detected in 200control DNA samples.

Sequence analysis of KCNQ2exon 2of the proband of Family 2revealed heterozygosity for a C →T transition (c.365C>T)resulting in the amino acid substitution S122L.Since the mutation eliminated a Sac I restriction site that is present in the wild-type allele,the presence of the mutation was visualized by PCR amplification of exon 2followed by restriction enzyme digestion with Sac I.All 3affected family members generated a digestion pattern consistent with the loss of the Sac I site in the mutant allele,while the three unaffected family members generated the wild-type digestion pattern (Fig.1B).This finding was also confirmed by direct sequence analysis of the exon 2PCR product from the six family members.S122is located in the second transmembrane segment of K V 7.2(Fig.2A)and is evolutionarily conserved in the

orthologous mouse and rat K V 7.2channels and also in human K V 7.3(Fig.2B).Mutations in this region have not been previously identified.The mutation was not observed in 400ethnically matched controls (800chromosomes).Electrophysiology

To assess the potential disease-causing role of the K V 7.2channel carrying the S122L mutation,we expressed it function-ally in https://www.sodocs.net/doc/5a6998928.html,evis oocytes.The mutation was introduced into the KCNQ2cDNA by site-directed mutagenesis.K +currents of homomeric WT and mutant channels,as well as heteromeric channels formed by coexpression with K V 7.3,were recorded from oocytes injected with the respective cRNAs using the two-electrode voltage clamp technique.

Heterologous expression of homomeric WT K V 7.2channels yielded voltage-dependent K +currents,elicited by depolarizing test pulses from a holding potential of ?80mV .These currents activated slowly at ?50mV and more positive potentials.Homomeric S122L channels were functional,but the onset of activation was shifted towards more depolarized potentials (

Fig.

Fig.2.Mutations in K V 7.2and K V 7.3channels identified in BFNC and evolutionary conservation of serine 122.(A)Schematic view of K V 7.2and K V 7.3subunits with all mutations that have been described so far shown as white symbols (Lerche et al.,2005and references therein,Singh et al.,2003),and the two novel mutations identified in this study shown as black symbols.(B)S122is located within the S2transmembrane segment of K V 7.2.This residue is conserved in the orthologous K V 7.2protein of human,mouse and rat as well as in human K V 7.3.GenBank accession numbers from top are:AY889405,AF490773,AF087453,AF071491,AY114213,AF105216,AF249278.

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3A).Maximal current amplitudes,analyzed at the end of a2-s pulse to+10mV and normalized in each experiment to the mean value of WT K V7.2currents,so that the data from different experiments could be pooled,were not significantly different between WT K V7.2and S122L channels.Furthermore,when the cRNAs encoding the WT and the mutant K V7.2subunits were injected in a0.5:0.5ratio,the maximal current amplitude remained unchanged(Fig.3B).

Activation curves were constructed from tail current amplitudes measured at?30mV(Fig.3C).We observed a positive shift in the voltage dependence of activation,with an increased slope for S122L channels.Therefore,the shift was most pronounced in the subthreshold range of an action potential,predicting a75%current reduction at?50mV(Figs.3A,C).For the channels comprising both WT K V7.2and S122L subunits,the observed rightward shift together with the altered slope was less pronounced.Furthermore, activation kinetics of S122L currents were slowed compared to those of the WT channel(Fig.3D).The time constants of activation,τact,obtained by fitting a first-order exponential function to the rising phase of the potassium current at various test potentials,were significantly different at potentials ranging from?40to+10mV(e.g.,at?30mV:τact=497±62ms(WT channel)vs.923±89ms(mutant channel)or856±88ms(WT+ mutant channel),p<0.01,n=10).No significant differences were observed for current deactivation which was recorded at various test potentials following a1.5-s depolarization to+50mV and quantified by fitting a first-order exponential function to the tail currents(Fig.3E).

Considering that heteromeric K V7.2/K V7.3channels might constitute the most abundant native form of the M-current in the brain(Jentsch,2000;Wang et al.,1998),we also studied the functional consequences of the S122L mutation in heteromeric assembly with K V7.3.Moreover,to mimic the potential condition of a BFNC patient,having one wild-type and one mutated KCNQ2 allele,and two wild-type KCNQ3alleles,we coexpressed K V7.2 WT,S122L and K V7.3in a1:1:2ratio(Fig.4).As illustrated in Fig.4A,maximal current amplitudes of the three different heteromeric channel preparations were almost identical when recorded3–5days after injection.As observed on the comparison of monomeric WT and mutant K V7.2channels,a depolarizing shift was observed in the voltage dependence of activation for S122L/ K V7.3compared to K V7.2/K V7.3heteromeric channels(Fig.4B), however,the slope of the activation curve was not significantly increased.There was also significant slowing of activation

