ライフサイエンスコーパス: mitral cell

1 for by passive electrical properties of the mitral cell.

2 orm synapses with principal neurons known as mitral cells.

3 zed glomeruli and a significant reduction in mitral cells.

4 3-Na(+)K(+)-ATPase was strongly expressed in mitral cells.

5 cerebellar Purkinje cells and olfactory bulb mitral cells.

6 ssed with whole-cell recording from pairs of mitral cells.

7 factory cortices in part by the birthdate of mitral cells.

8 gmine (20 mM) sharpened the ORF responses of mitral cells.

9 e how the cortex integrates inputs from bulb mitral cells.

10 nsmission between olfactory bulb granule and mitral cells.

11 r (GL) excision failed to increase mIPSCs in mitral cells.

12 s exert strong tonic GABAergic inhibition of mitral cells.

13 s and thereby modulate inhibitory drive onto mitral cells.

14 e absence of the detyrosinylated form in the mitral cells.

15 ses and gate dendrodendritic inhibition onto mitral cells.

16 scillations in populations of olfactory bulb mitral cells.

17 mediated synaptic inputs derived from output mitral cells.

18 resulting in phase-locked GABA release onto mitral cells.

19 nnervation pattern suggested for all teleost mitral cells.

20 evoke robust responses in a small subset of mitral cells.

21 uli despite relatively maintained input from mitral cells.

22 cells, reflecting the prolonged response in mitral cells.

23 ced responses in the gamma-glomerulus and in mitral cells.

24 layer 5 pyramidal neurons and olfactory bulb mitral cells.

25 ate and promotes spike timing variability in mitral cells.

26 strated a greater propensity to stutter than mitral cells.

27 olarization and afterhyperpolarizations than mitral cells.

28 s odor information relayed by olfactory bulb mitral cells.

29 ved stronger afferent-evoked excitation than mitral cells.

30 te the timing, rather than the existence, of mitral cell action potentials and perform their computat

31 ary granule cell EPSPs evoked in response to mitral cell action potentials in rat (both sexes) brain

32 fting the balance of principal tufted versus mitral cell activity across large expanses of the MOB in

33 onic dose-response relationship, suppressing mitral cell activity at high and low, but not intermedia

34 Most of our knowledge about mitral cell activity has been obtained from recordings i

35 f lateral inhibition causes decorrelation of mitral cell activity that is evoked by similar stimuli,

36 al cells) that could be capable of modifying mitral cell activity through the release of GLP-1.

37 milar inputs, while improving propagation of mitral cell activity to cortex.

38 generation of reliable temporal patterns of mitral cell activity.

39 Specifically, we measured how mitral cells adapt to continuous background odors and ho

40 tion potential ("spike") firing, wherein all mitral cells affiliated with a glomerulus either engaged

41 the degree of overlap in ORFs of individual mitral cells after exposure to odorant stimuli.

42 dly synchronized spikes (lag < or = 5 ms) in mitral cells, along with oscillatory activity at the gam

43 We suggest that persistent responses in mitral cells amplify the incoming sensory information an

44 t antennal lobe projection neurons (PNs)-the mitral cell analogs.

45 rth, slowed the morphological development of mitral cells and arrested the maturational changes in me

46 ot nonrewarded, odor representations in both mitral cells and associated granule cells of the olfacto

47 ther, distinct temporal response profiles in mitral cells and external tufted cells could be attribut

48 Evoked and spontaneous slow oscillations in mitral cells and external tufted cells were broader and

49 In the forebrain, Neurog1 lineages include mitral cells and glutamatergic interneurons in the olfac

50 ectivity at dendrodendritic synapses between mitral cells and interneurons.

51 ized odor-evoked responses of olfactory bulb mitral cells and interneurons.

52 increased the activity-dependent labeling of mitral cells and juxtaglomerular cells but not of tyrosi

53 al airflow, lateral inhibition was weaker in mitral cells and less modulated in tufted cells.

54 C) receives direct input from olfactory bulb mitral cells and piriform cortical pyramidal cells and i

55 ensures fast, reliable communication between mitral cells and their homotypic glomeruli, binding them

56 merulus only, mechanosensitive modulation of mitral cells and their postsynaptic neuropils was found

57 channel, which is predominantly expressed in mitral cells and whose gene-targeted deletion causes a "

58 lfactory bulbs, in dot-like terminals around mitral cells, and in the fibers of the medial olfactory

59 at out of the hundreds of compounds present, mitral cells are activated by single compounds.

