ライフサイエンスコーパス: synaptic

1 nt and shrinkage that are accompanied by the synaptic accumulation or removal, respectively, of the A

2 Dopamine neuron synaptic actions vary across the striatum, involving var

3 several studies have explored the effect of synaptic activation on beta-amyloid, little is known abo

4 t the interaction between glutamate-mediated synaptic activity and TrkB signaling is imperative to BD

5 ustering behavior through the measurement of synaptic activity at the single-cell level, thus providi

6 ascr#3 imprinting is mediated by increased synaptic activity between the ascr#3-sensing ADL neurons

7 cs and enhances mitochondrial biogenesis and synaptic activity in APP mice; and that SS31 may confer

8 Loss of synapses or alteration of synaptic activity is associated with cognitive impairmen

9 rence electrode, they often reflect those of synaptic activity occurring in distant sites as well.

10 t roles of AMPARs in governing bidirectional synaptic and behavioral plasticity in the CNS.

11 tered neuronal activity, we investigated the synaptic and network effects that occur 1 week after Pte

12 and marked a reorganization of expression of synaptic and schizophrenia-susceptibility genes.

13 a subunit-containing receptors underlie both synaptic and tonic glycinergic currents.

14 Utilizing expression of a virally encoded synaptic anterograde tracer, AAV-SynaptoTag, followed by

15 We further demonstrate how this novel synaptic arrangement enables DSGCs to encode direction r

16 ion of enlarged intraluminal vesicles within synaptic boutons.

17 ile filopodia as well as in later-stabilized synaptic boutons.

18 he soma affect neurotransmitter release from synaptic boutons.

19 The IHC ribbon synapse structure, synaptic Ca(2+) currents, and otoferlin distribution wer

20 n single spines, we provide a spatial map of synaptic calcium signals along dendritic arbors of hippo

21 ontribute to the specificity and strength of synaptic changes associated with learning and memory.

22 lts suggest that ubiquitous unreliability of synaptic changes evinces metaplasticity that can provide

23 ocampus is critical for episodic memory, and synaptic changes induced by long-term potentiation (LTP)

24 leus of the solitary tract (NTS) neurons for synaptic characterization and compared them with unlabel

25 e for reuptake of neurotransmitters from the synaptic cleft to terminate a neuronal signal and enable

26 Diverse molecular mechanisms regulate synaptic composition and function in the mammalian nervo

27 neurons interacting with each other through synaptic connection between axons and dendrites, therefo

28 The generation of precise synaptic connections between developing neurons is criti

29 Divergent synaptic connections did not contribute directly to the

30 We reconstructed the morphologies and synaptic connections of all 983 neurons within the three

31 d in the extrastriate cortex where they form synaptic connections with spines and small-diameter dend

32 pses towards weakening, while preserving the synaptic connections within active neuronal assemblies.S

33 ntributes to behavioral deficits by altering synaptic connections, and RhoA-ROCK inhibition enhances

34 ce of the Ising model couplings to infer the synaptic connectivity in in silico networks of neurons a

35 reactive fiber innervation and bidirectional synaptic connectivity.

36 ndamental events during the establishment of synaptic connectivity.

37 ut patterns, and systematically varied their synaptic connectivity.

38 the hindbrain, DA terminals form traditional synaptic contacts with auditory efferent neuronal cell b

39 The cellular and synaptic correlates of pheromonal learning, however, rem

40 , justifying the conductance-based nature of synaptic couplings.

41 he amplitude and duration of excitatory post synaptic currents near the action potential threshold.

42 hough field potentials (FPs) may reflect the synaptic currents of neurons near the recording electrod

43 cells in the guinea pig retina and monitored synaptic currents that were evoked by visual stimulation

44 By direct recording of synaptic currents, we also show that motoneurons are act

45 la neuromuscular junction indicate that many synaptic defects in unc-104-null mutants are mediated in

46 The trisomic Ts65Dn mouse model of DS shows synaptic deficits and reproduces the essential cognitive

47 h of modulating Abeta levels and attenuating synaptic deficits in AD.SIGNIFICANCE STATEMENT beta-Site

48 Synaptic depression attenuates the sensitivity to DCS fr

49 in vesicle clustering defects and increased synaptic depression.

