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1 apyramidal symptoms liability, sedation, and catalepsy.
2 genous GLP-1R to reverse haloperidol-induced catalepsy.
3 ctoriness of PRS rats to haloperidol-induced catalepsy.
4 5-HT(2A)-dependent manner, in the absence of catalepsy.
5 ption and hypothermia, with no difference in catalepsy.
6 ockdown mice, and were essentially devoid of catalepsy.
7 ed locomotor activity, but in the absence of catalepsy.
8 one were assessed for locomotor activity and catalepsy.
9 chotic drug with a high propensity to induce catalepsy.
10 f lithium to potentiate haloperidol-mediated catalepsy.
11 agonism, causing analgesia, hypomotilty, and catalepsy.
12 st to haloperidol, AC-260584 did not produce catalepsy.
13 he effects of haloperidol and risperidone on catalepsy.
14 lso potentiated the effect of risperidone on catalepsy.
15  significantly augmented risperidone-induced catalepsy.
16 he drug was without effect on vertical cling catalepsy.
17 striatal neurons but not haloperidol-induced catalepsy.
18 69L, but not clozapine, completely prevented catalepsy.
19   NT69L (up to 5 mg/kg i.p.) did not produce catalepsy.
20 g/kg), or vehicle did not induce significant catalepsy.
21  50% of the subjects, D-NAME did not produce catalepsy.
22  motor impairment characterized by rigidity, catalepsy, akinesia, and tremor.
23 acute D(2)R antagonist (haloperidol)-induced catalepsy and chronic haloperidol-induced enkephalin mRN
24 significant increases in horizontal bar test catalepsy and fore- and hindlimb paw retraction latencie
25 gly, haloperidol produced significantly less catalepsy and inhibition of locomotor activity in D2L-/-
26 ic window over hypolocomotion, sedation, and catalepsy and no observable conditioned place preference
27 se-dependently decreased haloperidol-induced catalepsy and reserpine-induced akinesia in rats.
28 ass receptors, remains effective in inducing catalepsy and striatal Fos/Jun expression in the D1 muta
29 dministration of THC produced dose-dependent catalepsy and suppression of motor activity.
30 oduced dose- and time-dependent hypothermia, catalepsy, and analgesia that were reversed by rimonaban
31 hypothermia, blockade of haloperidol-induced catalepsy, and change in blood glucose, cortisol and T(4
32 rphine-induced climbing, haloperidol-induced catalepsy, and D-amphetamine- and cocaine-induced locomo
33 d reduced locomotor activity, increased ring catalepsy, and hypoalgesia in hotplate and formalin test
34 esponses, including hypomotility, analgesia, catalepsy, and hypothermia.
35         'Waxy flexibility', 'posturing' and 'catalepsy' are among the well-recognised motor abnormali
36  of WIN 55,212-2 (10 microg) did not produce catalepsy as determined by the bar test.
37 e why ibogaine and noribogaine do not induce catalepsy, as demonstrated in our study, in contrast to
38 ian effects by reversing haloperidol-induced catalepsy at very low doses (MED = 0.04 mg/kg p.o.).
39 antipsychotic drug, haloperidol, in inducing catalepsy behavior.
40 tiated Delta(9)-THC-induced hypoactivity and catalepsy but failed to alter Delta(9)-THC-induced analg
41                By itself NT77L did not cause catalepsy, but it moderately reversed haloperidol-induce
42 y showed potentiation of haloperidol-induced catalepsy by ciproxifan, an imidazole-containing H3R ant
43 hich was most likely secondary to the severe catalepsy caused by these compounds.
44 d cannabimimetic effects (e.g., hypothermia, catalepsy, CB1-dependent withdrawal signs) after systemi
45 ethanone mesylate, dose-dependently produced catalepsy, decreased locomotion, and reduced the amplitu
46 transport response intensity, vertical cling catalepsy duration, and dorsal immobility duration.
47 , while extrapyramidal side effects, such as catalepsy, emerged only at much higher occupancies ( > 8
48                              In contrast, no catalepsy-enhancing effects were observed when selective
49      Indeed, co-treatment with EWH prevented catalepsy, hippocampal oxidative stress, cholinergic dys
50                      Delta9-THC-induced ring-catalepsy, hypomobility, and hypothermia were completely
51 10 (1) exhibited strong CNS side effects, in catalepsy, hypothermia, and motor incoordination assays.