kinetics Fig.3.Heterologous expression of homomeric K V7.2channels,comprised of either WT,or S122L mutant subunits.(A)Representative current traces recorded from Xenopus laevis oocytes injected with cRNA encoding either WT K V7.2or S122L mutant channels.Currents were elicited by depolarization from?80to +10mV,in10mV steps,followed by a0.5s pulse to?30mV to measure the tail current amplitude,and normalized to the maximum current amplitude at +10mV.The holding potential was at?80mV.(B)Relative current amplitudes for K V7.2,S122L and channels comprising both K V7.2and S122L compared at the end of the2-s pulse to+10mV.(C)Conductance–voltage relationships for homomeric K V7.2and S122L and K V7.2+S122L channels.Lines represent fits to a standard Boltzmann function:I/I max(V)=1/(1+exp[(V?V0.5)/k],where I/I max is the normalized tail current amplitude,V0.5the voltage of half-maximal activation and k a slope factor.Parameters for K V7.2were V0.5=?37±2mV,k=?10.0±0.4mV,n=13;for S122L:V0.5=?31.0±0.7mV,k=?7.5±0.3mV, n=20;and for K V7.2+S122L:V0.5=?34.9±0.7mV,k=?7.4±0.4mV,n=8.(D)A first-order exponential function was fit to the time course of activation yielding the time constantτact.The difference between the WT and the S122L or K V7.2+S122L channels was statistically significant(p<0.05)for most of the voltage range.(E)Deactivation kinetics for WT K V7.2and S122L mutant channels.The tail current decay at different test potentials,following a1.5s depolarization to+50mV,was fit by a first-order exponential function,yielding a deactivation time constantτdeact,n=10.Circle,WT K V7.2channels;Square, S122L channels;Diamond,WT K V7.2+S122L channels.

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in the voltage range from ?50to +10mV (e.g.,at ?30mV:τact =345±18ms (S122L/K V 7.3)vs.476±24ms (K V 7.2/K V 7.3),p <0.001,n =10),as shown in Fig.4C.When S122L and WT K V 7.2were coexpressed with K V 7.3subunits in a 1:1:2ratio,we still observed subtle changes in channel gating,in the same direction as for the other experiments,but they did not reach statistical significance (Figs.4B,C).Discussion

In Family 1we identified a novel KCNQ2mutation predicted to generate a protein that is 37%shorter at the C-terminal end (S247X).Since S247X channels will lack the pore region,as well as the C-terminus containing the assembly domain of K V 7.2/K V 7.3channels (Schwake et al.,2003;Maljevic et al.,2003),we anticipate that it will be non-functional,thus causing BFNC by haploinsufficiency as observed for most of the other known mutations (Jentsch,2000;Lerche et al.,2005).In Family 2we identified the amino acid substitution S122L within the second transmembrane (S2)segment of the K V 7.2K +channel.Functional expression of this mutation in Xenopus oocytes revealed a unique gating defect characterized by a shift of the voltage dependence of activation leading to a large reduction in current amplitude and slowing of the activation time course specifically in the subthres-hold range of an action potential.The biophysical analysis of this mutant channel has identified an important role for the S2segment in voltage-dependent gating.

Several BFNC mutations that affect voltage-dependent gating of K V 7.2channels have been reported.The two missense mutations,R207W and R214W,located in the S4transmembrane segment resulted in prominent depolarizing shifts of the activation curves (+30mV and +15mV ,respectively)that were accompanied by dramatic slowing of the activation kinetics (Dedek et al.,2001;Castaldo et al.,2002),consistent with the function of the S4segment as a voltage sensor.Another BFNC mutation located at the C-terminus,also affected the voltage sensitivity of K V 7.2and shifted the activation curve by about +10mV ,probably by interfering with regulatory protein-binding to the K V 7.2C-terminus (Borgatti et al.,2004).Some of the mutations reported by Singh et al.(2003)had similar,but less striking effects on channel gating.These mutations induced a parallel shift of the activation curve that occurred over the whole voltage range of channel activity.In contrast,S122L channels only displayed altered activation kinetics at subthreshold voltages between ?60and ?30mV while other parameters such as maximum current amplitudes (both for homomeric K V 7.2and heteromeric K V 7.2/K V 7.3channels)were unaltered,indicating that the functional expression of the protein in the cell membrane was probably unaffected.However,we cannot exclude the possibility that the S122L mutation could affect channel trafficking to the membrane without changing the maximal current amplitude (for example by reducing the surface expression or the stability of the channel but increasing its open probability).It has been previously suggested that the M-current plays a critical role in the regulation of neuronal excitability and response patterns at subthreshold potentials of the neuron,at which only a few other ion channels are active (Jentsch,2000;Brown and Adams,1980;Rogawski,2000;Delmas and Brown,2005).The genetic and pathophysiological results presented here support this hypothesis,as they establish the pathogenic role of this non-inactivating K +channel as a regulator of neuronal firing in the subthreshold voltage

range.