50 Our results suggest that this aberrant synaptic development of auditory brainstem circuits migh

51 umulation of alpha-synuclein, and subsequent synaptic disruption, occur in absence of dopaminergic ne

52 n mouse olfactory bulb slices to measure the synaptic dynamics of afferent-evoked input at physiologi

53 ct of acute DCS (10-20 V m(-1) for 3-5 s) on synaptic dynamics with constant rate (5-40 Hz) and Poiss

54 ggest that impaired mitophagy contributes to synaptic dysfunction and cognitive deficits by triggerin

55 glutamate receptors, ultimately resulting in synaptic dysfunction and loss.

56 Together, these experiments define synaptic dysfunction at NMJs experiencing ALS-related de

57 Patients suffer from early synaptic dysfunction prior to Tau aggregate formation, b

58 ere is ample consensus that preventing early synaptic dysfunction would be an effective therapeutic s

59 o involve alterations of neural circuits via synaptic dysfunction, the underlying molecular mechanism

60 otal role in Abeta-induced mitochondrial and synaptic dysfunction.

61 idative stress, as well as mitochondrial and synaptic dysfunction.

62 events both Abeta binding and Abeta-mediated synaptic dysfunctions.

63 ce experiments, is consistent with increased synaptic efficacy caused by ATP.

64 This increase in synaptic efficacy correlates with reduced phosphorylatio

65 ultrastructural characteristics of enhanced synaptic efficacy that were coordinated with changes in

66 lts in long-term changes in cortico-striatal synaptic efficacy under the control of the amygdala.

67 mplitude, demonstrating that slow changes in synaptic efficacy, combined with sustained sensory input

68 ple mechanisms for homeostatic regulation of synaptic efficacy, including heterosynaptic plasticity,

69 equency and increased amplitude of GABAergic synaptic events.

70 We find that synaptic excitation and intrinsic excitability are coreg

71 -pain-related amygdala plasticity by driving synaptic excitation of CeA neurons.

72 Knockout of the OGT gene decreased the synaptic expression of the AMPA receptor GluA2 and GluA3

73 n of Panx1 in microglia abolished the spinal synaptic facilitation and ameliorated the sequelae of mo

74 revican simultaneously controls cellular and synaptic forms of plasticity in PV+ cells by regulating

75 ative phosphorylation can fuel low-frequency synaptic function and inhibiting both underlies loss of

76 propose that the overall lack of changes in synaptic function and plasticity in DBN deficient mice m

77 sk gene for major mood disorders involved in synaptic function and related intermediate phenotypes.

78 s complementarity extends to these proteins' synaptic function as well.

79 he presynaptic compartment but do not impair synaptic function in fly neurons.

80 Evidence from research on both autophagy and synaptic function suggests that there are links between

81 nt to many aspects of disrupted neuronal and synaptic function, increased permeability to inflammator

82 DR) proteins are causally linked to abnormal synaptic function, neuronal growth and survival are unkn

83 erentially impaired excitatory or inhibitory synaptic functions in an isoform-specific manner.

84 ling (e.g., GluA1, PRRT2) with no changes in synaptic GABAergic proteins.

85 The loss of synaptic GluA2 is caused by rapid trafficking of GluA2-c

86 How synaptic growth is terminated after reaching proper size

87 hat there are links between the two and that synaptic homeostasis during aging requires autophagy to

88 es dominated by associative plasticity or by synaptic homeostasis.

89 for example, variation in genes involved in synaptic homoeostasis are implicated in autism spectrum

90 eptor neurons) resistant to direct and trans-synaptic infection from the spinal cord with rabies viru

91 ion is required for preventing the spread of synaptic inhibition between adjacent EB lamina.

92 Multiple forms of synaptic inhibition compartmentalized the GAC dendritic

93 In contrast, synaptic inhibition is unaffected by changes in firing o

94 m by which GABABRs are able to modulate fast synaptic inhibition.

95 1D channels, which activate upon cholinergic synaptic input and amplify EPSPs, thus indicating a cons

96 show how, via this D2R-dependent phenomenon, synaptic input can enhance the excitability of prefronta

97 reactive puncta suggesting that they receive synaptic input from bipolar cells.

