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1  endogenous dynorphin from pronociceptive to antinociceptive.
2    It is the most potent known phenylmorphan antinociceptive.
3 ain processing capacity are characterized as antinociceptive.
4       Studies have described both a pro- and antinociceptive action following 5-HT2A-receptor activat
5     These compounds were evaluated for their antinociceptive action in two analgesia animal models.
6            Derm-sap treatment attenuated the antinociceptive action of both intrathecal and systemic
7  the spinal cord probably contributes to the antinociceptive action of cholinergic agents.
8 onal role of spinal GABA(B) receptors in the antinociceptive action of intrathecal cholinergic agents
9 e of the important mechanisms underlying the antinociceptive action of intrathecal cholinergic agents
10  thermal stimuli, (2) are necessary for full antinociceptive action of morphine (intrathecal or syste
11                                          The antinociceptive action of morphine microinjected into th
12 rate studies: First, we determined the acute antinociceptive action of morphine, the rate of developm
13 s are more sensitive than female rats to the antinociceptive action of morphine.
14  The role of spinal GABA(B) receptors in the antinociceptive action of muscarine was also determined.
15 u opioid receptors in the spinal cord in the antinociceptive action of opioids.
16 eline nocifensive responding and (2) reduced antinociceptive action of systemic morphine.
17                             Furthermore, the antinociceptive action produced by intrathecal muscarine
18 or most drugs, there was a sex difference in antinociceptive action, and the impact of deletion of th
19 ment, intoxication, stimulation of appetite, antinociceptive actions (particularly against pain of ne
20 genous dynorphin had both pronociceptive and antinociceptive actions after nerve injury and induced G
21  desensitization of the channel resulting in antinociceptive actions against chemical stimulus modali
22 ll controversial, as both pronociceptive and antinociceptive actions have been reported.
23 or activation can mediate the prokinetic and antinociceptive actions of 5-HT(4)R agonists.
24  receptor may be responsible for some of the antinociceptive actions of certain CB2 receptor ligands.
25  (RVM) is a crucial site for the supraspinal antinociceptive actions of opioids.
26 gion are a potentially critical site for the antinociceptive actions of opioids.
27 nociceptin) which may mediate nociceptive or antinociceptive actions was determined using the [35S]GT
28 d 17a highlighted good anti-inflammatory and antinociceptive activities.
29   A series of pan-agonists was evaluated for antinociceptive activity (55 degrees C tail flick) in mi
30 l by electrophysiology and for their in vivo antinociceptive activity (acetic acid-induced writhing a
31 oying mu-, delta-, or kappa-agonism, but the antinociceptive activity after i.v. administration could
32           Analogue 2 produced dose-dependent antinociceptive activity following intravenous administr
33 nflammatory agent in an animal model and had antinociceptive activity in a pain model, which supports
34 Compounds 13 and 14 were evaluated for their antinociceptive activity in acute experimental models of
35                                Tiagabine had antinociceptive activity in both phase 1 (neurogenic pai
36                            E139 and E138 had antinociceptive activity in both phases of the formalin
37 onclusion our results indicate that E139 has antinociceptive activity in the formalin and hot plate t
38 ate (E139), an anticonvulsant enaminone, has antinociceptive activity in the hot plate test.
39 cular NPQ/spexin and NPQ 53-70 also produced antinociceptive activity in the warm water tail withdraw
40 s (Ki(delta) = 0.72 nM; Ki(mu) = 1.1 nM) and antinociceptive activity in vivo together with an increa
41 ble to activate TREK-1 and displaying potent antinociceptive activity in vivo.
42 dition, SIB-1663 (s.c. or i.c.v.) attenuated antinociceptive activity NIC given by the same route sug
43                                          The antinociceptive activity of an NT agonist (NT69L) and mo
44                                  The in vivo antinociceptive activity of compound 5b was evaluated by
45 48, a GABAB receptor antagonist, blocked the antinociceptive activity of E139.
46               In this study we evaluated the antinociceptive activity of five anilino enaminones E139
47  chemical stimulation (formalin) and (2) the antinociceptive activity of intrathecal and systemic mor
48                                          The antinociceptive activity of the cinnamoyloxycodeinones (
49  systemic administration of CYM51010 induced antinociceptive activity similar to morphine, and chroni
50 were partially sensitive to MEC, whereas the antinociceptive activity was completely sensitive to MEC
51                                      In vivo antinociceptive activity was demonstrated for 5c, 5d, an
52 rinic acetylcholine receptors appear to have antinociceptive activity, and acetylcholine release in t
53          In the hot plate test only E139 had antinociceptive activity.
54  with these two ligands have shown promising antinociceptive activity.
