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1 ted increase in cytosolic calcium levels and spinogenesis.
2 rogenic regulation of the DH influences mPFC spinogenesis.
3 portantly, foot-shock alone did not increase spinogenesis.
4 t E2-mediated activity in the DH drives mPFC spinogenesis.
5 eoglycan syndecan-2 (SDC2) induces dendritic spinogenesis.
6 tum to other brain regions through augmented spinogenesis.
7 ic spines during the developmental period of spinogenesis.
8  cargo locally to support synapse growth and spinogenesis.
9 nA2-RasGAP activity is necessary to suppress spinogenesis.
10  not correlated with LTP, but with increased spinogenesis.
11 the NMDA receptor abolished activity-induced spinogenesis.
12 uggesting fasting induced synaptogenesis and spinogenesis.
13  any activity in the regulation of dendritic spinogenesis.
14 role of the proteasome in activity-dependent spinogenesis.
15  actin depolymerizing factor is required for spinogenesis.
16 tivation of Rac1, an established enhancer of spinogenesis.
17 rowth, branch formation, synaptogenesis, and spinogenesis.
18 xpression increases during a period of rapid spinogenesis.
19  and subsequent morphological changes led to spinogenesis.
20 tial loss of dendritic filopodia involved in spinogenesis.
21 g time-lapse imaging have reported increased spinogenesis.
22 ombinant profilins rescued the impairment in spinogenesis, a hallmark in Fragile X syndrome, thereby
23                    The enhancement in evoked spinogenesis after Drd1 activation or ketamine treatment
24  enhancement in activity-dependent dendritic spinogenesis and behavioral effects induced by ketamine.
25 necessary and sufficient for fasting-induced spinogenesis and excitatory synaptic activity, and that
26  ion transport function, KCC2 also regulates spinogenesis and excitatory synaptic function through in
27  the elaborate responses of the spine during spinogenesis and experience-dependent plasticity.
28 l thalamus connectivity, intra-PFC dendritic spinogenesis and expression of the layer 4 marker RORB.
29 a demonstrate that GPER-mediated hippocampal spinogenesis and memory consolidation depend on JNK and
30 n-B3 controls axon targeting and coordinates spinogenesis and neuronal activity within the amygdala.
31  DeltaFosB induction and prevented increased spinogenesis and sensitized amphetamine reward.
32 Although the molecular mechanisms underlying spinogenesis and spine synapse formation are being delin
33 over, disrupting TSP2-alpha2delta-1-mediated spinogenesis and synapse generation in NAcSh decreases c
34     Moreover, disrupting TSP2-a2d-1-mediated spinogenesis and synapse generation in NAcSh decreases c
35  synaptic adhesion GPCR that is required for spinogenesis and synaptogenesis in mice and rats.
36  receptor gamma co-activator 1alpha inhibits spinogenesis and synaptogenesis.
37 y supporting the involvement of drebrin A in spinogenesis and synaptogenesis.
38  of neurons, in vivo, in time to orchestrate spinogenesis and synaptogenesis.
39 utilized during cocaine experience to induce spinogenesis and the generation of AMPA receptor-silent
40 ortex where Cbln2 was recently implicated in spinogenesis, and the cerebellum where Cbln1 is known to
41 exity and outgrowth toward TCA clusters; (3) spinogenesis; and (4) tuning of excitatory inputs.
42         Moreover, anxiogenesis and amygdalar spinogenesis are also triggered by chronic stress in con
43 induced enhanced drug reward, DeltaFosB, and spinogenesis are dependent on mating-induced dopamine D1
44             The activation of Rac1 initiates spinogenesis at an early stage and regulates the functio
45 rticostriatal synapse formation and striatal spinogenesis, but can itself be repressed by Foxp2 throu
46 ports, PTEN knockdown may not induce de novo spinogenesis, but instead may increase synaptic activity
47              Multiple proteins have roles in spinogenesis, but until now, a regulatory role for actin
48                  The regulation of dendritic spinogenesis could explain the association of CTTNBP2 wi
49 se of Mef2c rescue vocalization and striatal spinogenesis defects of Foxp2-deletion mutants.
50 icating the importance of estradiol-mediated spinogenesis for female sexual receptivity (81.43 +/- 7.
51 equently exhibit differential adaptations in spinogenesis, glutamatergic receptor trafficking, and in
52  the specific effect of CTTNBP2 on dendritic spinogenesis, here we investigate whether CTTNBP2NL has
53 all RhoGTPase, contributes to the absence of spinogenesis in immature neurons.
54  therapy (ET) enhances cognition and induces spinogenesis in neuronal circuits.
55 hese data demonstrate that estradiol-induced spinogenesis in the ARH is an important cellular mechani
56 a delayed onset of anxiety-like behavior and spinogenesis in the basolateral amygdala (BLA) of rats.
57 ty-like behavior, concomitant with increased spinogenesis in the basolateral amygdala.
58                     In addition to promoting spinogenesis in the cortex, (+)-JRT produces therapeutic
59  mTOR activation is necessary for E2-induced spinogenesis in the DH and mPFC.
60 glutamate uncaging/imaging to focally induce spinogenesis in the medial prefrontal cortex, directly i
61  spine density and uncaging-evoked dendritic spinogenesis in the medial prefrontal cortex, whereas op
62 t ketamine rapidly enhances glutamate-evoked spinogenesis in the medial prefrontal cortex, with timin
63 t inhibitory avoidance (IA) induces mushroom spinogenesis in the medium spiny neurons (MSNs) of the d
64 tes habituation by increasing stress-induced spinogenesis in the pPVT, increasing coherent neural act
65 e molecular mechanisms regulating E2-induced spinogenesis in vivo are largely unknown.
66 Until now, it has been assumed that enhanced spinogenesis increased excitatory input received by the
67 Galphas activation was sufficient to enhance spinogenesis induced by glutamate photolysis in both dSP
68 the functional translation of BDNF-triggered spinogenesis into clearly defined morphological spine ty
69              We show that DOCK10 function in spinogenesis is mediated mainly by Cdc42 and its downstr
70 c psychedelics and that TBG-induced cortical spinogenesis is required for the sustained antidepressan
71                         The initial stage of spinogenesis is thought to begin with the emergence of a
72          Excitatory spine synapse formation (spinogenesis) is a poorly understood yet pivotal period
73   Consistent with its normal role of slowing spinogenesis, loss of Icam5 induced precocious stubby sp
74                         A profound dendritic spinogenesis occurs concurrent with the connectivity inc
75 E2 treatment elicits ERK- and mTOR-dependent spinogenesis on CA1 and mPFC pyramidal neurons, effects
76 n the living brain, we found that prefrontal spinogenesis plays a critical role in sustaining specifi
77               We find that glutamate-induced spinogenesis requires opening of NMDARs (N-methyl-D-aspa
78           Ketamine increases evoked cortical spinogenesis through dopamine Drd1 receptor (Drd1) activ
79 sion by recruiting AMPARs to synapses during spinogenesis, thus providing a mechanistic link between
80  through HIF-1alpha, mediates VEGF-dependent spinogenesis to underlie the EE-induced antidepressant-l
81 se data demonstrate that neurons undertaking spinogenesis upregulate actin expression, that actin ove
82             Surprisingly, estrogen-activated spinogenesis was associated with a decrease in CA1 hippo
83                                   Prefrontal spinogenesis was required for the long-term maintenance
84 ly, WRP function is critical at the onset of spinogenesis, when dendritic filopodia are prevalent.
85 n when they are not observable, constraining spinogenesis while preserving mature spines may be impor
86 n when they are not observable, constraining spinogenesis while preserving mature spines may be impor