Fig. 4.Heterologous expression of heteromeric K V 7.2/K V 7.3channels harboring WT K V 7.2and/or S122L mutant channels.(A)Current amplitudes measured at the end of a 2-s depolarizing test pulse to +10mV .Xenopus oocytes were injected with K V 7.2+K V 7.3or S122L+K V 7.3cRNA in a 1:1and K V 7.2+S122L+K V 7.3cRNA in a 1:1:2ratio;n =6–10.(B)Activation curves for the three coexpressions obtained from the tail current amplitudes as in Fig.3.Parameters were as follows:V 0.5=?39.6±0.7mV ,?38.6±0.6mV ,and ?35.2±0.3mV;slope factor k =?7.4±0.3mV ,?7.0±0.4mV ,and ?7.4±0.3mV for K V 7.2+K V 7.3,K V 7.2+S122L+K V 7.3and S122L+K V 7.3coexpressions,respectively;n =18–21.(C)Time constant of activation,τact ,obtained by a first-order exponential fit to the rising phase of potassium currents at various test potentials.Statistically significant differences (p <0.05)between K V 7.2+K V 7.3and S122L+K V 7.3,were observed for most of the voltage range.Inset:representative current traces at ?50mV ,normalized to the maximal current amplitude at +10mV ,illustrating the difference in the current amplitude and activation kinetics for different heteromeric channels at this potential.Circle,WT K V 7.2+K V 7.3channels;Square,S122L+K V 7.3channels;Diamond,WT K V 7.2+S122L +K V 7.3channels.

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K V7.2interacts with K V7.3channels via their C-termini leading to a large increase in current amplitude in in vitro systems(Yang et al.,1998;Schwake et al.,2003;Maljevic et al.,2003;Selyanko et al.,2000),suggesting that this interaction also plays an important role within the brain.However,the neuronal expression patterns of K V7.2and K V7.3channels are still unclear and published studies have revealed both similarities and differences(Cooper et al., 2000;Roche et al.,2002;Devaux et al.,2004;Weber et al.,2006; Geiger et al.,2006).When mutant and WT K V7.2channels were coexpressed either in a1:1ratio or in a1:1:2ratio with K V7.3in oocytes(the latter would be expected in an affected heterozygous individual),the effects of the mutation were still apparent but much less pronounced,and the1:1:2coexpression did not attain statistical significance.However,data generated from recordings in oocytes may not accurately reflect the neuronal environment and,in particular,the coexpression of both channels in the brain might be variable with higher expression of KCNQ2in cells that may be important for the generation of seizures.Moreover, functional changes in developing or mature neurons that only express K V7.2channels or have delayed KCNQ3expression might be sufficient to cause BFNC(Tinel et al.,1998;Weber et al.,2006; Geiger et al.,2006).The functional data presented here together with the results of the genetic analysis,which did not reveal a second mutation in KCNQ2or KCNQ3and showed the absence of the c.365C>T mutation in800control chromosomes,support the conclusion that S122L is the causal mutation in Family2.

The S122L mutation resides in the S2segment,close to its predicted extracellular end.In Shaker voltage-gated K+channels, an interaction between negative residues of the S2segment and the positive residues of the voltage sensing S4segment has been convincingly shown and contributes significantly to gating charge movement accompanying activation(Papazian et al.,1995).Other functional studies(Monks et al.,1999)as well as the crystal structure of a voltage-gated K+channel(Long et al.,2005) confirmed the interplay between S2and S4segments in channel gating.We present here indirect evidence,that the S2segment may play a similar role in K V7.2channels and speculate that the S122L substitution affects voltage-dependent activation by partially disrupting an interaction between the S2and S4segments. Acknowledgments