98 releasing peptide (Grp), that receive direct synaptic input from both pain and itch primary sensory n

99 expectedly long dendrites, which may receive synaptic input from the cerebral cortex and other brain

100 t the lateral habenula (LHb) receives direct synaptic input from the PFC and that activation of LHb n

101 tory synchrony is evident in the spontaneous synaptic input in mitral cells (MCs) separated up to 220

102 convergence of muscle and cutaneous afferent synaptic input onto individual projection neurons.

103 bility is presumed to arise from overlapping synaptic input, its precise relationship to local circui

104 als in a pacemaker pattern in the absence of synaptic input, the intrinsic properties that underlie t

105 ents (e.g., NMDAR-mediated Ca(2+) influx) by synaptic input.

106 ectivity both from excitatory and inhibitory synaptic inputs from other neurons and from their own in

107 el indicates that the spatial arrangement of synaptic inputs onto dendrites could play a significant

108 ion conductances, inhibitory and excitatory synaptic inputs that differ among this cell population.

109 ons by integrating excitatory and inhibitory synaptic inputs.

110 t sufficient to compensate for a decrease in synaptic integration of alpha1(Q177K)beta GlyRs.

111 Appropriate growth and synaptic integration of GABAergic inhibitory interneuron

112 r HCN channels, given their ability to alter synaptic integration, in the expression of forelimb move

113 gnition functions were examined by analyzing synaptic integrity and performing animal behavior on T1R

114 d neuron loss, elevated levels of markers of synaptic integrity that was linked to improved cognition

115 Collagen XIII was found to affect synaptic integrity through binding the ColQ tail of acet

116 lesterol to support neuronal homeostasis and synaptic integrity.

117 Trans-synaptic interactions between neurexins (Nrxs) and neuro

118 Surprisingly, the number of simultaneous synaptic joints decreases rapidly after saturation of th

119 By combining trans-synaptic labeling, ultrastructural analysis, calcium ima

120 6 to 9 when Muller arbors first colonize the synaptic layers beginning in stereotyped inner plexiform

121 Within only two synaptic layers, a large number of parallel information

122 pendent plasticity (ITDP) is a circuit-based synaptic learning rule by which paired activation of ent

123 e spacing effect is a phenomenon detected at synaptic level, which determines the specificity and the

124 stically, neuroligin deletions decreased the synaptic levels of neurotransmitter receptors and had no

125 Third, delta suppresses alpha6 synaptic localization by preventing assembly with GARLHs

126 einopathies, direct evidence for the precise synaptic localization has been difficult to achieve due

127 P) cleaving enzyme 1 (BACE1) trafficking and synaptic localization significantly influence its beta s

128 mpartments and colocalized with the putative synaptic markers in young neurons derived from human neu

129 eurons from human PSCs with a high degree of synaptic maturation.

130 ganglion cells (RGCs) process and integrate synaptic, mechanical, swelling stimuli with light inputs

131 nal amacrine cells in mouse retina forms the synaptic mechanism responsible for long-range coherent a

132 is process; however, the neural circuits and synaptic mechanisms by which distinct populations of RVM

133 Neuronal inhibition can occur via synaptic mechanisms or through tonic activation of extra

134 dopamine D4 receptor (hD4R) is maintained in synaptic membranes is not known.

135 As synaptic modifications by drugs of abuse are often tied

136 the dendritic trafficking itinerary for key synaptic molecules in rat cortical neurons.

137 gregates that are associated with changes in synaptic morphology.

138 truct PNS neurons and their hitherto unknown synaptic networks in the tadpole larva of a sibling chor

139 Deeper exploration of the brain's vast synaptic networks will require new tools for high-throug

140 key missing signaling effector in the common synaptic NMDA-R-CaMKII-SynGap-Ras-BRaf-MEK-ERK transduct

141 the extracellular microenvironment regulates synaptic NMDAR signaling.

142 creases muscle fiber size, enhances the post-synaptic NMJ area, reduces the abnormal accumulation of

143 ulation of Abeta at nerve terminals leads to synaptic pathology and ultimately to neurodegeneration.

144 actin clearance and recovery correlated with synaptic phosphatidylinositol 4,5-bisphosphate (PIP2) an

145 tructures, to quantitatively investigate the synaptic phosphorylated alpha-synuclein pathology in dem

146 Synaptic plasticity (e.g., long-term potentiation [LTP])

147 Spike timing-dependent synaptic plasticity (STDP) serves as a key cellular corr

148 ive morphological, electrophysiological, and synaptic plasticity alterations.