60 merulus depends on chemical transmission but mitral cells are also electrically coupled.

61 implications of these putative subclasses of mitral cells are discussed.

62 Mitral cells are major projection neurons of the olfacto

63 tory bulb, odor representations by principal mitral cells are modulated by local inhibitory circuits.

64 Here, we show that assemblies of AOB mitral cells are synchronized by lateral interactions th

65 aracter of their synapses with the principal mitral cells--are sufficient to restructure the network

66 that are 4x larger and contain twice as many mitral cells as those of the sympatric black vulture (Co

67 les showed that excitatory synaptic input to mitral cells as well as dendrodendritic inhibition was u

68 ributed to slow dendrodendritic responses in mitral cells, as blocking this slow current in mitral ce

69 main form of lateral transmission within the mitral cell assembly.

70 Cav3.x-mediated Ca(2+) influx from even one mitral cell at membrane potentials between -65 and -50 m

71 While mitral cells at rest were also excited by raphe activati

72 The physiological mechanism underlying mitral cell autorhythmicity involves cyclic activation o

73 et of CR neurons, the loss of which prevents mitral cell axon innervation and LOT formation.

74 Specifically, mitral cell axons form the lateral olfactory tract (LOT)

75 Electrical stimulation of mitral cell axons in the lateral olfactory tract (LOT) r

76 Aergic interneurons were directly excited by mitral cell axons.

77 e found that early- and late-generated mouse mitral cells became differentially distributed in the do

78 otential and current (Ih) is stereotypic for mitral cells belonging to the same glomerular circuit.

79 ngle units recorded extracellularly from the mitral cell body layer were further identified as mitral

80 evoked fast GABAergic inhibitory currents in mitral cells but failed to activate D(2) receptor-mediat

81 or responsiveness and pairwise similarity of mitral cells but had little impact on tufted cells.

82 Additionally, GL excision reduced sIPSCs in mitral cells by 50%, suggesting that periglomerular cell

83 l cell body layer were further identified as mitral cells by antidromic activation of the lateral olf

84 ry bulb slices elicited the GABAergic LTP in mitral cells by enhancing postsynaptic GABA receptor res

85 the activation of a cohort of narrowly tuned mitral cells by odor mixtures is read out synaptically b

86 tivation within glomerular circuits sharpens mitral cell chemoreceptive fields, even in the absence o

87 nic cholinergic receptor activation sharpens mitral cell chemoreceptive fields, likely via intraglome

88 Some mitral cells closely followed the response time course o

89 e both combinatorially and temporally sparse mitral cell codes.

90 Since mitral cells commonly respond to odours by burst firing

91 re, we find that longer-latency responses in mitral cells, compared with tufted cells, are due to wea

92 olfactory processing that is dependent upon mitral cell convergence and integration onto cortical ce

93 tral cells, as blocking this slow current in mitral cells converted mitral cell responses to a transi

94 e role of connexin-mediated gap junctions in mitral cell coordinated activity.

95 activity showed that at least two classes of mitral cells could be distinguished.

96 e combination of large olfactory bulbs, high mitral cell counts and a greatly enlarged nasal cavity l

97 excitability and synaptic integration in AOB mitral cell dendrites, and we show that dendrites of acc

98 s, which measure electrical coupling between mitral cell dendrites, were high in young mice, but decr

99 ested homotypic connectivity with individual mitral cell dendritic arbors projecting only to glomerul

100 We found overlapping clusters of CTB-labeled mitral cell dendritic branches (CTB(+) ) in TRPM5-GFP(+)

101 Finally, we show that mitral cell dendritic refinement occurs just after the c

102 cate that the monosynaptic afferent input to mitral cells depends on the strength of odorant stimulat

103 evidence for excitatory interactions between mitral cells despite the lack of direct synaptic connect

104 We conclude that mitral cells do not have center-surround receptive field

105 citatory postsynaptic current (EPSC) between mitral cells emerged by P30.

