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1 ey hair), and thermal sensitivity (hot plate/tail flick).
2 k: 70-75%; jump: 60-81%) and beta-endorphin (tail-flick: 100%; jump: 93%) analgesia elicited from the
3 the PAG significantly reduced both morphine (tail-flick: 70-75%; jump: 60-81%) and beta-endorphin (ta
4 Antinociception studies using a radiant-heat tail flick analgesia method demonstrated that lambda-car
5 hine before norBNI responded strongly in the tail-flick analgesia assay to a subsequent challenge wit
10 knockout mice displayed shorter latencies on tail flick and hot plate tests for spinal and supraspina
11 ueductal gray were determined using both the tail flick and the foot withdrawal responses to noxious
12 were confirmed in the antinociceptive tests (tail-flick and acetic acid writhing) in mice, which demo
14 strength, and heat nociception, measured by tail-flick and hindlimb withdrawal tests, were not affec
15 ), for pharmacological activity in the mouse tail-flick and hot-plate assays, and for hypothermia and
16 iled to produce antinociception in the mouse tail-flick and hot-plate assays, engender nicotine-like
18 ams of CGP 35348 antagonized the increase in tail-flick and hot-plate latency produced by either dose
19 in vivo for antinociception activity in the tail-flick and hot-plate models of acute pain and for th
20 on, 5g was a nicotine antagonist in both the tail-flick and hot-plate tests, whereas 8a was an antago
21 glion neurons, and (3) no change in baseline tail-flick and hotplate reflex nocifensive responses.
22 ormalin test, and the thermal (49 degrees C) tail-flick and increasing-temperature (3 degrees C/min)
23 ine-6beta-glucuronide (M6G) analgesia on the tail-flick and jump tests differed in potency in the per
25 25 and 250 nmol and the resulting effects on tail-flick and nociceptive foot-withdrawal latencies wer
29 was evaluated for antinociception using the tail-flick and von Frey assays in mice pretreated with l
30 es to noxious thermal stimulation (hotplate, tail flick) and to persistent noxious chemical stimulati
32 In the present study, hot-water-immersion tail-flick antinociception assays at 52 degrees C on mic
33 hand, the mutant mice react normally in the tail flick assay and acetic acid-induced writhing tests.
37 times more potent than morphine in the mouse tail-flick assay (ED(50) = 0.05 mg/kg), and (-)-(1R,5R,
38 a partial agonist effect in the 55 degrees C tail-flick assay and a full agonist effect in the acetic
42 ater analgesia, as assayed in the warm water tail-flick assay, in NET-knock-out (-KO) mice than in wi
53 ociception was measured using a radiant heat tail-flick assay; mechanical sensitivity was measured us
54 cies in the hot plate and the high-intensity tail flick assays (hypoalgesia), but there was no differ
55 harmacological manipulations utilized in our tail-flick assays on GM1-treated mice provide a novel bi
61 tar S-DHPG (0.1, 1.0, 10 mM) does not change tail flick latencies or paw withdrawal latencies to heat
62 ive to NMDA antagonism, but not hot plate or tail flick latencies, which were insensitive to NMDA ant
66 (ED50=30 microg) in significantly increasing tail-flick latencies with longer durations of action.
67 nd time-dependent increase in high-intensity tail-flick latencies with maximal effects observed at a
68 tagonist, did not antagonize the increase in tail flick latency (TFL) produced by microinjection of L
69 activity of compound 5b was evaluated by the tail flick latency test, giving an ED50 of 2.5 mg/kg.
