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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.
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
21 evidence is cited for a form of denervation supersensitivity in causalgia and for increased expressi
24 ng the well described phenomenon of dopamine supersensitivity indicating that apomorphine not only re
25 tub3Delta, supporting the idea that benomyl supersensitivity is a rough measure of microtubule insta
26 induction of IEGs, that D1 dopamine receptor supersensitivity is attributable to a switch to ERK1/2/M
29 an axon reflex and that alpha-adrenoreceptor supersensitivity occurs in the presynaptic portion of th
31 posed to levodopa, and these may result from supersensitivity of postsynaptic striatal dopamine D1 an
32 In vitro calcineurin digestion shows that supersensitivity of S603 dephosphorylation is an inheren
33 homeostasis are accompanied by a pronounced supersensitivity of the mice to the locomotor effects of
35 of sympathetic neurotransmission, selective supersensitivity of the vascular smooth muscle to sympat
36 ression of AtRGS1 complemented the pheromone supersensitivity phenotype of a yeast RGS mutant, sst2De
37 in had a thermal instability and phosphatase supersensitivity similar to that of the A638 and E638 mu
38 uples Gpa1p from Sst2p, results in pheromone supersensitivity similar to the sst2 mutant, and promoti
40 cyclase responses instead of displaying the supersensitivity that had been seen in the young group.
41 was present in only 1 patient, and pupillary supersensitivity to 2.5% phenylephrine was not observed.
42 owing that purine synthesis inhibitors cause supersensitivity to A. tumefaciens transformation in thr
43 ne auxotrophs were identified that exhibited supersensitivity to A. tumefaciens-mediated transformati
44 These findings support a model of cerebellar supersensitivity to alcohol-related tissue volume defici
46 sed dispersion of action potential duration, supersensitivity to beta-adrenergic receptor stimulation
49 tients with endothelial dysfunction and that supersensitivity to exogenous nitrates is not clinically
50 ted vegetative growth and rescued cells from supersensitivity to fluoride, but homozygous diploids fa
52 oportion to its abundance and thereby caused supersensitivity to microtubule disruptive drugs such as
57 tation of oxytocin neurones does not involve supersensitivity to the noradrenergic input, or hypersen
58 hypothermia as well as pronounced behavioral supersensitivity upon challenge with the nonselective mu
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