55   A flexible linker was required to maintain antinociceptive activity.
56                Morphine remains an excellent antinociceptive agent in these mice.
57  significant interest for the development of antinociceptive agents, is blocked by low nanomolar conc
58  centrally mediated (supraspinal and spinal) antinociceptive (analgesic) activity in various pain mod
59  15d-PGJ2 cream associated with MNs provides antinociceptive and anti-inflammatory effect, and can of
60 viable therapeutic approach to enhance their antinociceptive and anti-inflammatory effects, as well a
61 eceptors in the spinal cord mediate both the antinociceptive and antiallodynic actions of intrathecal
62 ) produced potent long-lasting (i.e., >24 h) antinociceptive and antiallodynic effects, which were bl
63 adation and therefore has been pursued as an antinociceptive and antiepileptic drug target.
64               One of the mechanisms by which antinociceptive and antiinflammatory effects of ADO can
65 is toxin (PTX)-sensitive manner and produces antinociceptive and antiinflammatory effects.
66 e development of spatiotemporally controlled antinociceptive and antiinflammatory therapy for arthrit
67 activities, is increasingly recognized as an antinociceptive and anxiolytic agent, effects which may
68  MOR-expressing dorsal horn neurons would be antinociceptive and of interest in the search for new ap
69 CB1) receptors has been shown to mediate the antinociceptive and other effects of systemically admini
70 re thought to act synergistically regulating antinociceptive and reward mechanisms.
71 raspinal injection of PAP protein has potent antinociceptive, antihyperalgesic, and antiallodynic eff
72 his mechanism also contributed to peripheral antinociceptive/antihyperalgesic effects of WIN because
73  inhibitors have been under investigation as antinociceptive, antiinflammatory, and anticonvulsant as
74      When administered systemically in mouse antinociceptive assays, N-benzyl-norBNI (1b) had only MO
75  tissue assays in vitro and in vivo in mouse antinociceptive assays.
76 n subjects were grouped as pronociceptive or antinociceptive based on whether they had greater thal-B
77 idant, anti-inflammatory, local anaesthetic, antinociceptive, cicatrizing, antiseptic, and especially
78 cending modulatory network with its pro- and antinociceptive components.
79 n turn could trigger descending serotonergic antinociceptive controls.
80 ectivity within and between default mode and antinociceptive descending modulation networks.
81 gnificant predictor of morphine half-maximal antinociceptive dose (ED50) values.
82 M also acutely displaced the spinal morphine antinociceptive dose-response curve to the right.
83 ightward displacement of the spinal morphine antinociceptive dose-response curve.
84     Unlike MOP receptor agonists, BU08028 at antinociceptive doses and approximately 10- to 30-fold h
85 gan does not produce locomotor inhibition at antinociceptive doses.
86 te or chronic pain, and for designing better antinociceptive drug therapies, such as the combined use
87 -Arg-Phe-NMeLys-NH(2), showed a long-lasting antinociceptive effect (>7 h), the peptides with d-Cit(2
88 06 (50-100 nmol/10 micro l) had its greatest antinociceptive effect against capsaicin-induced behavio
89 scle nociceptors, resulting in an unexpected antinociceptive effect against chronic mechanical hypera
90 gs indicate that gabapentin has a measurable antinociceptive effect and a stronger antihyperalgesic e
91                                         This antinociceptive effect can be blocked by lesions of brai
92 ice with DF2593A did not produce any further antinociceptive effect compared with C5aR(-/-) mice trea
93 SCI rats, the current data do not support an antinociceptive effect from an acute blockade of central
94                    12 g showed a significant antinociceptive effect in both models and is proposed as
95 that hyperbaric oxygen (HBO2) can produce an antinociceptive effect in models of acute pain.
