ライフサイエンスコーパス: calbindin

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

2 nolabeling with tyrosine hydroxylase (TH) or calbindin.

3 lls positive for the calcium-binding protein calbindin.

4 ar dye injection or with an antibody against calbindin.

5 stochemistry and was moderately stained with calbindin.

6 histochemistry, and immunocytochemistry for calbindin.

7 microtubule-associated protein 2 (MAP2), and calbindin.

8 are non-GABAergic cells (79%) and devoid of calbindin.

9 as indicated by labeling for calretinin and calbindin.

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

11 er levels of calretinin and higher levels of calbindin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 up 1 are Renshaw cells and intensely express calbindin and coexpress parvalbumin and calretinin.

30 hat cleaved caspase-3-positive cells express calbindin and DARPP-32, but not somatostatin, parvalbumi

31 In contrast, PSA-NCAM, calbindin and GAD67 immunohistochemistry did not reveal

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

33 The PI(P) division stained darkly for calbindin and lightly for CO and AChE.

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

35 Combined calbindin and mitochondrial marker immunofluorescence sh

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

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

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

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

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

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

42 characterized by less neuropil staining for calbindin, and by distinct, intensely stained patches of

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

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

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

46 ith the cell-selective immunomarkers Prox-1, calbindin, and neurofilament.

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

48 Calbindin- and calretinin-expressing SNC populations sho

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

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

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

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

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

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

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

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

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

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

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

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

61 )1 subtypes and the calcium-binding proteins calbindin, calmodulin and calreticulin in areas vulnerab

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

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

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

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

70 Other striatal markers such as calbindin, calretinin, and the cannabinoid-1 receptor we

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

72 CRF-IR never colocalized with IR for calbindin, calretinin, neuropeptide Y, serotonin, or som

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 Furthermore, mean calbindin cell cross-sectional area was increased in fem

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

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

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

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

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

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

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

96 Calbindin-containing cells were stained using an antibod

97 Reduced density of calbindin-containing interneurons in the prefrontal cort

98 leasing peptide (GRP), which is found within calbindin-containing retinorecipient cells and causes ph

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

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

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

102 Last, oxidized calbindin D(28k) binds Ca(2+) with lower affinity than d

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

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

105 The interactions between calbindin D(9k) (S100D) and the detergent dodecyl phosph

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

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

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

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

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

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

112 specific analysis of the data indicates that calbindin D(9k) has a core of three tightly packed helic

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

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

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

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

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

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

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

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

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

122 ity and to lack evidence for the presence of calbindin D-28k, parvalbumin, and protein kinase C-gamma

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

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

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

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

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

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

129 Calbindin D28k can be reconstituted from six synthetic p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 -3 and parasubiculum neurons had a transient calbindin-expression, which declined with age.

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

168 nic FYN/hAPP mice had striking depletions of calbindin, Fos, and phosphorylated ERK (extracellular si

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

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

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

172 Calbindin immuno-labeling excluded Purkinje cell axonal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 ral neurons in this group receive convergent calbindin-IR Renshaw cell inputs.

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

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

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

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

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

198 d with calretinin-li but colocalization with calbindin-li was not observed.

199 tly colocalized with either calretinin-li or calbindin-li.

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

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

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

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

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

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

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

207 During inhibition, calbindin-negative neurons exhibit increased sensitivity

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

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

210 electively activates tyrosine hydroxylase in calbindin-negative neurons.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 relation between NAA/Cr and neuronal counts, calbindin, or MAP2 was found.

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

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

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

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

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

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

235 3 interneuron populations, with 71% loss of calbindin (p=0.001), 60% loss of calretinin (p=0.001), a

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

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

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

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

240 nal cortex, cholinergic innervation targeted calbindin patches.

241 ta activity, cholinergic innervation avoided calbindin patches.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 The firing of calbindin-positive interneurons targeting dendrites was

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

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

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

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

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

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

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

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

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

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

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

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

271 Calbindin-positive Renshaw cell number was decreased sig

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

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

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

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

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

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

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

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

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

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

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

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

284 -hand Ca2+-binding proteins, parvalbumin and calbindin, significantly altered the relationship betwee

285 aberrant dendritic arborization and reduced calbindin staining intensity.

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

287 pattern related to quantified calretinin and calbindin staining levels.

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

289 mic acid decarboxylase 67, calretinin and/or calbindin, suggest that new neurons in both regions are

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

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

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

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

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

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

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

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

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

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