ライフサイエンスコーパス: calbindin

1 acidic protein, doublecortin, calretinin and calbindin).

2 y proteins that bind calcium in the cytosol (calbindin).

3 arly in neurogenesis (serotonin, calretinin, calbindin).

4 factor 6 (ATF6) or activated caspase 12 and calbindin.

5 er levels of calretinin and higher levels of calbindin.

6 nolabeling with tyrosine hydroxylase (TH) or calbindin.

7 lls positive for the calcium-binding protein calbindin.

8 ar dye injection or with an antibody against calbindin.

9 hese co-express the calcium-binding protein, calbindin.

10 changes resulted in increased expression of calbindin 1 in CD (260%; P<0.05).

11 ated upstream of the RE1 binding site in the calbindin 1 promoter, and 1 CpG site within the calbindi

12 time course of changes in PC physiology with calbindin-28 K changes showing the first small, but sign

13 cause of fructose-mediated downregulation of calbindin 9k.

14 ll loss that was confirmed with staining for calbindin, a calcium binding protein enriched in Purkinj

15 tetraploid neurons in this structure express calbindin, a marker of neostriatal-matrix spiny neurons,

16 ote GABAergic AC differentiation and repress calbindin(+) ACs, whereas its dominant-negative form has

17 eurons as well as a simultaneous increase of calbindin(+) ACs.

18 be converted into a calcium-sensing switch (calbindin-AFF) by duplicating the C-terminal half of the

19 An interneuron marker calbindin and a mitosis marker p-H3 showed down-regulati

20 preferentially the neurochemical classes of calbindin and calretinin neurons in the upper layers of

21 bulin and two populations were identified by calbindin and calretinin staining.

22 stry for the Ca(2+)-binding proteins (CaBPs) calbindin and calretinin to investigate the primary gust

23 Although varied amounts of calbindin and calretinin were found within each tonotopi

24 tors, gephyrin; the calcium binding proteins calbindin and calretinin; the NR1 subunit of the N-methy

25 Inactivation resulted in a distribution of calbindin and ChAT in spinal gray matter regions where t

26 Using two markers for Renshaw cells (calbindin and cholinergic nicotinic receptor subunit alp

27 oup of GABAergic interneurons that coexpress calbindin and in half of the cases parvalbumin.

28 en examined the co-localization of pERK with Calbindin and Lmx1b, which are expressed by excitatory n

29 Combined calbindin and mitochondrial marker immunofluorescence sh

30 The calbindin and nNOS immunostained neurons were the most c

31 aradigms and processed for immunostaining of calbindin and reelin.

32 Although calbindin and S100B have a low sequence homology, they s

33 to dentate gyrus granule cells, coexpressed calbindin and the homeobox protein Prox1.

34 r, area 32 terminals targeted preferentially calbindin and, to a lesser extent, calretinin neurons, w

35 Approximately 40% express calbindin and/or parvalbumin, while few express calretin

36 Calbindin D28k (calbindin) and S100B enhance IMPase-1 activity.

37 Interestingly, calbindin+ and calretinin (CalR)+ periglomerular neurons

38 We show that calretinin+, calbindin+, and dopaminergic (TH+) periglomerular OB int

39 other interneurons (expressing parvalbumin, calbindin, and calretinin) we studied.

40 rious calcium-binding proteins (parvalbumin, calbindin, and calretinin) within the PPC.

41 of the calcium-binding proteins parvalbumin, calbindin, and calretinin--using dual-immunofluorescence

42 ng the calcium-binding proteins parvalbumin, calbindin, and calretinin.

43 of neurons with CaBPs, including calretinin, calbindin, and parvalbumin, and to compare this distribu

44 and contacts between relaxin-3 terminals and calbindin- and calretinin-positive neurons.

45 e hamster SCNce, numerous cells contain both calbindin- and NeuN-IR.

