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1 r characterized by episodes of imbalance and incoordination.
2 es that manifest as attacks of imbalance and incoordination.
3 esis that culminate in nr PN death and motor incoordination.
4 cute manifestation of CP55,940-induced motor incoordination.
5 accentuating effect on ethanol-induced motor incoordination.
6 d in the expression of ethanol-induced motor incoordination.
7 sant-like effect without eliciting locomotor incoordination.
8 this breed is manifested by muscle weakness, incoordination and life-threatening collapse after inten
10 fferent behavioral effects of ethanol, motor incoordination and sedation, appear to be regulated by P
11 however, linked by common symptoms of motor incoordination and typically associated with deficiency
14 us system-depressant agents, including motor incoordination, anxiolysis, and the elicitation of signs
15 ent markedly inhibited ethanol-induced motor incoordination as well as CHA's accentuation of ethanol'
16 be prevalent in patients with neuromuscular incoordination, as with cerebral palsy, or after surgery
20 cells; however, there was still an apparent incoordination between granule decondensation and exocyt
21 hibitor, significantly accentuated the motor incoordination by ICB CP55,940 (15 microg), providing fu
22 ct phenotype, including chorea and dystonia, incoordination, cognitive decline, and behavioural diffi
23 r that resembles human SCA1, featuring motor incoordination, cognitive deficits, wasting, and prematu
24 ephalography (EEG), impaired motor activity, incoordination, hypoglycorrhachia, microencephaly, decre
25 c restriction dramatically rescues the motor incoordination, imbalance and the associated neuropathol
27 tion of cannabinoid (CP55,940)-induced motor incoordination in mice by the adenosine A(1) receptor-se
28 researchers examining ethanol-induced motor incoordination in mice, but it should be applicable to o
29 s found to induce a faster recovery of motor incoordination in rotarod experiments and a shorter seda
31 velop an adult-onset neurologic phenotype of incoordination, involuntary limb clasping, seizures, and
32 ginning with increased activity, followed by incoordination, loss of postural control, and eventually
33 modulates acute ethanol (i.p.)-induced motor incoordination (MI) through receptor mediated mechanism(
34 conditions, all characterized by progressive incoordination of gait and limbs and by speech and eye-m
37 because of differing patterns of weakness or incoordination of the facial muscles, lips, tongue, pala
38 lethal neurological disease characterized by incoordination, postural abnormalities, difficulties wit
39 to significantly alter ethanol-induced motor incoordination probably due to their mutual functional a
41 nd Kcnc3-null mutant mice both display motor incoordination, suggested in mice by increased lateral d
42 CB CP55,940 (15 microg) attenuated the motor incoordination suggesting a modulation by an endogenous
43 a(9)-THC- and Delta(9)-THC+CHA-induced motor incoordination suggesting coupling of CB(1) receptor to
44 xhibit postural and kinetic tremor and motor incoordination that is characteristic of essential tremo
45 sinergic modulation of ethanol-induced motor incoordination, the effect of direct intracerebellar adm
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