We thank the families for their participation in this study and Professor Thomas Jentsch for providing the KCNQ2and KCNQ3 cDNAs.This work was supported by grants from Citizens United for Research in Epilepsy(CURE),March of Dimes Birth Defect Foundation(#5-FY02-250)and NIH research grant NS046484to AE,and from the Fritz-Thyssen-Stiftung,the Deutsche For-schungsgemeinschaft(DFG,Le1030/9-1),the Bundesministerium für Bildung und Forschung(BMBF/NGFN2),and the Land-esforschungsschwerpunkt Baden-Württemberg to H.L.,and a fellowship of the University of Ulm to S.M.H.L.is a Heisenberg fellow of the DFG.This study was also supported in part by PHS grant M01-RR00039from the General Clinical Research Centers Program,NIH,National Center for Research Resources. References

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《我喜欢的作文》我喜欢的作文（一）：我喜欢的一本书每个人都有自己喜欢的一本书，我也不例外。在我家的书橱上，有着一本我喜欢的书――《名人故事》。当我第一次接触这本书时，我爱不释手，立刻被它那古色书香吸引住了。封面上，爱因斯坦和爱迪生的画像印入眼帘。画像旁，写着几个引人注目的大字――名人故事。看到这，我不由自主的把书翻开，津津有味的品读起来。经过这本书，我明白了以前从未认识过的名人。原先，朱德幼时喜欢听天国名将石达开的故事，这竟成为他走向革命道路的起点；毛泽东决心以救国救民为自己的职责；郭沫若要做中国的歌德；田汉要做中国的席勒；华盛顿能文能武，为美国的独立建立了赫赫功劳、、、、、、这本书里的名人们的一个个感人至深的故事，总是激励着我通向成功的途径。被人誉为东方神鹿的王军霞，在上初中时，学校离家有四公里远。这段路程对于一个14岁的女孩来说实在够远的了，为了给家里省钱，王军霞放下了买自行车骑回学校的念头，毅然地做出了一个惊人的决定――以步代车，开始了每一天来回跑足足十六公里的路程的生涯。她这种精神感动了我。《名人故事》这本书激励着我前进，让我明白了许多名人故事，让我从中受到启发，我怎能不喜欢呢？我喜欢的作文（二）：我喜欢的歌每个人都有自己喜欢的一首歌，当然，我也不例外。在这些数不胜数的歌中，我最喜欢的一首歌就是《隐形的翅膀》。每当我听起这首歌，我就会情不自禁地想起那件事记得有一次英语考试，我才考了80分，而我们班居然有几个人满分。从那次起，我开始变的闷闷不乐的。课堂上，我不用心发言。下课了，看不到同学们与我玩耍的情景。我觉得同学们都在嘲笑我老师似乎看出了我的心思，在一次课堂上，老师问我们有没有听过《隐形的翅膀》这首歌，听过这首歌的同学都大声地唱起来，我被这美妙动人的歌声吸引住了，回家后，我搜索了这首歌并尝试着学唱。每一次，都在徘徊孤单中坚强。每一次，就算很受伤也不闪泪光。我明白，我一向有双隐形的翅膀，带我飞，飞过绝望从此，我不再自卑。我喜欢这首歌，因为它让我在绝望中找到期望，在自卑中给了我鼓励。我喜欢的作文（三）：我喜欢的花有人喜欢高傲的牡丹花，有人喜欢美丽的玫瑰花但我喜欢的却是千姿百态的菊花。

作文(我喜欢的一个汉字)

题目：我喜欢的一个汉字要求：说说自己喜欢的一个汉字，以及为什么喜欢它。我喜欢的一个汉字爱，是我最喜欢的一个汉字，你们知道为什么吗？因为，对待朋友，对待动物，乃至人类，你付出多少爱，你就会拥有多少爱。有了爱，人们之间的距离为零；有了爱，人们之间可以无话不谈；有了爱，能将我们的心拉得更近。原先，我最喜欢的是“强”字。因为，我读过张海迪的故事，读过保尔的故事…… 当时，我认为他们是坚强的、勇敢的。他们不怕任何阻拦，勇往直前。我当时喜欢“强”字，是因为我读过爱迪生的故事，他不怕失败，研究、发现、创造，当时，我也认为他是坚强的、勇敢的。再比如比尔·盖茨，他十分的勇敢，在当时他家人强烈反对下，毅然跨出了校门，去创造他的网络世界，我当时也认为他是坚强的、勇敢的。像这样的例子还有很多，很多。正是因为他们，我当时才喜欢“强”字。可是，现在回想起来，我错了，张海迪为什么不怕种种阻挠，而学习呢？因为爱。因为她爱学习！爱迪生为什么不怕失败呢？因为爱。因为他爱发明创造。比尔·盖茨为什么不顾家人的强烈反对，一定要跨出校门，去创建自己的网络世界呢？也是因为爱。他爱网络…… 同学们，你们为什么喜欢“爱”这个字了吗？请记住我的一句话：“…种瓜得瓜，种豆得豆。?你在付出爱的同时，也会得到同样的爱。就像种瓜、种豆一样。不管是关爱、友爱……你都能得到同样的爱！” 我喜欢的一个汉字我喜欢的一个汉字“爱” 爱是一泓泉水，滋润你的心田；爱是一杯清茶，处处散发浓香；爱，是在你危难时的帮助；是你难过时的安慰。父爱.母爱.友爱······发自内心的美好。我们都清楚的记得，都不会忘记2010年4月14日这个令人悲痛的日子。青海玉树发生了701纪大地震。许多同胞都倒在废墟里，面对这突如其来的灾难，我们都献出了自己的一份爱心。如今，已有1万多同胞成功的克服了困难，而那2千多不幸的呢，却倒在了废墟里。而这些活下来的同胞是靠着坚强的意志活了下来。身为一名少先队员，我们为你们感到骄傲。现在，我想说的是，不要因为失去亲人而再痛苦了，振作起来吧，我们手拉手，共同克服这难关吧。爱，可以是一句慰问的话语，可以是自己小小的一份力，而现在我想说的是，只要人人都献出一份爱，才可以创造美好和谐的家园，让我们共同加油吧！