149 Synaptic plasticity and homeostatic regulation of synaps

150 n mGluR-LTD and is involved in many forms of synaptic plasticity and learning and memory.

151 ral window of CaMKII activation required for synaptic plasticity and learning.

152 Here, we analyzed events of structural synaptic plasticity at the single-synapse level after di

153 fy distinct expression patterns and roles in synaptic plasticity for AKT isoforms in the hippocampus.

154 y for improving manual skills is mediated by synaptic plasticity in a region of motor cortex that, be

155 d optogenetics to examine whether changes in synaptic plasticity in D1- versus D2-MSN GABAergic synap

156 ether, these data reveal that cocaine-evoked synaptic plasticity in PL-mPFC is reversible in vivo, an

157 ta indicate that neuron-derived E2 modulates synaptic plasticity in rodent BLA sex-dependently.

158 studies, we developed the working model that synaptic plasticity in the nucleus accumbens is central

159 lescent aged mice identifies a novel form of synaptic plasticity in VTA GABA cells, and the synaptic

160 udy identifies a novel form of glutamatergic synaptic plasticity in VTA GABA neurons, a currently und

161 ll activity.SIGNIFICANCE STATEMENT Long-term synaptic plasticity is a fundamental property of the bra

162 PP and that the Abeta-mediated impairment of synaptic plasticity is accompanied by presynaptic effect

163 sm in neurons and astrocytes, and ultimately synaptic plasticity loss evident by a decreased long-ter

164 l-specific alterations in CREB signaling and synaptic plasticity may underlie certain nicotine withdr

165 opriate spike patterns could drive long-term synaptic plasticity remained unknown.

166 w negative images are formed at the level of synaptic plasticity rules, cells, and circuits.

167 show that achieving cocaine use reversed the synaptic plasticity underpinning the motivation to seek

168 on of NF-kappaB signaling decreased cortical synaptic plasticity via HDAC2.

169 difying rules that govern activity-dependent synaptic plasticity, addictive drugs can derail the expe

170 ablishment of the body axis, cell migration, synaptic plasticity, and a vast range of other biologica

171 synthesis in mature axons may play a role in synaptic plasticity, axonal arborization, or functional

172 me serine racemase after CCI injury improved synaptic plasticity, brain oscillations, and learning be

173 AKT is indirectly implicated in synaptic plasticity, but its direct role has not been st

174 Although LTM is sustained by structural synaptic plasticity, how synapses integrate spaced stimu

175 ecp2-deficient neurons also lack homeostatic synaptic plasticity, likely due to reduced levels of EEA

176 orders including cognitive decline, impaired synaptic plasticity, reduced sociability, hyperactivity

177 in both neuronal excitability and short-term synaptic plasticity-parameters that critically govern ne

178 k parameters arising from learning-dependent synaptic plasticity.

179 cortical development or experience-dependent synaptic plasticity.

180 nsmission in humans that may favor increased synaptic plasticity.

181 ptor (D1R) expression, and ensures long-term synaptic plasticity.

182 cal regions, a function that requires marked synaptic plasticity.

183 nt and selective means to enhance memory and synaptic plasticity.

184 pine development and its modification during synaptic plasticity.

185 NMDA receptors and is involved in mediating synaptic plasticity.

186 specificity and the precision in structural synaptic plasticity.

187 HFD-induced metabolic changes and preserved synaptic plasticity.

188 ctions in NMDA receptor-mediated hippocampal synaptic plasticity.

189 release neuroactive molecules and influence synaptic plasticity.

190 neuronal excitability and altered short-term synaptic plasticity.SIGNIFICANCE STATEMENT Schizophrenia

191 cue-induced drug seeking requires transient synaptic potentiation (t-SP) of cortical glutamatergic s

192 ally is sufficient to recapitulate transient synaptic potentiation and reinstate cocaine seeking.

193 Hebbian plasticity to facilitate associative synaptic potentiation in prefrontal excitatory circuits.

194 T-type current blockade also prevented synaptic potentiation induced by postsynaptic action pot

195 ith AMPAR surface diffusion markedly impairs synaptic potentiation of Schaffer collaterals and commis

196 This cAMP-driven synaptic potentiation requires the activation of both pr

197 ivation engages several kinetically distinct synaptic processes that profoundly alter the discharge r

198 formation in CA1 pyramidal neurons but shape synaptic properties and that NL1 specifically is require

199 Importantly, changes in synaptic properties appear to be good predictors of vuln

200 Each layer develops unique synaptic properties but molecular mechanisms that mediat

201 ly auditory deprivation alters intrinsic and synaptic properties in the ACx.