96 opressin (HE) has previously demonstrated an antinociceptive effect in rats with a hind paw inflammat
97 ning were also evaluated for their potential antinociceptive effect in vivo and pharmacokinetic prope
98                   An additive or synergistic antinociceptive effect induced by simultaneous administr
99               We have demonstrated that this antinociceptive effect is centrally-mediated and is depe
100 ceptor knockout (KO) mice, we show that DHCB antinociceptive effect is primarily due to its interacti
101                      We hypothesize that the antinociceptive effect is through the modulation of the
102 study provides a molecular mechanism for the antinociceptive effect of acetaminophen and discloses sp
103 eted mice showed a 5.5-fold tolerance to the antinociceptive effect of acute morphine compared to pla
104 ts demonstrated that after nerve injury, the antinociceptive effect of acute morphine was significant
105                Our results indicate that the antinociceptive effect of buprenorphine in mice is micro
106           In support of this hypothesis, the antinociceptive effect of buprenorphine, but not morphin
107  5 min of the cobalt chloride injection, the antinociceptive effect of carbachol stimulation was bloc
108 tment with rimonabant completely blocked the antinociceptive effect of centrally administered WIN 55,
109 R heteromer selective antibody augmented the antinociceptive effect of DPDPE in vivo, and the DOR-KOR
110 ed on these experimental findings, the acute antinociceptive effect of HBO2 appears to involve neuron
111 specifically in the spinal cord in the acute antinociceptive effect of HBO2 in mice.
112                                          The antinociceptive effect of HBO2 was also significantly at
113 s evaluated for its potential to enhance the antinociceptive effect of intrathecal morphine in the ra
114    CatWalk gait analysis also supported that antinociceptive effect of l-THP as demonstrated by resto
115        We designed this study to investigate antinociceptive effect of l-THP in acute and chronic pai
116    The underlying mechanisms involved in the antinociceptive effect of MCS are not clearly understood
117  of DMSO (0, 0.2, 2, or 20%) would alter the antinociceptive effect of microinjecting morphine into t
118                             Tolerance to the antinociceptive effect of microinjecting morphine into t
119 4 (50 microg, i.c.v.) significantly enhanced antinociceptive effect of morphine (P < 0.05), through a
120  of CART (55-102) significantly enhanced the antinociceptive effect of morphine in the tail-flick tes
121 es that endogenous glutamate counteracts the antinociceptive effect of morphine in the vPAG.
122 reatment doses of methocinnamox, the maximal antinociceptive effect of morphine was decreased in fema
123            We have previously shown that the antinociceptive effect of nitrous oxide (N(2)O) in the r
124                    NTS2 is important for the antinociceptive effect of NT69L and morphine.
125 tor antagonist, levocabastine attenuated the antinociceptive effect of NT69L and the combined effect
126 hereas testosterone replacement restored the antinociceptive effect of OFQ in GDX males.
127 tors might induce tolerance, we measured the antinociceptive effect of the kappa agonist U50,488 usin
128                                          The antinociceptive effect of WIN55,212-2 was attenuated rel
129 ), and diestrous rats produced a significant antinociceptive effect on both tests.
130 rmalin, indicating that that fraction has an antinociceptive effect on inflammatory pain models.
131               We demonstrate a comprehensive antinociceptive effect on mechanical, cold and deep tiss
132 hyperbaric oxygen (HBO(2)) produces an acute antinociceptive effect that is dependent on nitric oxide
133                                              Antinociceptive effect was monitored at selected time po
134 inhibitors significantly reduced DOR-induced antinociceptive effect whereas inhibitors of 5-lipoxygen
135 ates visceral pain perception, indicating an antinociceptive effect, possibly through GPR35 receptors
136  rat TMJ skin did not induce any significant antinociceptive effect.
137 k test a dose of 2 mg/kg was required for an antinociceptive effect.
138 uced transgenic mice and measured the drug's antinociceptive effect.
139  protein to its receptors, thereby restoring antinociceptive effect.
140 rimary sensory afferents is known to have an antinociceptive effect.
141 e but at a slower rate than tolerance to its antinociceptive effect.
142 ugs displayed a supraspinal, but not spinal, antinociceptive effect.
143 fferent nerve pathways, as well as having an antinociceptive effect.
144 ining the nociceptive threshold and that its antinociceptive effects are closely linked to opioidergi
145  hypolocomotor, hypothermic, anxiogenic, and antinociceptive effects are not.
146 enetic activation of the PFC produces strong antinociceptive effects in a rat model (spared nerve inj
147 is idea, antagonist 18i (30 mg/kg ip) showed antinociceptive effects in an animal model of mild nerve
148                  In vivo, SAR127303 produces antinociceptive effects in assays of inflammatory and vi
149 ghest dose of 2 g/kg resulted in significant antinociceptive effects in both assays.