我喜欢作文

我喜欢作文我喜欢作文(精选15篇) 我喜欢作文（一）：我喜欢我喜欢冬天的雪，在某个早晨或傍晚，飘飘洒洒的飞来。我喜欢那份纯洁的白，我喜欢那种飞舞的自然。我喜欢春天彩色的蝴蝶，那轻盈的舞姿，绚丽的翅膀吸引了我。花海中她们就是海鸥，寻找着自我的需要。我喜欢春风，他所过之处一片绿色，吹走冬天的气息，带来鲜花与嫩草。我喜欢夏日的夜空，繁星就如同一颗颗闪烁的珍珠，装点着夜空每一处的角落。我喜欢秋天的田野，玉米和大豆总在瑟瑟秋风中摇曳，那农民便是金色海洋中的鱼民，从田地里扑捉着丰收的欢乐。我喜欢那远处树木的最终一片落叶，因为那预示着来年又一次的嫩叶要生长。我喜欢梦。梦见自我有一只神奇的法杖，实现我美丽的梦想。我还梦见自我有一位魔法朋友，我们一齐去游玩远方。我梦见自我是一位侠女，斩妖除魔，救民四方。我也喜欢花。富贵的牡丹、淡雅的茉莉、圣洁的水仙、鲜艳的山茶、多姿的月季、绚烂的杜鹃，或者山谷里可爱的小野花，她们开得同样美丽，同样多彩。

我喜欢微笑。不管是我对别人，还是别人对我，微笑同样真切。我也喜欢音乐。从古典优美的声音中，我觉得一切都那么充一切都那么完美。我喜欢朋友。他们在我倾诉烦恼时认真地听，开导我，每当这时，我就觉得什么东西流入心底，十分温暖。我喜欢生活，感激一切让我喜欢的事物！我喜欢作文（二）：我喜欢我喜欢清澈的小溪，喜欢小溪叮咚的声音；但更喜欢将我的脚，当作小木桨，在水面上轻轻划过；让那清爽的感觉，流进我的血液。我喜欢郁郁葱葱的森林，喜欢森林清鲜的空气；但更喜欢将我的手，当作一阵风，在树身上慢慢拂过：让那自然的感觉，传播我的身体。我喜欢明朗的天空，喜欢天空偶尔的几声鸟叫；但更喜欢将我的耳朵，当作收音机，在天空中悄悄收着；让那清脆的声响，传送我的四肢。我喜欢广阔的大地，喜欢大地上的一花一草；但更喜欢将我的眼睛，当作望眼镜，在大地上静静地看着：让那美丽的风景，镶在我的大脑。