106 etween two dissimilar odorants, responses of mitral cell ensembles to the two odorants gradually beca

107 Trains of action potentials in one mitral cell evoked autoexcitation in the stimulated cell

108 cose concentrations showed glucose-dependent mitral cell excitability as evaluated by current-clamp e

109 buted to lateral excitation during concerted mitral cell excitation or by single-cell activity if glu

110 es emerge as a result of the balance between mitral cells' excitatory inputs and inhibition provided

111 It has been proposed that olfactory bulb mitral cells exhibit this functional circuitry, with exc

112 Mitral cells exhibited a more sharply tuned molecular re

113 The mitral cells exhibited two main types of morphologies wi

114 Mitral cells express low-voltage activated Cav3.3 channe

115 degree of colocalization, some amygdalopetal mitral cells extended dendrites to non-TRPM5-GFP glomeru

116 In addition, the late-generated mitral cells extended substantially stronger projections

117 In the olfactory bulb, individual mitral cells fired action potentials in response to ligh

118 We show that odor-elicited changes in mitral cell firing rate were larger and more frequently

119 er, increases UP state amplitude and impacts mitral cell firing rate.

120 within the EPL, but it has little effect on mitral cell firing rates and hence does not sharpen olfa

121 Careful alignment of mitral cell firing with the phase of the respiration cyc

122 ling to investigate signal processing in the mitral cells, focusing on the glomerular dendritic tuft.

123 re represented by a combination of activated mitral cells, forming reproducible activation maps in th

124 Potassium currents in olfactory bulb mitral cells from Kv1.3 null mice have slow inactivation

125 analysis of glomeruli confirmed that mitral-mitral cell gap junctions on distal apical dendrites con

126 t in connexin36(-/-) mice, which lack mitral-mitral cell gap junctions.

127 e nervus terminalis ganglion innervating the mitral cell/glomerular layer (MC/GL).

128 Compared to external tufted cells, mitral cells have a prolonged afferent-evoked EPSC, whic

129 ared odor-elicited changes in firing rate of mitral cells in awake behaving mice and in anesthetized

130 tatory interactions in a glomerulus, whereas mitral cells in different networks engage in long-lastin

131 The second order neurons, mitral cells in mammals and projection neurons in insect

132 urons) include Purkinje cells in cerebellum, mitral cells in olfactory bulb, and photoreceptors in re

133 ability and rates and shorter latencies than mitral cells in response to physiological afferent stimu

134 Recordings from mitral cells in the absence of both subunits reveal a re

135 influenced the input-output relationship of mitral cells in the AOB and MOB differently showing a ne

136 in rodents have established that a subset of mitral cells in the main olfactory bulb (MOB) projects d

137 l odorants activate only a small fraction of mitral cells in the mouse main olfactory bulb (MOB).

138 We recorded from individual mitral cells in the OB in anesthetized rats to determine

139 rebral cortex including pyramidal cells, and mitral cells in the olfactory bulb and is not expressed

140 ating that the readout of olfactory input by mitral cells in the olfactory bulb can be modified by be

141 racterize the morphology and distribution of mitral cells in the olfactory bulb of adult zebrafish, D

142 As a consequence of these changes, across mitral cells in the olfactory bulb, individual odors sho

143 t of dendrodendritic synapses of granule and mitral cells in the olfactory bulb.

144 Spiking responses of mitral cells in the rat olfactory bulb adapt to, and rec

145 e synchronous oscillations in olfactory bulb mitral cells in vitro.

146 Our findings suggest that mitral cells in zebrafish may be more similar to mammali

147 on between olfactory bulb principal neurons (mitral cells) in vitro.

148 ocal connections with the majority of nearby mitral cells, in contrast to the sparse connectivity bet

149 b, gap junctions between apical dendrites of mitral cells increase excitability and synchronize firin

150 sic biophysical properties of olfactory bulb mitral cells influences population coding of fluctuating

151 cell excitatory postsynaptic potentials and mitral cell inhibition were also potentiated by theta-bu

152 y in the gamma-glomerulus is conveyed to the mitral cells innervating this specific neuropil.

153 at PCs respond faithfully and selectively to mitral cell inputs arriving as a synchronized gamma freq

154 ally integrate several functionally distinct mitral cell inputs.