202 nal simulations suggest that dendrodendritic synaptic properties prevent individual principal cells f

203 ing unique morphological, physiological, and synaptic properties.

204 (mTORC1), a signaling pathway that regulates synaptic protein synthesis.

205 Furthermore, stress-induced deficits in synaptic proteins and decreases in dendritic density and

206 We conclude that synaptic proteins have evolved to limit possible contact

207 ears earlier than the outer plexiform layer, synaptic proteins, and ribbons are first reliably recogn

208 We used iExM to visualize synaptic proteins, as well as the detailed architecture

209 tination-directed proteasomal degradation of synaptic proteins, presumably mediated by lysine 48 (K48

210 s indicate a role for complement proteins in synaptic pruning and neurodevelopment.

211 Significantly, similar to synaptic puncta, neuronal processes also exhibit medial-

212 We further show that this synaptic rearrangement requires the activity-dependent,

213 mmon vesicles onto spatially segregated post-synaptic receptors clusters, but a pre-synaptic segregat

214 there is no therapeutic strategy to promote synaptic recovery in the injured brain.

215 astrocytes and injured neurons that promotes synaptic recovery in the ischemic brain.SIGNIFICANCE STA

216 Taken together, synaptic recruitment of young neurons generates sparse a

217 ABSTRACT: Synaptic refinement and strengthening are activity-depen

218 equency Ca(2+) oscillations are required for synaptic refinement and the response to the muscle-deriv

219 view centers on the intrinsic properties and synaptic regulation that control the activity of dopamin

220 nervous system, signals pass across multiple synaptic relays on their way to a destination, but littl

221 ted with a decrease in temporal precision of synaptic release at the first central auditory synapse,

222 Activity-dependent synaptic remodeling occurs during early-use critical per

223 naptic plasticity in VTA GABA cells, and the synaptic remodeling that can occur after Delta(9)-tetrah

224 onse to protocols inducing LTP of inhibitory synaptic responses (iLTP).

225 g proteins and reduced complexity of the sub-synaptic reticulum, which could be rescued by pre- but n

226 sely associated with the release site at the synaptic ribbons.

227 Synaptic scaling is a key homeostatic plasticity mechani

228 Our results show that synaptic scaling sustains strength of the respiratory mo

229 KIV) is a key sensory/effector in excitatory synaptic scaling that senses perturbations in firing thr

230 post-synaptic receptors clusters, but a pre-synaptic segregation of cholinergic and glutamatergic re

231 release indeed does not produce a prolonged synaptic signal after a stimulus train and does not cont

232 ed extracellular Wg ligand and nuclear trans-synaptic signal transduction, as well as downstream misr

233 ion of scaffold proteins used for assembling synaptic signaling complexes.

234 Thus, neurexins nucleate an overall trans-synaptic signaling network that controls synapse propert

235 he ascr#3-sensing ADL neurons and their post-synaptic SMB motor neuron partners via increased express

236 Given that synaptic spines are dynamic structures which regulate ne

237 To identify molecular modulators of synaptic stability and degeneration, we have used the Cl

238 nstream signaling cascades that regulate the synaptic state.

239 on, but not AMPA receptor blockade, prevents synaptic stimulation from facilitating D2R-induced ADPs,

240 In this study, we investigated the effect of synaptic stimulation on Tau pathology and synapses in in

241 Changes in synaptic strength and connectivity are thought to be a m

242 ic factor (BDNF), a key player in regulating synaptic strength and learning, is dysregulated followin

243 Synaptic strength at excitatory synapses is determined b

244 el is associated with transient increases in synaptic strength at prefrontal cortex synapses in the n

245 udies have shown that PE enhances excitatory synaptic strength by facilitating an anti-Hebbian form o

246 As a result, synaptic strength exceeds acceptable levels and damages

247 ich could be mediated by enhanced excitatory synaptic strength in ventral tegmental area (VTA) dopami

248 and the maintenance of augmented excitatory synaptic strength in VTA DA neurons and increased addict

249 uronal processes is key to the alteration of synaptic strength necessary for long-term potentiation,

250 iated by activity-dependent modifications of synaptic strength within neuronal circuits.