我喜爱的书刊作文12篇

《我喜爱的书刊作文》我喜爱的书刊作文（一）：我喜爱的书刊《意林》是我喜爱的书刊。我与《意林》相识，还是得益于朋友的牵线搭桥。那几本厚厚或薄薄的《意林》一出现，便深深的吸引了我。不管疲劳时，还是闲暇时，我都会捧一本《意林》看得津津有味。《意林》栏目众多，但都是一些意趣横生、意味深长的小故事。它于短小精悍的故事中，展现人的灵性，折射人在生活中灵光一现，体现人生哲理。因此许多小故事让我记忆深刻、深受启发。有一个故事名字叫一步改变一生。故事讲了著名导演张艺谋去一个小山村选演员。他一连问了好几遍：谁想演电影？村民们都不吱声。这时，一个长相并不漂亮的女孩站了出来，还边唱边扭了一段，引的村里人哈哈大笑。没想到这个勇敢的姑娘被张导选中，还在影片中出演女主角，之后她名声大燥。从这个故事中我懂得了有时候不要轻视那小小的一步，它可能会改变人的一生。所以我学会了勇敢，相信自我以后遇到事情会更有自信、更勇敢一些。阅读是一个有生命的过程，在阅读中，仿佛故事中的主人公都变得活灵活现起来，给我讲述、与我交流。《意林》真是小故事大智慧，小幽默大道理，小视角大意境。它鼓舞了我的智慧和心灵。我认为，读《意林》是一件很惬意的事，它能够让你忘却疲劳，沉浸在那些哲理的小故事中。《意林》，它就像一缕温情的阳光，照耀人性的每一个角落；就像一把智慧的钥匙，将打开成功的通道；就像一位心心相印的朋友，将和我一齐提升人生的境界。我喜爱的书刊作文（二）：我喜爱的书刊学习之余我喜欢看书来充实自我的生活，从识字以来我看了很多的书：有《简爱》、《安娜卡列尼娜》、《傲慢与偏见》等世界名著，有《红楼梦》、《西厢记》、《三国演义》等中国古典小说，还有很多当代小说，其中，我最喜欢看的是反映我们读书生活的校园小说。在看过的校园小说中，我最爱读的一本就是《三重门》，它是一本批评现行教育制度的书。《三重门》描述了一群高一学生的读书生活。主人公雨翔是个很有个性的人物。他敢跟老师唱反调，逃课，逃夜，他把应试教育批得面目全非，视教育制度为草芥。我很佩服主人公的敢做敢当，不畏权势。《三重门》之所以吸引了广大学生朋友的目光，我想主要是这本书的作者韩寒是一个传奇人物。他刚上高一就能写出一部轰动全国的书，有的学生说韩寒写出了他们的心声，把他们隐藏在心底多年的心理话都说了出来，觉得十分痛快。也有人说韩寒自高自大，目中无人，复制钱钟书的思想，因为《三重门》的文笔跟《围城》的很相似，总之，韩寒成了学生们的偶像，家长们担心的对象。