46 Numbers of tyrosine hydroxylase-, calbindin-, and calretinin-expressing interneurons were

47 Double labeling with SNAP25 and calbindin antibodies demonstrated that horizontal cell p

48 ium-binding proteins such as parvalbumin and calbindin are molecular markers for interneuron subtypes

49 r GABA transporter, and parvalbumin, but not calbindin, are colocalized with the presynaptic varicosi

50 ation of the neuronal markers calretinin and calbindin, as assessed by real-time PCR and immunofluore

51 he vast majority of cells within DLM express calbindin, based both on immunocytochemistry (ICC) for c

52 many of the nerve cell bodies surrounded by calbindin baskets belong to motor neurons and ascending

53 sed on immunoreactivity and association with calbindin baskets, a finding that may have significant f

54 c oxide synthase and their relationship with calbindin baskets.

55 al interneurons and a selective reduction of calbindin-, but not parvalbumin- or calretinin-expressin

56 We propose that chronic suppression of calbindin by DeltaFosB is one mechanism through which in

57 were obtained with immunohistochemistry for calbindin (CALB), parvalbumin (PARV), glutamic acid deca

58 ropeptide Y (NPY)-, somatostatin (Som)-, and calbindin (Calb)-immunoreactive interneurons express col

59 )1 subtypes and the calcium-binding proteins calbindin, calmodulin and calreticulin in areas vulnerab

60 so show the focal and indiscriminate loss of calbindin(+), calretinin(+), parvalbumin/system A transp

61 focused on neurons with immunoreactivity for calbindin, calretinin and nitric oxide synthase and thei

62 nst Go-alpha, protein kinase C, parvalbumin, calbindin, calretinin, and choline acetyltransferase wer

63 ypes we used antibodies against parvalbumin, calbindin, calretinin, and neural nitric oxide synthase

64 emistry of choline acetyltransferase (ChAT), calbindin, calretinin, and parvalbumin to mark interneur

65 -expressed with the calcium-binding proteins calbindin, calretinin, and parvalbumin.

66 se-3 as well as the calcium binding proteins calbindin, calretinin, and parvalbumin.

67 an the Ca(2+)-binding proteins (parvalbumin, calbindin, calretinin, and secretagogin) studied to date

68 c oxide synthase, choline acetyltransferase, calbindin, calretinin, and serotonin, aiming to accurate

69 sine hydroxylase, choline acetyltransferase, calbindin, calretinin, and serotonin, to establish accur

70 ium-binding proteins, including parvalbumin, calbindin, calretinin, and the calcium-sensitive enzyme

71 type molecular markers, such as parvalbumin, calbindin, calretinin, N-terminal EF-hand calcium-bindin

72 and coronal sections were immunolabeled for calbindin, calretinin, NeuN, and reelin.

73 ene c-fos in neurons containing parvalbumin, calbindin, calretinin, or calcium/calmodulin-dependent k

74 Using antibodies to calbindin, calretinin, parvalbumin, and nitric oxide syn

75 iform cortex) have cells that express either calbindin, calretinin, parvalbumin, somatostatin, vasoac

76 mportant subtype of interneurons, expressing calbindin (CB(+) ), receives cortical inputs.

77 he expression of the calcium-binding protein calbindin (CB) during embryonic to adult stages to map o

78 ned the distribution of parvalbumin (PV) and calbindin (CB) expression in cortical regions and thalam

79 inding proteins (CaBPs) parvalbumin (PV) and calbindin (CB) have shown age-related density changes th

80 ern of calretinin (CR), parvalbumin (PV) and calbindin (CB) immunoreactivity and its corrected relati

81 correspond to poor, intermediate and strong calbindin (CB) labelling, respectively.

82 ergic neurons displayed immunoreactivity for calbindin (CB) or calretinin (CR), but not parvalbumin (

83 calcium-binding proteins calretinin (CR) and calbindin (CB), and the synthetic enzyme for nitric oxid

84 Brains were labeled with antibodies against calbindin (CB), parvalbumin (PV), calretinin (CR) and ne

85 analyzing the expression of calretinin (CR), calbindin (CB), parvalbumin, and various neuropeptides,

86 erved a predominant inhibitory drive of deep calbindin (CB)-immunonegative PCs that contrasts with a

87 s, and the subset of cartridges that contain calbindin (CB+).

