戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1  underlie vHPC lesion-induced behavioral DA 'supersensitivity'.
2 secretion by residual axons, and denervation supersensitivity.
3 as higher expression resulted in the loss of supersensitivity.
4  mouse models of psychostimulant or dopamine supersensitivity.
5 echanism contributes to central dopaminergic supersensitivity.
6 be responsible for the development of D(2)DR supersensitivity.
7 ion may be an underlying cause of behavioral supersensitivity.
8 nists due to the development of postsynaptic supersensitivity.
9  were accompanied by dopamine D2/D3 receptor supersensitivity.
10 urse reminiscent of experimental denervation supersensitivity.
11 se fat pads and results in vagal denervation supersensitivity.
12 ed vasoconstriction and possible denervation supersensitivity.
13                                     Receptor supersensitivity accounts for some but not all aspects o
14 ture of CRPS I, we investigated whether this supersensitivity also occurs in the sudomotor system.
15 t elimination of GRK5 results in cholinergic supersensitivity and impaired muscarinic receptor desens
16 riety of phenotypes were observed, including supersensitivity and resistance to the microtubule-desta
17 way that enhance this RO-specific DNA damage supersensitivity by promoting ectopic recombination betw
18 the development and expression of behavioral supersensitivity compared to rats treated with quinpirol
19 avioral phenotypes that includes amphetamine supersensitivity, hyperexploratory behavior and rotarod
20                                 The dopamine supersensitivity hypothesis cannot account for the time
21  evidence is cited for a form of denervation supersensitivity in causalgia and for increased expressi
22                         alpha-Adrenoreceptor supersensitivity in many tissues has been described in p
23 llow gradual resolution of dopamine receptor supersensitivity in the minority of patients with TRS wh
24 rsed by L-DOPA and evidence of "dopaminergic supersensitivity" in the striatum.
25 ng the well described phenomenon of dopamine supersensitivity indicating that apomorphine not only re
26  tub3Delta, supporting the idea that benomyl supersensitivity is a rough measure of microtubule insta
27 induction of IEGs, that D1 dopamine receptor supersensitivity is attributable to a switch to ERK1/2/M
28 sure exerted by paclitaxel binding, and drug supersensitivity is lost.
29                                         This supersensitivity is reversed when CRPS I resolves.
30 ced dopamine supersensitivity, or behavioral supersensitivity, is a problematic consequence of long-t
31 an axon reflex and that alpha-adrenoreceptor supersensitivity occurs in the presynaptic portion of th
32        The time course of fluoxetine-induced supersensitivity of hypothalamic 5-HT2A/2C receptors was
33 posed to levodopa, and these may result from supersensitivity of postsynaptic striatal dopamine D1 an
34    In vitro calcineurin digestion shows that supersensitivity of S603 dephosphorylation is an inheren
35                       LID is associated with supersensitivity of striatal dopaminergic signaling and
36  homeostasis are accompanied by a pronounced supersensitivity of the mice to the locomotor effects of
37                        It is understood that supersensitivity of the striatonigral pathway underlies
38  of sympathetic neurotransmission, selective supersensitivity of the vascular smooth muscle to sympat
39               Antipsychotic-induced dopamine supersensitivity, or behavioral supersensitivity, is a p
40 ression of AtRGS1 complemented the pheromone supersensitivity phenotype of a yeast RGS mutant, sst2De
41  sufficient to prevent antipsychotic-induced supersensitivity, pointing to an entirely novel therapeu
42 in had a thermal instability and phosphatase supersensitivity similar to that of the A638 and E638 mu
43 uples Gpa1p from Sst2p, results in pheromone supersensitivity similar to the sst2 mutant, and promoti
44          Here we demonstrate that behavioral supersensitivity stems from long-lasting pre, post and p
45 malization of striatal dopaminergic receptor supersensitivity than wild-type grafts.
46  cyclase responses instead of displaying the supersensitivity that had been seen in the young group.
47 was present in only 1 patient, and pupillary supersensitivity to 2.5% phenylephrine was not observed.
48 owing that purine synthesis inhibitors cause supersensitivity to A. tumefaciens transformation in thr
49 ne auxotrophs were identified that exhibited supersensitivity to A. tumefaciens-mediated transformati
50 These findings support a model of cerebellar supersensitivity to alcohol-related tissue volume defici
51 C-3 and melanoma cell line A375-C6 conferred supersensitivity to apoptotic stimuli.
52 sed dispersion of action potential duration, supersensitivity to beta-adrenergic receptor stimulation
53 ng from the non-Hermitian skin effect to the supersensitivity to boundary conditions, have been widel
54                                         This supersensitivity to dephosphorylation in vitro was also
55 n growth rate, they demonstrate an intrinsic supersensitivity to DNA-damaging agents.
56 tients with endothelial dysfunction and that supersensitivity to exogenous nitrates is not clinically
57 ted vegetative growth and rescued cells from supersensitivity to fluoride, but homozygous diploids fa
58                  In addition to the striatal supersensitivity to induction of the permeability transi
59 oportion to its abundance and thereby caused supersensitivity to microtubule disruptive drugs such as
60              Low expression of beta4a caused supersensitivity to paclitaxel, whereas higher expressio
61 tant exhibits a synergistic, or "synthetic," supersensitivity to pheromone.
62                        Mice lacking PRs show supersensitivity to the antiseizure responses of progest
63 lay enhanced filamentous differentiation and supersensitivity to the MAPK signal.
64 tation of oxytocin neurones does not involve supersensitivity to the noradrenergic input, or hypersen
65 hypothermia as well as pronounced behavioral supersensitivity upon challenge with the nonselective mu
66 gic interneurons in situ could contribute to supersensitivity without receptor upregulation.