52 bjects, whereas L-NAME (3200 mg/kg) produced catalepsy in 50% of the subjects, D-NAME did not produce
53 oup II mGluRs induces a dramatic reversal of catalepsy in a rat model of PD.
54 also active in reversing haloperidol induced catalepsy in a rodent preclinical model of Parkinson's d
55                     7-NI (32 mg/kg) produced catalepsy in all subjects, whereas L-NAME (3200 mg/kg) p
56 d their enantiomers for efficacy and lack of catalepsy in animal models.
57  dependently counteracts haloperidol-induced catalepsy in mice from 30 mg/kg by the oral route.
58 ritoneal administration: haloperidol-induced catalepsy in mouse and the rat 6-hydroxydopamine (6-OHDA
59                                Resistance to catalepsy in PRS rats did not depend on reductions in bl
60        GPR6 IAG reversed haloperidol-induced catalepsy in rats and restored mobility in the bilateral
61 firm that haloperidol and risperidone caused catalepsy in rodents, driven by strong antagonism of D(2
62 loperidol induces parkinsonism in humans and catalepsy in rodents.
63 ose CP55,940 (10 mg/kg daily, i.p.) produced catalepsy in WT mice, which precluded determination of a
64 t stress during pregnancy, were resistant to catalepsy induced by haloperidol (0.5-5 mg/kg i.p.) or r
65 ity, including antinociception, hypothermia, catalepsy, locomotor activity, and in the drug discrimin
66 st the potentiation of antipsychotic-induced catalepsy may result from pharmacokinetic drug-drug inte
67 ce, compound 34 was orally active in the rat catalepsy model at 3 mg/kg.
68  be orally active in the haloperidol induced catalepsy model, a well-established antiparkinsonian mod
69  been shown to be orally active in the mouse catalepsy model.
70  and 18a showed good oral efficacy in rodent catalepsy models of Parkinson's disease.
71  mouse and rat models of haloperidol-induced catalepsy, mouse and rat models of reserpine-induced aki
72  mouse and rat models of haloperidol-induced catalepsy, mouse model of reserpine-induced akinesia, ra
73  and 1.0 mg/kg, respectively) showed extreme catalepsy on day 1, but significantly decreased cataleps
74                AM404 produced no significant catalepsy or analgesia, two typical effects of direct-ac
75 out affecting signaling pathways involved in catalepsy or certain mood-related behaviors.
76            No changes in haloperidol-induced catalepsy or MK-801-induced locomotion were seen followi
77 s were observed at doses that do not produce catalepsy or peripheral adverse effects associated with
78 tivity in rats at doses that did not produce catalepsy or peripheral adverse effects of other mAChR a
79  at dose levels not able to induce sedation, catalepsy, or learning impairment in passive avoidance.
80  NR1-KD animals, and it produced very little catalepsy relative to haloperidol.
81 a(9)-THC), including analgesia, hypothermia, catalepsy, rotarod locomotor impairment, or conditioned
82 l selective breeding for haloperidol-induced catalepsy, starting from three mouse populations of incr
83                                 Finally, rat catalepsy studies confirmed the restricted permeation of
84 fects of the drug, yet enhanced tolerance to catalepsy, suggest that development of cannabinoid drugs
85 responding, and elicit a much lower level of catalepsy than haloperidol.
86 actions, discriminative stimulus effects and catalepsy, that are very selective for NMDA antagonists
87 augmented haloperidol (0.19mg/kg SC)-induced catalepsy, this lithium effect was not attenuated by adm
88  of early-life stress on haloperidol-induced catalepsy using the rat model of prenatal restraint stre
89 eractivity and apomorphine-induced climbing; catalepsy was assessed by measuring step-down latency; s
90 of heroin were abolished, and heroin-induced catalepsy was increased.
91            Enhanced tolerance to THC-induced catalepsy was observed in betaarr2-KO mice.
92           However, haloperidol (HAL)-induced catalepsy was unchanged in either D2GSK3beta(-/-) or D1G
93 and behaviors (antinociception, hypothermia, catalepsy) were assessed in beta-arrestin2-knockout (bet
94 alepsy on day 1, but significantly decreased catalepsy when tested again on days 7 and 21.
95 h NOS inhibitors were effective in producing catalepsy, which is an effect commonly produced by compe
96                       However, we found that catalepsy, which is thought to reflect the EPS of typica
97 t it moderately reversed haloperidol-induced catalepsy with an ED(50) of 6.0 mg/kg (i.p.).