155 The direct inhibitory synaptic input engages mitral cell intrinsic membrane properties to generate in

156 The mitral cell is the primary output neuron and central rel

157 embrane potential recorded in olfactory bulb mitral cells is an emergent, homotypic property of local

158 ound that the lateral inhibition received by mitral cells is gated by postsynaptic firing, such that

159 SE, the efficacy of glutamatergic LE between mitral cells is highly variable and mediated by calcium-

160 it has been suggested that sensory input to mitral cells is indirect through feedforward excitation

161 or brain size among birds, but the number of mitral cells is proportional to the size of their olfact

162 trong stimuli evoked sustained firing in AOB mitral cells lasting up to several minutes.

163 eration of 5T4-positive granule cells in the mitral cell layer does not change significantly over tim

164 mRNA and immunoreactivity were found in the mitral cell layer of the olfactory bulb, the Purkinje ce

165 s study shows that the majority of zebrafish mitral cells likely innervate a single glomerulus rather

166 to many glomeruli, and second-order neurons (mitral cells) link to multiple glomeruli via branched pr

167 ctory bulb and its neuromodulatory effect on mitral cell (MC) first-order neurons.

168 tions in a cell-type-specific manner between mitral cells (MCs) and GCs or between MCs and EPL intern

169 ivity, population-level interactions between mitral cells (MCs) and granule cells (GCs) can generate

170 ence-dependent plasticity between excitatory mitral cells (MCs) and inhibitory internal granule cells

171 nd inhibition at reciprocal synapses between mitral cells (MCs) and local interneurons.

172 e mapped the functional connectivity between mitral cells (MCs) and OB interneurons in a cell-type-sp

173 Responses of olfactory (OB) bulb mitral cells (MCs) and tufted cells (TCs) are known to d

174 In the mouse olfactory system, mitral cells (MCs) and tufted cells (TCs) comprise paral

175 ibition between pairs of olfactory bulb (OB) mitral cells (MCs) and tufted cells (TCs) is linked to a

176 classes of the mammalian olfactory bulb, the mitral cells (MCs) and tufted cells (TCs), differ marked

177 illatory synchrony in the activity of output mitral cells (MCs) appears to result from interactions w

178 uppress stimulus-evoked excitation of output mitral cells (MCs) at another glomerulus for interstimul

179 e (NA) increases GABA inhibitory input on to mitral cells (MCs) by exciting GCs.

180 ABSTRACT: Mitral cells (MCs) contained in the main (MOB) and acces

181 onergic afferents are largely excitatory for mitral cells (MCs) in the MOB where 5-HT2A receptors med

182 Synchronized firing of mitral cells (MCs) in the olfactory bulb (OB) has been h

183 e tested how background odors are encoded by mitral cells (MCs) in the olfactory bulb (OB) of male mi

184 ormation flow from the periphery onto output mitral cells (MCs) of the olfactory bulb (OB) has been t

185 evident in the spontaneous synaptic input in mitral cells (MCs) separated up to 220 mum (300 mum with

186 DA directly hyperpolarized mitral cells (MCs) via D(2)-like receptors and slightly

187 n of subthreshold oscillations (STOs) in the mitral cells (MCs) with inhibitory granule cells (GCs).

188 ectedly, AON axons also directly depolarized mitral cells (MCs), enough to elicit spikes reliably in

189 principal neurons of the olfactory bulb, the mitral cells (MCs), sparing the other principal neurons,

190 tors (nAChRs) in regulating the responses of mitral cells (MCs), the output neurons of the olfactory

191 Here we report that Nrp2-positive (Nrp2(+)) mitral cells (MCs, second-order neurons) play crucial ro

192 membrane excitability of projection neurons (mitral cells, MCs) that dramatically curtailed their res

193 lateral excitation (LE) provides a means of mitral cell-mitral cell communication.

194 anges last many minutes we suggest that such mitral cell-mitral cell interactions provide the glomeru

195 een fluorescent protein, we recorded from P2 mitral cells (MT cells) while selectively stimulating P2

196 flects differential expression between local mitral cell networks processing distinct odour-related i

197 ve been hypothesized to represent tufted and mitral cell networks, respectively.

198 ponses in a linear fashion while maintaining mitral cell odor preferences.

199 ur results demonstrate the dynamic nature of mitral cell odor representations in awake animals, which

200 adual and long-lasting (months) weakening of mitral cell odor representations.