70 BLA resulted in a time dependent increase in tail flick latency that was attenuated by preadministrat
71 dy, the effects of phenylephrine infusion on tail flick latency was determined before and after salin
73 ndently increased mean arterial pressure and tail flick latency, but had inconsistent effects on neur
74 or 3 mg kg(-1) d(-1) FP15 reversed increased tail-flick latency (a sign of reduced pain sensitivity);
75 or nonpaced) showed significant increases in tail-flick latency (TFL) within 5 s (time 0) after matin
76 iferative responses by 80% and elevated both tail-flick latency and plasma corticosterone when compar
77 Controls showed a pronounced elevation in tail-flick latency following presentation of 90-dB white
78 s, manifested by rapid onset of decreases in tail-flick latency for periods >3 h after drug administr
80 antagonists by themselves did not alter the tail-flick latency or the analgesic effect of deltorphin
85 slightly blocked anti-nociception in a naive tail-flick model, while enhancing morphine-induced preci
86 placements displayed analgesic ED50s on the tail-flick (morphine: 1.4 microgram, M6G: 0.06 microgram
87 placements displayed analgesic ED50s on the tail-flick (morphine: 1.7 microgram, M6G: 0.1 microgram)
88 placements displayed analgesic ED50s on the tail-flick (morphine: 2.1 microgram, M6G: 0.2 microgram)
92 hippocampal infusions had greater analgesia (tail flick, paw lick), less anxiety behavior (plus-maze,
93 began during the 50 msec after onset of the tail flick, peaked within 200 msec, and outlasted the du
94 uation of 1, 2e, and 2f sc in mice using the tail-flick procedure indicated that they are selective d
95 ring associated with the noxious heat-evoked tail flick reflex were used to classify neurons as "on-c
100 ations that eliminated the inhibition of the tail-flick reflex restored vocalization to thermal stimu
101 the hind leg produced a facilitation of the tail-flick reflex that was significantly reduced in spin
106 e relationship between the inhibition of the tail-flick response and brain-mediated responses to noci
109 gray using both the foot-withdrawal and the tail-flick responses to noxious radiant heating in light
111 v administration as measured analgesia using tail-flick (spinal involvement) and hot-plate (supraspin
112 nociception in the hotplate; however, in the tail flick test a dose of 2 mg/kg was required for an an
113 .07 and 0.04 microg/kg, respectively, in the tail flick test and only 35 and 0% inhibition at 20 and
114 rkedly increased withdrawal latencies in the tail flick test and reduced responses to subcutaneous fo
116 ference conditioning for reward effects, the tail flick test for nociception, and a measure of locomo
117 ad no effect on the altered responses in the tail flick test in aged rats, and in general, had no eff
119 s (13l and 11b) showed analgesic response in tail flick test which was blocked by pretreatment with n
120 the epibatidine analogues are full agonists (tail flick test) in producing antinociception after intr
121 ) or their combination and their behavior in tail flick test, reflective of spinal antinociception an
125 n the dose-response curve to morphine on the tail-flick test (a pain sensitivity assay), suggesting e
127 ll found Delta9-THC-induced analgesia in the tail-flick test and other behavioral (licking of the abd
128 intrathecally, all produced analgesia in the tail-flick test but only 5a produced analgesia in the ho
129 blocked OFQ/N(1-17)-induced analgesia on the tail-flick test elicited from the amygdala, and whether
136 rophenyl analogue (5e) (AD50 = 0.0003 in the tail-flick test) was the most potent and selective analo
139 t as well as the peak (15 min) effect on the tail-flick test, analgesia elicited by either endomorphi
140 stress-induced analgesia as detected by the tail-flick test, but decreased the potency of the opioid
141 tinociception produced by morphine using the tail-flick test, but not that using the foot-withdrawal
142 tent and long lasting antinociception in the tail-flick test, indicating that 13a was able to permeat
144 ayed relatively lower antinociception on the tail-flick test, resulting in significantly increased ED
163 en microinjected into the DRN at the time of tail-flick testing, 8-OH-DPAT also effectively prevented
164 reduce nociceptive responses in hot plate or tail flick tests of homozygous mu receptor knockout mice
167 mal thermal nociception in the hot-plate and tail-flick tests, and had similar olfactory, auditory an
172 ow that facilitation of a spinal nociceptive tail-flick (TF) reflex induced by stimulation in the NGC
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