251 r glutamate, AMPA receptors are critical for synaptic strength, and dysregulation of AMPA receptor-me

252 Thus, basal synaptic strength, short-term plasticity, and homeostasi

253 This protein loss also caused an increase in synaptic strength, suggesting that spontaneous neurotran

254 y as a novel therapeutic strategy to restore synaptic strength.

255 lization of rewarded STDP and hard limits on synaptic strength.

256 circuits are further modified by excitatory synaptic strengthening as well as a transient surge in f

257 ver, Neto2 Ser-409 phosphorylation inhibited synaptic targeting of GluK1 because, unlike WT Neto2 and

258 eptors and the connections of their specific synaptic targets.

259 t roles in the outer segment, cell body, and synaptic terminal of photoreceptors.

260 rate of exocytosis from a subset of cortical synaptic terminals within the EC and in this way, constr

261 protective effects against mitochondrial and synaptic toxicities in APP transgenic mice.

262 Consistent with the role of synaptic trafficking of AMPA-type of glutamate receptors

263 ovel framework of analysis and comparison of synaptic transmission alterations in neurodegenerative d

264 onset) does not require the participation of synaptic transmission and is mediated by diffusion of po

265 cking is a critical regulatory mechanism for synaptic transmission and neural function.

266 tance of kinesin-3 based axonal transport in synaptic transmission and provide novel insights into th

267 Thus, synaptic transmission and the expression of LTP are depe

268 (AMPARs) mediate the majority of excitatory synaptic transmission and their function impacts learnin

269 KEY POINTS: Synaptic transmission at the endbulb of Held was assesse

270 e also show that MYO acts in vivo to inhibit synaptic transmission between neurons in the escape resp

271 opic neurotransmitter receptors mediate fast synaptic transmission by functioning as ligand-gated ion

272 Synaptic transmission controls brain activity and behavi

273 Reduced synaptic transmission correlates with increased levels o

274 we report the finding of activity-invariant synaptic transmission delays as a functional adaptation

275 In contrast, synaptic transmission delays in mice varied depending on

276 ogy was employed to measure excitability and synaptic transmission in DMS and midbrain neurons.

277 dent effects of corticosterone on inhibitory synaptic transmission in the rat PL were determined usin

278 (LTP) is a rapid and persistent increase in synaptic transmission that is thought to be affected in

279 nction and inhibiting both underlies loss of synaptic transmission via massive vesicle release and su

280 Anaesthetic molecules act on synaptic transmission via the allosteric modulation of l

281 To enhance synaptic transmission, mice inhaled CO2 to induce an aci

282 in homeostatic downscaling of glutamatergic synaptic transmission.

283 netic elimination causes a complete block of synaptic transmission.

284 S to date, associated with genes involved in synaptic transmission.

285 o short- and long-term changes in excitatory synaptic transmission.

286 Ch release by inhibiting the function of pre-synaptic UNC-2/CaV2 calcium channels.

287 We show that cell depolarization increases synaptic vesicle dopamine content prior to release via v

288 a major presynaptic phosphatase that couples synaptic vesicle endocytosis to the dephosphorylation of

289 of the SNARE four-helix bundle that mediates synaptic vesicle fusion and used it to study vesicle fus

290 tagmin that promote Ca(2+) activation of the synaptic vesicle fusion machinery.

291 pecific scaling of several components of the synaptic vesicle machinery, including the vesicular glut

292 We also found that synaptic vesicle pool recovery from depletion was sensit

293 it adds the neuronal Munc13 proteins and the synaptic vesicle priming process that they control to th

294 bility that Syt1 rings could pre-form on the synaptic vesicle to facilitate docking.

295 They mediate the priming step that renders synaptic vesicles fusion-competent, and their genetic el

296 cellular Ca(2+) and diminution of releasable synaptic vesicles.

297 duced striatal synaptosomal mitochondria and synaptic vesicular proton pump protein (V-ATPase H) leve

298 fferent layers of the network can coordinate synaptic weight updates.

299 l system of Drosophila larvae by mapping the synaptic wiring diagram and neurotransmitters.

300 The complete synaptic wiring diagram of the LON paves the way to unde