201 inhibitory granule cells and makes principal mitral cell odor responses more sparse and temporally dy

202 This enabled mitral cell odor-evoked ensemble activity to be analyzed

203 f awake, head-fixed mice and found that some mitral cells' odor representations changed following the

204 particular has been hypothesized to regulate mitral cell odorants receptive fields (ORFs) and behavio

205 Here, we show that mitral cells of the accessory olfactory bulb release glu

206 differently showing a net effect on gain in mitral cells of the MOB, but not in the AOB.

207 synchronous infra-slow bursting activity in mitral cells of the mouse accessory olfactory bulb (AOB)

208 he outputs from a single type of neuron, the mitral cells of the mouse olfactory bulb, to identical s

209 ium spiny neurons of the striatum and tufted-mitral cells of the olfactory bulb, has gone unnoticed a

210 ulation can be observed in the glomeruli and mitral cells of the olfactory bulb, using calcium imagin

211 sory neurons of the olfactory epithelium and mitral cells of the olfactory bulb.

212 0, the Ca(2+) sensor for IGF1 secretion from mitral cells, or deletion of IGF1 receptor in the olfact

213 ate that Cx36-mediated gap junctions between mitral cells orchestrate rapid coordinated signaling via

214 ated in a manner predicted by the changes in mitral cell ORFs by cholinergic drugs.

215 , we observed that the membrane potential of mitral cells oscillates between UP and DOWN states at a

216 used simultaneous whole-cell recordings from mitral cell pairs to show that a direct form of chemical

217 Coupled AMPA responses between mitral cell pairs were absent in the knockout, demonstra

218 Instead, each mitral cell performs a specific computation combining a

219 This mitral cell plasticity is odor specific, recovers gradua

220 m synapses onto distal tuft-like branches of mitral cell primary dendrites.

221 tic depression, dendrodendritic circuitry in mitral cells produces robust amplification of brief affe

222 In the olfactory bulb, principal neurons (mitral cells) project apical dendrites to a common glome

223 upling as well as correlated spiking between mitral cells projecting to the same glomerulus was entir

224 eral excitation in paired recordings between mitral cells projecting to the same glomerulus.

225 synchronized by their excitatory inputs from mitral cells, providing a means to coordinate GABA relea

226 glomerular stimulation, we demonstrate that mitral cells receive direct, monosynaptic input from olf

227 ering an individual glomerulus revealed that mitral cells receive monosynaptic afferent inputs.

228 nce, the AOB network topology, in which each mitral cell receives input from multiple glomeruli, enab

229 mpared the electrophysiological responses of mitral cells recorded from the accessory olfactory bulb

230 hat the synaptic charge was 5-fold larger in mitral cells, reflecting the prolonged response in mitra

231 While it is known that mitral cells release vesicular glutamate from their apic

232 We conclude that mitral cells represent natural odorant stimuli by acting

233 Responses of mitral cells represent the results of the first stage of

234 cortical neurons receive input from multiple mitral cells representing broadly distributed glomeruli.

235 ritic circuitry in external tufted cells and mitral cells, respectively, tunes the postsynaptic respo

236 Moreover, olfactory bulb output mitral cells respond to a single stimulation of the sens

237 One cohort of mitral cells responded exclusively to male urine; these

238 Mitral cells responded to high frequency ORN stimulation

239 In cell-attached recordings, mitral cells responded to high frequency stimulation wit

240 A quantitative model indicates that mitral cell responses can be explained by just a handful

241 ore, selective PV cell inactivation enhances mitral cell responses in a linear fashion while maintain

242 gly, calcium imaging experiments reveal that mitral cell responses in M71 transgenic mice are largely

243 this slow current in mitral cells converted mitral cell responses to a transient response profile, t

244 ls of the bulb by specifically decorrelating mitral cell responses to enable odor separation.

245 merular inhibition could suppress excitatory mitral cell responses to odorants.

246 and mGluR1 receptor antagonists, converting mitral cell responses to transient response profiles.

247 may be important for the specificity of AOB mitral cell responses.

248 The sustained response in mitral cells resulted from dendrodendritic amplification

249 st, muscarinic receptor activation increases mitral cell spike synchronization and field oscillatory

250 ulb inhibition on the pairwise statistics of mitral cell spiking.