88 A bilateral reduction (20%) in calbindin cell density was found in patients (controllin

89 stem activity was necessary for the ChAT and calbindin changes.

90 active intestinal peptide (VIP), calretinin, calbindin, cholecystokinin, and somatostatin.

91 A significant number of BrdU/NeuN- and BrdU/calbindin-colabeled cells were observed in topographical

92 compared our in silico model of the IMPase-1/calbindin complex with the crystal structure of S100B.

93 The majority of calbindin-containing cells in the mature brain are doubl

94 otentiated light-induced c-Fos expression in calbindin-containing cells of the ventral SCN in early a

95 clock in diurnal rodents, and activation of calbindin-containing suprachiasmatic cells may be involv

96 , GFP expression was found in infragranular, calbindin-containing, layer 1-targeting ("Martinotti") c

97 The biological function of calbindin D(28k) appears to be tied to the redox state o

98 Human calbindin D(28k) is a Ca(2+) binding protein that has be

99 arbonic anhydrase II and the 30 kDa protein, calbindin D(28K).

100 ay represent an important mechanism by which calbindin D(9k) achieves high affinity binding while min

101 Further, a wide distribution of calbindin D(9k) among tissues has argued for its biologi

102 We have demonstrated that calbindin D(9k) can be converted into a calcium-sensing

103 At neutral pH, Ca(2+)-loaded calbindin D(9k) does not associate with DPC micelles.

104 We produced mice with the mutant calbindin D(9k) gene by injecting the E14.1 ES cell subl

105 We discovered a frameshift deletion in the calbindin D(9k) gene in an ES cell line, E14.1, that ori

106 binding on the side-chain methyl dynamics of calbindin D(9k) have been characterized by (2)H NMR rela

107 The role of calbindin D(9k) in the cell is discussed, along with the

108 Thus, calbindin D(9k) is not required for viability, reproduct

109 Calbindin D(9k) knockout mice were indistinguishable fro

110 blastocysts and proved that these mice lack calbindin D(9k) protein.

111 Since the discovery of calbindin D(9k), its role in intestinal calcium absorpti

112 ecular dynamics simulations of ubiquitin and calbindin D(9k).

113 ofluorescent labeling for: 1) calretinin, 2) calbindin D-28K (CB), 3) parvalbumin, 4) neurocalcin, 5)

114 alcium-binding proteins parvalbumin (PV) and calbindin D-28K (CB).

115 Placental calbindin-D(9K) expression in NL fetuses was marginally

116 er, probably mediated by modifying placental calbindin-D(9K) expression.

117 of the intracellular calcium-binding protein calbindin-D(9K), previously shown to be rate-limiting fo

118 Calbindin D28k (calbindin) and S100B enhance IMPase-1 ac

119 lcium-binding proteins parvalbumin (PVB) and calbindin D28k (CB) are coexpressed in large subpopulati

120 ding ratio (kappa) after complete washout of calbindin D28k (Cb), kappafixed, displayed a substantial

121 ssential tremor and 39 control brains, using calbindin D28k immunohistochemistry on 100-microm cerebe

122 Calbindin D28k, a highly conserved protein with Ca2+-sen

123 ontain nonpyramidal cells immunoreactive for calbindin-D28K (CALB), parvalbumin (PARV), and calretini

124 atiotemporal analysis of the localization of calbindin-D28k (CB) and calretinin (CR) immunoreactive s

125 calcium-binding proteins calretinin (CR) and calbindin-D28k (CB) have been widely used to characteriz

126 teins calretinin (CR), parvalbumin (PV), and calbindin-D28k (CB) to characterize the gecko auditory s

127 of three cytosolic calcium-binding proteins: calbindin-D28k (CB), calretinin (CR), and parvalbumin (P

128 lar sections were stained with antibodies to calbindin-D28k (to visualize Purkinje cells) and vesicul

129 solution structure of disulfide-reduced holo-calbindin-D28k has been determined by NMR, while the str

130 etermined by NMR, while the structure of apo calbindin-D28k has yet to be determined.