我喜欢(700字)作文

精选作文:我喜欢(700字)作文我喜欢春天。走在春天的小径上，花儿露出甜美的微笑；风儿送来芬芳的花香；鸟儿向我亲切地问好。我喜欢这种笑容，这种花香和这种亲切，我更喜欢拥有这一切的春天！我喜欢夏天。坐在阴凉的树荫下，喜欢荷花的美貌，像亭亭玉立的姑娘；喜欢扇子的摇摆声，像音乐家，弹奏着不同节奏的乐曲；喜欢西瓜的香甜清凉，像魔术师，把人们火热的身体感受到清凉的舒适。我更喜欢将我的喜欢都集合在一起的夏天！我喜欢秋天。走在硕果累累的果树下，金黄的树叶躺在树妈妈的怀抱中，沉醉在秋天最美的时候。美的是五颜六色的水果，美的是金灿灿的地毯，美的是黄澄澄的小雨，但更美的是人们脸上快乐的笑容。更美的是他们的化妆师秋天！我喜欢冬天。坐在家门口的板凳下，期待是当一片片绒毛般的雪花谁在大地妈妈身上时，雪花女儿变成了大地妈妈最温暖的小棉袄，陪着妈妈一起欣赏着孩子的打雪仗，堆雪人时无邪的笑声，那是给女儿和妈妈最大的回报，因为她们是笑容的收集师冬天！我喜欢森林。走进森林，抖抖耳朵有心听，鸟儿是最着名的音乐家，树叶是最着名的伴奏师，她们演奏的是最着名的《自然协奏曲》。动动鼻子仔细嗅，即将开放的桂花是霸气外露的，已经冬眠的桃花也是芬芳扑鼻的，她们是森林有名的香奈儿。摸摸心灵轻轻看，从茂密的树叶间的缝隙钻进来的阳光，是那样的温暖、明亮，幽幽的森林又添了一份耀眼的景色！&& 我喜欢大自然，它让我心中燃起了那么多的喜欢，它让我的心变得彩色，让我也感受到了彩色的大自然，因此，我深深地喜欢着这可爱美丽的大自然！&& 我喜欢生活，并且深深地喜欢能在我心里充满了这么多的喜欢！重庆沙坪坝区重庆大学附属小学六年级:刘?毅篇一：我喜欢作文800字我喜欢作文800字幸福，或许很简单，更或许很复杂；生活，或许很简单，更或许很复杂；自己，或许很简单，更或许很复杂；喜欢，或许很简单，更或许很复杂。———题记我喜欢在课间十分钟一边哼哼曲调，一边沐浴漫无目的反射在我肩头上的太阳光，一边欣赏粉笔灰在空中肆意跳跃的舞步。听，窗外树枝上的鸟儿伴随我唱和；瞧，微风拂过，两鬓发丝妖娆可爱的舞动着；看，窗外的榕树在当伴舞，树叶在伴奏——“沙沙沙”。随着铃声，又进入了课堂。等待下一个十分钟。我喜欢音乐，一个人，静静地。我喜欢流行歌曲，吉他的狂野激情，小提琴的温柔婉转，钢琴的意味深长，都令我神往，我好似被带进了一个神奇的世界，在那小提琴也疯狂，吉他也轻悠，钢琴也变得雄伟，这是音乐奇侠世界，在这个世界里，找不到一丝杂念。不知何时，我也成为了音乐奇侠?? 我喜欢看书，独自坐在家里的书桌前，翻动着手中的页码，任春风吹拂，任阳光灿烂，任时间匆匆从我身旁流去。独自得读着自己喜欢的书，徜徉在书的海洋里，闻着书香的气息，看着哲人的事迹，这是对心灵的浇灌。我喜欢在忙绿了一天后，贪婪的趴在桌上，拿起一支笔，在那夹着香气的淡蓝色本子上，记载这一天中的趣事和收获。不管是快乐的还是不快乐，不管是否忧愁都毫无顾忌，毫无保留的倒叙在本子上，当窗外得灯红酒绿隐设于黑暗，我坐在转椅上，忘我的写下去，我写下的那一行行凌乱无序的文字，将会成为长大后的回忆。我喜欢雨后的彩虹，我喜欢看七色中最外层的那一色，淡淡的，很优雅。彩虹在天上呆腻了，便来到了地面上，调皮的我，在水面上跳跃，溅起一丝水花，捣乱了七色的顺序。我跑到桥头，站在顶端，我想抓住彩虹飞到那天上去，它却与我一起疯狂，跑到了湖面。周边河畔的金柳，是夕阳中的新娘，波光里的艳影，在我心头荡漾；??那柳阴下的一潭，不是清泉，是那雨后虹，揉碎在

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我喜欢的作文我喜欢的作文20篇我喜欢的作文（一）：我最喜欢的楚霸王我最喜欢的楚霸王楚霸王项羽于我来说，有种说不出的魅力。他似乎有种与生俱来的魔力，牵引着我们去了解他，敬仰他，在历史的舞台上，他完美的诠释了他那不平凡的一生，无阕风云、生死浮沉，谁的红装，谁的天下，一个朝代的覆灭，群雄逐鹿，横刀立马，谁能主宰天阙，金戈铁马，割喉烈酒，饮鸩止渴，谁又能完美的诠释这一切。仅有项羽，唯有英雄项羽才能完美的诠释。当楚汉之争临近终结时，项羽还是不肯服输，虽然明白这一站注定会失败，而他注定是那个失败者，但他毫不畏缩，只要还有一丝期望，饮鸩止渴又何足畏惧，我曾想过，乌江的最终一站，项羽为何会失败，归根究底他就是太正义了，不会做卑鄙小人的事，其实，在乌江一战的时候，他只须事先命人在乌江水里洒一点毒药，然后等到真正的刘邦开战时，再把刘邦的士兵引导江水中，让其自生自灭，血染乌江也好，惨不忍睹也罢，只要能胜利，管他用什么无耻的手段。只是，他没有，他没有这样做！正是因为骨子里的正义和不服输，才让他成为后人景仰的大英雄，项羽用他的一生告诉我们：做人就要正义，就算死也要做