150  pathway accounts for essentially all of the antinociceptive effects in males, although females appea
151 tral nervous system (CNS), 3 exerts profound antinociceptive effects in mice and rats, which result f
152 enosine A(1) receptor (A(1)AR) agonists have antinociceptive effects in multiple preclinical models o
153 ociceptive effects, and offer opioid-sparing antinociceptive effects in myriad preclinical inflammato
154 addition, compound 28 exerted dose-dependent antinociceptive effects in several neuropathic pain mode
155 aversion, but elicited CB1 receptor-mediated antinociceptive effects in the chronic constriction nerv
156 (3a) is orally active and has dose-dependent antinociceptive effects in wild-type mice.
157                                          The antinociceptive effects of 3a were completely abolished
158 improved metabolic stability and could block antinociceptive effects of a KOR selective agonist, FE20
159 rphine pellets demonstrated tolerance to the antinociceptive effects of acute systemic morphine admin
160                                          The antinociceptive effects of AMP, when combined with the a
161  identify which subtypes are involved in the antinociceptive effects of cholinergic receptor activati
162 l via GIRK channels, as indicated by greater antinociceptive effects of GABA(B) or mu-opioid receptor
163                      Both pronociceptive and antinociceptive effects of HA are mediated by activation
164                        Importantly, both the antinociceptive effects of heroin and acquisition of her
165                   Thus, in tolerant rats the antinociceptive effects of high doses of morphine appear
166 ease does not contribute to tolerance to the antinociceptive effects of microinjecting morphine into
167 ntribution of endogenous RGS proteins to the antinociceptive effects of morphine and other opioid ago
168 th morphine into the vPAG enhanced the acute antinociceptive effects of morphine as measured by a lef
169 uced microglial reactivity and preserved the antinociceptive effects of morphine in male rats.
170 st nor-binalorphimine completely blocked the antinociceptive effects of morphine in morphine-infused
171         The increase greatly potentiated the antinociceptive effects of morphine in rAAV-muOR-infecte
172 ylamine blocked NSIA in rats tolerant to the antinociceptive effects of morphine, but, in contrast to
173 spinal afferents were less responsive to the antinociceptive effects of morphine, especially in the n
174 ependence disappears in rats tolerant to the antinociceptive effects of morphine, which may account f
175 n has been shown to produce tolerance to the antinociceptive effects of morphine.
176 al gray (PAG), a central locus mediating the antinociceptive effects of morphine.
177 le; thus, the sensitivity of the male to the antinociceptive effects of OFQ is not simply attributabl
178                                          The antinociceptive effects of OFQ were dose dependent in ma
179 ment of tolerance and cross-tolerance to the antinociceptive effects of opioid and cannabinoid-specif
180           Sigma-1 antagonism potentiates the antinociceptive effects of opioid drugs, so sigma-1 rece
181                 These data explain the rapid antinociceptive effects of peripherally administered CCR
182                        Here we show that the antinociceptive effects of spinal and systemic administr
183 2AR-dependent dissociation in the beneficial antinociceptive effects of THC and its detrimental amnes
184 gands (5d and 7b) were able to attenuate the antinociceptive effects of the cannabinoid agonist CP55,
185                                          The antinociceptive effects of the CB(2) receptor-selective
186  to acute THC and decreased tolerance to the antinociceptive effects of the drug, yet enhanced tolera
187  opioid analgesia, and underlies part of the antinociceptive effects of the widely prescribed tricycl
188 ), produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bre
189     In this study, we sought to evaluate the antinociceptive effects of various combinations of ethan
190 s, such as naloxone and naltrexone, elicited antinociceptive effects similar to that of partial agoni
191 s, the opioid antagonist naltrexone elicited antinociceptive effects similar to those of partial agon
192      Neurotensin (NT) is a neuropeptide with antinociceptive effects that are mediated through NT rec
193              Recently, BTX was found to have antinociceptive effects that are probably independent of
194 ese results demonstrate that l-THP possesses antinociceptive effects through spinal Sig-1R mechanism
195 aV1.7)-blocking toxin (ProToxin-II) to exert antinociceptive effects without motor impairment.
196 ding of how antidepressant drugs exert their antinociceptive effects, and new developments regarding
197 and monoacylglycerol lipase produce reliable antinociceptive effects, and offer opioid-sparing antino
198 serin (2mg/kg), at these doses, have similar antinociceptive effects, whereas the agonist, DOI, produ
199 oduced a PLA(2)-dependent synergism in their antinociceptive effects.