131 s mutant PS1 and the calcium binding protein calbindin-D28k in ECL2 are also susceptible to lesion-in

132 Calbindin-D28k is a calcium binding protein with six EF

133 The calcium-binding protein calbindin-D28k is critical for hippocampal function and

134 The structure of apo calbindin-D28k is in an ordered state, transitioning int

135 Calbindin-D28k is known to bind four calcium ions and up

136 Calbindin-D28k is unique in that it functions as both a

137 for the first time, the specific regions of calbindin-D28k undergoing conformational changes between

138 ned genetic disruption of parvalbumin-alpha, calbindin-D28k, and calretinin in mice with patch-clamp

139 f gamma-aminobutyric acidergic interneurons (calbindin-D28k, calretinin, parvalbumin) in 13 HD cases

140 Co-localization with calbindin-D28k, H(+)-ATPase, aquaporin-2, and pendrin sh

141 controlled by a native fast calcium buffer, calbindin-D28k, maintaining a lower vesicular release pr

142 f conformational change between apo and holo calbindin-D28k.

143 These and previous results using calbindin D9k null mutant mice illustrate that molecular

144 cium-binding proteins calmodulin, S100B, and calbindin D9k.

145 ndin-D9k null (knockout) pups generated from calbindin-D9k knockout females fed a vitamin D-deficient

146 Our results show that in calbindin-D9k knockout pups, a maternal vitamin D-defici

147 We found that calbindin-D9k null (knockout) pups generated from calbin

148 First, it is directly necessary to generate Calbindin expressing interneurons from ventro-lateral pr

149 refinement, the CST no longer terminated in calbindin-expressing areas but did so where ChAT interne

150 This observation confirms that the calbindin-expressing cells in DLM are not GABAergic, in

151 atum, as well as with dopamine receptor- and calbindin-expressing cells within the lateral septum, th

152 Calbindin-expressing cells-located in the central core-c

153 pproximately 30% of all PG cells and include calbindin-expressing neurons.

154 Ectopic calbindin-expressing principal cells develop relatively

155 cystokinin-expressing interneurons to target calbindin-expressing principal cells is diminished.

156 We identify calbindin-expressing principal cells which are mispositi

157 ch seizures chronically suppress hippocampal calbindin expression and impair cognition.

158 Moreover, levels of DeltaFosB and calbindin expression are inversely related in the DG of

159 tion, and to demonstrate a sex difference in calbindin expression levels in the fibers of the DLM-to-

160 The early group upregulates calbindin expression soon after becoming postmitotic and

161 fB during early differentiation and maintain calbindin expression throughout life.

162 of entorhinal cortex and parasubiculum: (i) calbindin-expression in layer-3 neurons decreased progre

163 -3 and parasubiculum neurons had a transient calbindin-expression, which declined with age.

164 ociated lipocalin, kidney injury molecule-1, calbindin), followed by a marker of cell cycle arrest (u

165 library: AGS3 (GPSM1), RGS10, RGS19 (GAIP), calbindin, GC1alpha2, GC1beta2, PDE5, PDE2A, amiloride-s

166 histone deacetylation at the promoter of the calbindin gene (Calb1) and downregulates Calb1 transcrip

167 In addition, we show that calbindin-, GIRK2-, and calretinin-expressing MbDA neuro

168 ery few WMICs containing parvalbumin, and no calbindin-immunopositive neurons.