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灯，好像在说：“小心点，不要撞到我。”在清洁工爷爷奶奶中，没有一个是不高兴的，因为他们是在为祖国清扫垃圾，如果没有他们的工作，我们就会生活在垃圾堆里。夏季的一天，一场雷雨过后，我们小区门口的下水道堵了，门前一片水溏，我下了楼正要去奶奶家，看到这场景，着急的不得了，突然那位清洁工奶奶冲过来，跑进水塘里，又是拖又是拽，才把垃圾清理掉，水这才慢慢的流下去，路人们都夸她是“清洁天使”，我跑过去谢了奶奶，心里想：“这可真是一个称职的清洁工人啊！” 又一个早晨，我们小区门口有一个垃圾桶，上面脏兮兮的，人们都不想接近它，扔垃圾都离的远远的，一位清洁工爷爷看见了，先打了盆水，然后拿上抹布从上到下，从左到右的擦鞋，擦得干干净净的，擦完后老爷爷才喘了一口气，我在心里想：“这位老爷爷真是不怕脏啊！” 有一种在城市里的“天使”叫清洁工，人们把他们叫做“清洁天使”！那一抹身影作文2我家里曾今有一条小狗，虽然它现在已近不在了，但是它那一抹棕色的身影，以及那一件件在它身上发生的有趣的事，常常浮现在我的脑海里。丢丢有一双水汪汪的大眼睛，黑黑的鼻头。由于它是我们在回家的路上捡的，所以就叫他“丢丢”。虽然它是一只博美犬，个头十分矮小，但可是十分勇敢，还很聪明。这不！

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动物还是植物都在冬眠的日子里喝一杯滚滚烫烫的热水。我喜欢黄昏，可能是太阳公公干了一天的活太累了，当他下班时，总要拄着拐杖并涨着通红的脸欲欲回家。我喜欢看书，当我执手握着那些丰富的知识时，总是觉得握着一脉优美的传统。小声的读着那优美的句子，就像是细细品味着浓郁清香的茶。我喜欢生活，喜欢这一切一切！关于我喜欢的作文（二）我喜欢春天的细雨，那儿还带着冬天的气息的雾中，细雨纵横交错交织成薄纱，笼罩着那寒冷。凉风欢快的吹来，吹散薄纱，拉来春天的象征。

我喜欢夏日的雷电，在原本喧哗，吵闹的世界里，一声轰隆隆的雷神打破了这个喧哗的世界，迎来大片凉风。我喜欢>秋天的风儿，秋风吹动了树枝，枫叶随着风的旋律，配着树枝摇动的沙沙声，跳出美丽，轻盈的舞蹈。我喜欢冬天的雪花，在那没有生命的大地上，雪花徐徐飘下，如芦花，似柳絮，像轻悠悠的鹅毛，无尽无休的飘着，飘着??宛如那美丽的银蝶在院中翩翩起舞，又想一群穿白纱裙的小舞女，伴着天空中传来的仙乐，轻轻盈盈地在空中飘舞着，旋转着，跳着舞蹈。这雪花把大地装扮成那样美丽，如仙境一般。我喜欢遐想，听那优美，抒情流畅的旋律，一幅幅快乐的画面使我陶醉，美丽的蓝河，那飘渺的绿野山间的小白屋子，我仿佛听到了对岸白桦林中的鸟语嗅到了那蝶恋蜂

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很远;北海的长廊默默地讲述着一个个故事。它的横梁和檐上都绘画着一幅幅画，每一幅画都是一个动人的故事。这些绘画精美、耐磨，久经风霜不褪色，每幅画还描了金边，让人赞不绝口。我喜欢北海。它是智慧的结晶，是中华民族的骄傲，是我们祖先用勤劳和智慧的双手创造出来的，所以，我喜欢北海。我喜欢的作文二：在我所有的朋友中,我最喜欢的是王安琪。她胖乎乎的脸蛋上中嵌着一双明亮的眼睛, 忽闪忽闪的,高高的鼻梁下面长着一双樱桃小嘴,每当她笑时,小嘴边就会出现可爱的小酒窝. 她不仅可爱还乐于助人记得有一次,放学后,我们都留在教室里做练习题,一道题让我犯难,着急地像热锅上的蚂蚁,我转头一看,看见安琪还在埋头思考,我走过去问她这道题该怎么做,她放下书,耐心地给我讲解,时间一分一秒地过去了,虽然我懂了,可她还剩下很多练习题还没有做,我惭愧地低下头.顿时,她握着我的手说;我们是朋友嘛,朋友不就应该互相帮助吗?没事,不就挨顿打吗,值得。我激动地流下了眼泪安琪无论有什么事,都要去书的海洋去游览一下,有一次,她看书看得住迷劳动,她妈妈叫她吃饭,她才不舍地放下书,去吃饭,因此我

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唯一移动的景。当穿过木桥后，蓦然回首，古朴的小木桥在眼中，多了几分沧桑。不知古时，有多少人走过这座桥，又有多少人看过这片雪林，这片静谧安详的雪林...... 我喜欢这些良辰美景，尽管有一天它会消失殆尽，但它已铭刻在我心间。文_缑一棽（泉州市第二实验小学）指导老师：潘晓峰

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