200 d half-lives of enkephalins, inducing potent antinociceptive effects.
201          The new diphenethylamines displayed antinociceptive efficacies with increased potencies than
202 tive allosteric modulator, was evaluated for antinociceptive efficacy and tolerance in models of neur
203      The resulting peptide, 4, exhibits full antinociceptive efficacy in the mouse warm water tail wi
204 , an ORL-1 receptor antagonist, enhanced the antinociceptive efficacy of buprenorphine in wild-type m
205            We have previously noted that the antinociceptive efficacy of morphine was significantly d
206 l and thermal stimuli accompanied by reduced antinociceptive efficacy of opioids and, in some models,
207       This tool may assist in predicting the antinociceptive efficacy of sigma1 receptor ligands.
208 al assays, and in vivo anti-inflammatory and antinociceptive efficacy.
209 rphine administration leads to a decrease in antinociceptive efficacy.
210                                           In antinociceptive evaluations using the warm-water tail-wi
211 d but not normal BAN and that NO may have an antinociceptive function and modulate bladder hyperactiv
212                                              Antinociceptive functions have been attributed to the PP
213 onists and cannabinoid preparations that are antinociceptive has important implications for the thera
214 ked reduction or complete elimination of the antinociceptive (hot plate test) effects of ethanol, oxo
215 l of the compounds were weak agonists in the antinociceptive, hypothermia, and spontaneous activity t
216 the acetylcholine agonist carbachol which is antinociceptive in the spinal cord.
217  have an enhanced TSP response compared with antinociceptive individuals, marked by facilitated ascen
218 ing reflects a balance of pronociceptive and antinociceptive influences; the contribution by the gast
219 kade of central CB1 receptors, HE's putative antinociceptive mechanism, in neuropathic SCI rats.
220       The data suggests a centrally mediated antinociceptive mechanism.
221                    The emerging diversity of antinociceptive mechanisms targeted by different classes
222 rvous system correlated with nociceptive and antinociceptive modulatory systems in mice.
223 ohol and nicotine have been shown to possess antinociceptive or analgesic effects.
224 eins as positive regulators of opioid spinal antinociceptive pathways.
225 rphine exposure may diminish spinal morphine antinociceptive potency by activating descending pain fa
226   Additionally, 7 demonstrated morphine-like antinociceptive potency in mice, indicating this compoun
227 ts with 0.32 mg/kg methocinnamox reduced the antinociceptive potency of morphine to that observed in
228 ue from female and male rats and reduced the antinociceptive potency of morphine.
229 cific RVM regions showing pronociceptive and antinociceptive processes (in line with previous animal
230 duced inflammatory pain enhanced the in vivo antinociceptive profile of i.p.-administered codeine (7
231  blood-brain barrier (BBB) correlated to its antinociceptive profile over a 168-h time course.
232 - and efflux and tissue biodistribution) and antinociceptive properties after peripheral administrati
233 mpound 13g exhibited the most potent in vivo antinociceptive properties, which are indicative of its
234  deficits induced by THC from its beneficial antinociceptive properties.
235 ly, this study aimed to evaluate whether the antinociceptive property of 15d-PGJ2 cream can be enhanc
236 ion of 15d-PGJ2 into the rat TMJ can provide antinociceptive relief against a subsequent noxious chal
237  with hyperbaric oxygen (HBO2) can elicit an antinociceptive response in models of acute pain.
238 hol and nicotine can result in a synergistic antinociceptive response that is at least partially medi
239  centrally in sickle mice correlative to the antinociceptive response.
240 t mice, GRK5 knockout mice exhibited reduced antinociceptive responses after morphine administration
241 1) receptor inverse agonist) were studied on antinociceptive responses following i.c. microinjections
242 retreatment with rimonabant had no effect on antinociceptive responses following intra-PAG improgan.
243 t were ineffective by themselves resulted in antinociceptive responses in both paradigms.
244  intra-accumbens dopamine release paralleled antinociceptive responses in naive and morphine pretreat
245 tions that betaarr2-KO mice display enhanced antinociceptive responses to acute THC and decreased tol
246 rks concerned with cognitive, autonomic, and antinociceptive responses to delivered and anticipated a
247 not differ from wild-type mice in short-term antinociceptive responses to morphine measured in the ta
248 eriaqueductal gray matter (vlPAG) attenuated antinociceptive responses to noxious thermal stimulation
249 ors interact synergistically to modulate the antinociceptive responses.