169 albumin-immunoreactive (PV-IR) interneurons, calbindin-immunoreactive (CB-IR) interneurons, and calre

170 Most calbindin-immunoreactive (IR) Renshaw cells survive to e

171 male mice showed a significant reduction in calbindin-immunoreactive cells (range: 36-67% lower), wh

172 We counted the number of calbindin-immunoreactive cells in 18 distinct nuclei of

173 ut mice but there was a notable reduction in calbindin-immunoreactive cells in midline/intralaminar/p

174 The spatial distribution pattern of calbindin-immunoreactive cells in the dorsal thalamus wa

175 m1 receptors are also expressed by 60% of calbindin-immunoreactive neurons and 40% of calretinin-i

176 Most paranigral VTA neurons also contained calbindin immunoreactivity, and approximately 25% of the

177 However, despite the importance of calbindin in both neuronal physiology and pathology, the

178 are little altered, there is a reduction of calbindin in Purkinje cell dendrites at 1 year of age, s

179 The levels of calbindin in the dentate gyrus correlated negatively wit

180 u pathology and exacerbated the depletion of calbindin in the dentate gyrus.

181 bitory neurons and preferentially innervates calbindin inhibitory neurons, which reduce noise by inhi

182 s a significant loss (57% reduction) of only calbindin interneurons (p=0.022) in HD cases dominated b

183 ChAT interneurons increased, while calbindin interneurons decreased during this period.

184 In contrast, the generation of calbindin interneurons is maximal during late embryogene

185 efinement, the CST terminated sparsely where calbindin interneurons were located and spared ChAT inte

186 No TRPC1/3/4/6-IR was found in calbindin-IR neurons.

187 ffuse dendritic endings, both contacting the calbindin-IR pedicles of double cones.

188 Calbindin is a calcium-binding protein (CBP) present in

189 Calbindin is preferentially expressed in medium spiny ne

190 In calbindin knock-out Purkinje cells, peak calcium increas

191 d number of proprioceptive glutamatergic and calbindin-labeled putative Renshaw cell synapses on thei

192 s innervating the midcochlea region, whereas calbindin levels were similar across the entire ganglion

193 Notably, increasing DG calbindin levels, either by direct virus-mediated expres

194 sensory trigeminal complex, the patterns of calbindin-like and substance P-like immunoreactivity, an

195 e immunofluorescence staining for IAA-RP and calbindin, many of these ribotide-immunoreactive neurons

196 ctions showed that 5-HT(7) receptor mRNA and calbindin mRNAs were concentrated in the same region of

197 The localization of 5-HT(7) receptors and calbindin mRNAs within the same regions suggests that th

198 The organization of calbindin-negative and calbindin-positive cells showed m

199 T-currents increase excitation efficacy onto calbindin-negative cells during dopamine inhibition, sug

200 ingly, these effects occurred selectively in calbindin-negative dopaminergic neurons within the SNc.

201 During inhibition, calbindin-negative neurons exhibit increased sensitivity

202 In the adult substantia nigra, calbindin-negative neurons specifically express high lev

203 pal cell populations (calbindin-positive and calbindin-negative neurons) which targeted the contralat

204 electively activates tyrosine hydroxylase in calbindin-negative neurons.

205 Thus, calbindin-positive and calbindin-negative SNc neurons differ substantially in t

206 al and stimulates dopamine (DA) release in a calbindin-negative subset of cells that are preferential

207 show that calbindin-positive dorsal tier and calbindin-negative ventral tier SNc dopaminergic neurons

208 ons can be divided into two populations: the calbindin-negative ventral tier, which is vulnerable to

209 The late group includes IaINs, are calbindin-negative, and express FoxP2 at the start of di

210 (PA) group showed a significant decrease in calbindin neurons and a paradoxical increase in neurons

211 PA decreased the density of calbindin neurons in layer II of the Anterior Insular Co

212 the middle cortical layers and more "matrix" calbindin neurons that project expansively to the upper

213 d by only 31% of parvalbumin neurons, 23% of calbindin neurons, and 25% of calretinin neurons.

214 neurons trend to compensate for the loss of calbindin neurons, at least within Anterior Insular Cort

215 pOFC axons were associated with dendrites of calbindin neurons, which are poised to reduce noise and

216 of these alterations probably by protecting calbindin neurons.