251 er responsiveness of AON neurons relative to mitral cells suggests that individual AON neurons synapt

252 Although the dendritic connectivity of AOB mitral cells suggests the capacity for broad integration

253 w that dendrites of accessory olfactory bulb mitral cells support action potential propagation and ca

254 ed with dendritic sectioning, indicated that mitral cell synchrony was mainly driven by inhibitory po

255 n zebrafish may be more similar to mammalian mitral cells than previously believed, despite variation

256 and in vivo, we identify a subpopulation of mitral cells that exhibit slow stereotypical rhythmic di

257 In the olfactory bulb the sets of mitral cells that project their apical dendrite to the s

258 s in the mammalian main olfactory bulb where mitral cells that project to the same glomerular unit di

259 sing OSNs is innervated by the population of mitral cells that projects to the MeA.

260 Only 27% of mitral cells that showed a response to odors in the anes

261 1 increases the firing frequency of neurons (mitral cells) that encode olfactory information by decre

262 e investigated the functional structure of a mitral cell, the principal output neuron in the rat olfa

263 l activity in mouse accessory olfactory bulb mitral cells, the direct neural link between vomeronasal

264 One view suggests that mitral cells, the primary output neuron of the olfactory

265 Mitral cells, the principal cells of the accessory olfac

266 The input-output transform performed by mitral cells, the principal projection neurons of the ol

267 Electrophysiological recordings showed that mitral cells, the target cells of newly generated intern

268 me that some rodent accessory olfactory bulb mitral cells-the direct link between vomeronasal sensory

269 iated in three different compartments of the mitral cell: the soma-axon region, the primary dendrite

270 ulate the activity of principal neurons, the mitral cells, through dendrodendritic synapses, shaping

271 and compare responses of AON neurons and MOB mitral cells to a panel of structurally diverse odorants

272 ential away from spike threshold could adapt mitral cells to background input without compromising th

273 The response of MOB mitral cells to brief (0.1 ms, 1-100 V) stimulation of t

274 imals have found that sustained responses of mitral cells to odorants are rare, suggesting sparse com

275 observed short-term plasticity could enable mitral cells to overcome autoinhibition and increase act

276 electrophysiological responses of individual mitral cells to volatile compounds in mouse urine.

277 Compared to mitral cells, tufted cells exhibited twofold greater exc

278 assess the degree of shared activity between mitral cells under physiological conditions, we analysed

279 The stimulation of mitral cells using a pattern that mimics activity of the

280 ally induce aftereffects, we photostimulated mitral cells using channelrhodopsin and recorded central

281 ask how effectively different populations of mitral cells, varying in their diversity, encode a commo

282 Moreover, the synchronized activity of mitral cells was decreased in the OB of adult TNR knock-

283 ed to phosphorylation, glucose modulation of mitral cells was rapid, less than one minute, and was re

284 The spontaneous activity of mitral cells was recorded in vivo from the main olfactor

285 However, correlated spiking in mitral cells was significantly reduced, as was electrica

286 , recurrent inhibition of principal neurons (mitral cells) was completely eliminated by the mGluR1 an

287 sponsiveness of AON neurons, the majority of mitral cells were activated by only one or two component

288 gly, a substantial number of thermosensitive mitral cells were also chemosensitive.

289 Functionally, odor-evoked responses of mitral cells, which are normally inhibited by abGCs, wer

290 size of their olfactory bulbs and numbers of mitral cells, which provide the primary output of the ol

291 ansient activity in the larger population of mitral cells, which respond to odorants during a small f

292 sulted from dendrodendritic amplification in mitral cells, which was blocked by NMDA and mGluR1 recep

293 slow intracellular Na(+) dynamics endow AOB mitral cells with a weak tendency to burst, which is fur

294 We also observed feedforward excitation of mitral cells with weak stimulation of the olfactory nerv

295 Mitral cells within a glomerulus show highly synchronize

296 Mitral cells within a single odorant receptor-specific n

297 , whose axons contact the dendritic tufts of mitral cells within olfactory bulb glomeruli.

298 trocytes within the OB express NFIA, whereas mitral cells within the OB express NFIB.

299 Assuming a broad inhibitory field, a mitral cell would be influenced by >100 contiguous glome

300 ases GABAergic spontaneous IPSCs (sIPSCs) in mitral cells, yet the presynaptic mechanism(s) involved