250 ygen at 3.5atm absolute) for 11min and their antinociceptive responsiveness was determined using the
251  conclude that nerve injury induces death of antinociceptive RVM neurons that can be reduced or aboli
252 dulla (VMM) are a major source of descending antinociceptive signals.
253                                              Antinociceptive studies with mice confirm that these gly
254                                              Antinociceptive synergy between intrathecally administer
255 emonstrating the PKC dependence of CLON-DELT antinociceptive synergy in mice.
256 eceptors (ARs) and opioid receptors produces antinociceptive synergy.
257 an alpha2AAR agonist required PKCepsilon for antinociceptive synergy.
258 sting the activation of brainstem-descending antinociceptive systems from the amygdala.
259 likely to subserve activating the descending antinociceptive systems of the brainstem from the amygda
260 timulation engages physiologically different antinociceptive systems to inhibit a spinal reflex, tail
261 c receptors that are activated by endogenous antinociceptive systems.
262                                              Antinociceptive testing in mice revealed 5 to be the mos
263 than the cinnamoylamino derivatives in mouse antinociceptive tests.
264 insic efficacy of opioid analgesics with two antinociceptive tests: hot water tail-withdrawal and ace
265  part of a program aimed at the discovery of antinociceptive therapy for inflammatory conditions, a s
266 pioid receptor function as a basis for novel antinociceptive therapy in arthritis.
267 rest, M119 was also able to attenuate acute, antinociceptive tolerance and dependence in mice treated
268 ly, these mice display substantially reduced antinociceptive tolerance and physical dependence.
269 elleted mice) enhanced the level of morphine antinociceptive tolerance assessed by the tail immersion
270 eated vlPAG morphine administration produces antinociceptive tolerance by modulating both pre- and po
271           Based on reports of suppression of antinociceptive tolerance by the delta antagonist naltri
272 dministration of CYM51010 resulted in lesser antinociceptive tolerance compared with morphine.
273 ation of NO production, antinociception, and antinociceptive tolerance development.
274 n, and indicate that NO is a key mediator of antinociceptive tolerance development.
275  kinase A (PKA) inhibitors reversed morphine antinociceptive tolerance in 3-day morphine-pelleted mic
276 entiate morphine antinociception and reverse antinociceptive tolerance in mice, through their ability
277 let-7 levels and partially attenuated opioid antinociceptive tolerance in mice.
278 S)-3,5-DHPG as well as in reversing morphine antinociceptive tolerance in mice.
279 that PKC or PKA inhibitors reversed morphine antinociceptive tolerance in mice.
280 in opiate withdrawal symptoms despite normal antinociceptive tolerance in the BDNF-deficient mice.
281 aarr2-KO) mice also fail to develop morphine antinociceptive tolerance in the hot-plate test, further
282                Moreover, KOR agonist-induced antinociceptive tolerance observed in vivo has also been
283 n of RSA 504 and RSA 601 did not demonstrate antinociceptive tolerance over 7 days of administration
284 or repeated morphine administration produced antinociceptive tolerance regardless of whether morphine
285 n addition, ABX prevented the development of antinociceptive tolerance to chronic morphine in both th
286  mechanical and thermal hypersensitivity and antinociceptive tolerance to morphine.
287 ompared to naive rats indicating that opioid antinociceptive tolerance was not present.
288 M1710 did not engage CB1 activity or produce antinociceptive tolerance, CB1-mediated cannabinoid with
289 fects, including persistent constipation and antinociceptive tolerance, limit its clinical efficacy.
290  14 did not produce locomotor effects, acute antinociceptive tolerance, or conditioned-place preferen
291 tagonists dose-dependently reversed morphine antinociceptive tolerance.
292 term use of morphine leads to development of antinociceptive tolerance.
293 en implicated in the development of morphine antinociceptive tolerance.
294 production coincided with the development of antinociceptive tolerance.
295 rsed the expression of 5- to 8-fold morphine antinociceptive tolerance.
296 ce only partly reversed the 45-fold level of antinociceptive tolerance.
297       Such pain may manifest behaviorally as antinociceptive tolerance.
298 d neuropathic pain and furthermore causes no antinociceptive tolerance.
299 eir effectiveness for oral application in an antinociceptive treatment regime.
300 e development of neuropathic pain and during antinociceptive treatment with these drugs alone or in c

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