217 ally superficial positions and the number of calbindin(+) neurons was increased three-fold in the mut

218 Furthermore, loss of calbindin, neuropeptide Y, parvalbumin, and GAD65-positi

219 A significant reduction of calbindin-, NPY (neuropeptide Y)-expressing, and choline

220 ce, renders parvalbumin interneurons but not calbindin or calretinin interneurons vulnerable and pron

221 pressed parvalbumin or somatostatin, but not calbindin or calretinin.

222 lls in PMD are not immunoreactive for either calbindin or parvalbumin, but a few fibers immunoreactiv

223 essing calcium-binding proteins parvalbumin, calbindin, or calretinin.

224 was stained for SMI32, acetylcholinesterase, calbindin, or calretinin.

225 Nissl bodies, myelin, acetylcholinesterase, calbindin, or cytochrome oxidase, we identified three PI

226 d inhibitory neurons labeled for calretinin, calbindin, or parvalbumin.

227 ress activated a proportion of parvalbumin-, calbindin-, or calcium/calmodulin-dependent kinase II-po

228 Parvalbumin-, but not somatostatin-, calbindin-, or cholecystokinin-expressing interneurons w

229 retinin-positive and some were parvalbumin-, calbindin-, or glutamic acid decarboxylase (GAD)-67-posi

230 blood in parabiosis (synaptophysin P = .02; calbindin P = .02) or following intravenous plasma admin

231 asma administration (synaptophysin P < .001; calbindin P = .14).

232 3 interneuron populations, with 71% loss of calbindin (p=0.001), 60% loss of calretinin (p=0.001), a

233 Brains were labeled with antibodies against calbindin, parvalbumin, calretinin, neuropeptide Y, and

234 be negative for the calcium-binding proteins calbindin, parvalbumin, or calretinin.

235 The relatively constant size of calbindin patches differs from cortical modules such as

236 es, and relatively constant neuron number in calbindin patches in medial/caudal entorhinal cortex.

237 and pyramidal cells, periodic arrangement of calbindin patches, and relatively constant neuron number

238 nal cortex, cholinergic innervation targeted calbindin patches.

239 ta activity, cholinergic innervation avoided calbindin patches.

240 differentiation of granular interneurons and Calbindin(+) periglomerular interneurons seemed unaffect

241 ated many OB interneurons, including TH+ and calbindin+ periglomerular interneurons.

242 l horn of the spinal cord and the numbers of calbindin-, PKC-gamma, and calretinin-expressing neurons

243 other retinal markers (tyrosine hydroxylase, calbindin, PKCalpha and Brna3), in R6/2 and Q175 mice at

244 bipolar cell nuclei (protein kinase C alpha/calbindin positive) with blur/loss of ON bipolar cell de

245 These cells are GABA, calretinin, and calbindin positive.

246 composed of two principal cell populations (calbindin-positive and calbindin-negative neurons) which

247 Thus, calbindin-positive and calbindin-negative SNc neurons di

248 trinsically photosensitive RGCs (ipRGCs) and calbindin-positive cells in the IPL.

249 reover, the laminar distribution of cortical calbindin-positive cells is altered.

250 The organization of calbindin-negative and calbindin-positive cells showed marked differences in en

251 Fewer GAD65/67-, Pax6-, calretinin-, and calbindin-positive cells were detected in the glomerular

252 Here, we show that calbindin-positive dorsal tier and calbindin-negative ve

253 degeneration in Parkinson's disease, and the calbindin-positive dorsal tier, which is relatively resi

254 neage commitment and on the specification of calbindin-positive interneurons in the dorsomedial corte

255 re was also an increase in the proportion of calbindin-positive interneurons in the dorsomedial corte

256 The firing of calbindin-positive interneurons targeting dendrites was

257 rom layers II/III to V/VI, and the number of calbindin-positive interneurons was slightly decreased.

258 Nor was there significant loss of calbindin-positive medium spiny projection neurons (MSNs

259 sity in some amygdalar nuclei, and decreased calbindin-positive neuron density in prefrontal cortex.

260 The number of calbindin-positive neurons in a patch increased from app

261 ondria in preferentially vulnerable striatal calbindin-positive neurons in moderate-to-severe grade H

262 Calretinin- and calbindin-positive neurons occurred throughout the senso

263 ceptions to this rule, in which the axons of calbindin-positive ON cone bipolar cells make ribbon syn

264 trees of layer 3 neurons largely avoided the calbindin-positive patches in layer 2.

265 eir progeny to deep granule interneurons and calbindin-positive periglomerular cells.

266 We confirm the existence of patches of calbindin-positive pyramidal cells across these species,

267 y similar in that in both species patches of calbindin-positive pyramidal cells were superimposed on

268 lar output preferentially targets patches of calbindin-positive pyramidal neurons in layer 2 of media

269 e grid-layout and cholinergic-innervation of calbindin-positive pyramidal-cells in layer-2 emerged ar

270 Calbindin-positive Renshaw cell number was decreased sig

271 +) transients in Dogiel Type II (mitotracker/calbindin-positive) neurons after a short delay (1-2 s),

272 sal-to-ventral, (ii) doublecortin in layer-2 calbindin-positive-patches disappeared dorsally before v

273 articipate in the DLM-to-LMAN projection are calbindin-positive.

274 gly, ectopic expression of a Ca(2+) chelator calbindin prevented the Golgi fragmentation, ATF-6 activ

275 based both on immunocytochemistry (ICC) for calbindin protein and in situ hybridization for calb mRN

276 therefore, we suggest that downregulation of calbindin protein expression in the dorsal thalamus of m

277 The early appearance of calbindin-pyramidal-grid-organization in layer-2 suggest

278 By contrast, genes (protein kinase C, calbindin, red/green opsin) that are expressed with a de

279 Islet2 and Lim3, we find the upregulation of calbindin, red/green opsin, rhodopsin, and a synaptic ma

280 not overlap with photoreceptors that express calbindin, red/green opsin, rhodopsin, and dystrophin.

281 of cognitive deficits reflects the degree of calbindin reduction in the hippocampal dentate gyrus (DG

282 which is consistent with previous studies of calbindin's backbone dynamics.

283 aberrant dendritic arborization and reduced calbindin staining intensity.

284 reparations and in vitro that calretinin and calbindin staining levels were heterogeneous.

285 pattern related to quantified calretinin and calbindin staining levels.

286 lized in a discrete subregion resembling the calbindin subnucleus previously described.

287 , and that a bipolar cell immunopositive for calbindin synapses onto the sublamina b processes of the

288 The ratio of neurons expressing Calbindin, TH, and VIP is selectively decreased while, f

289 d basket-like structures, immunoreactive for calbindin, that likely underlie synaptic inputs to speci

290 parvalbumin-immunonegative, some expressing calbindin; they innervated interneurons mostly in the de

291 bpopulation of cholinergic neurons coexpress calbindin through embryonic and postnatal development, b

292 oteins, namely, parvalbumin, calretinin, and calbindin, to characterize the nucleus accumbens and asc

293 acterized the distribution of calretinin and calbindin, two regulators of intracellular calcium that

294 By contrast, calbindin was not co-expressed with aromatase in any reg

295 s expressed Lmx1b, but no co-expression with Calbindin was observed.

296 a (PKCalpha), and the horizontal cell marker calbindin were localized by immunofluorescence and immun

297 Purkinje cells, identified by the marker calbindin, were severely depleted and, although not TUNE

298 e high proportion of WMICs immunoreactive to calbindin, whereas in primates (macaque monkey, lar gibb

299 y 20% of tetraploid cortical neurons express calbindin, which is mainly expressed in layers II-III, w

300 nation with markers for cone photoreceptors (calbindin, XAP-1) and ON bipolar cells (guanine nucleoti