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Journal articles on the topic 'Agonism avoidance'

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Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Spasov, Alexander A., Edwin E. Zvartau, Olesya Iu Grechko, Natalya V. Eliseeva, Yuliya V. Semenova, Olga A. Dravolina, Pavel M. Vasiliev, and Vera A. Anisimova. "Study of aversive and p38 mapk-inhibitory properties of kappa-agonist with analgesic activity – compound RU-1205." Research Results in Pharmacology 6, no. 3 (September 25, 2020): 59–65. http://dx.doi.org/10.3897/rrpharmacology.6.54558.

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Introduction: The clinical use of kappa-opioid agonists, despite their lack of significant drug potential, is limited by the development of severe sedation, dysphoria, depression, and anhedonia. To this date, there are kappa-opioid receptor agonists lacking these side effects due to the selective activation of intracellular signal transmission pathways without p38-MAPK-kinase activation. Materials and methods: We analyzed assessment of the docking energy of compound RU-1205 to the p38-MAPK active center by the method of similarity to SB203580. The study of possible aversive properties of RU-1205 (0.01–1 mg/kg s.c.) conducted in the tests of the intravenous self-administration and drug differentiation with butorphanol (0.01–0.3 mg/kg). The study of p38 MAPK-inhibitory activity was studied by the ability of RU-1205 to change the aversive properties of U50488 (10 mg/kg i.p.) compared to MAPK-kinase inhibitor SB203580 in the conditioned place avoidance test. Results: The spatial similarity coefficient of the RU-1205 molecule with SB203580 by the molecular conformation method was 1.14 (high similarity), and the docking energy was -8.7 Kcal/mol. RU-1205 did not possess any properties similar to those of butorphanol and did not demonstrate any primary reinforcing aversive properties in the development of intravenous self-administration reaction. Compound RU-1205 did not demonstrate any aversive properties in the conditioned place avoidance test, and reduced the development of aversion caused by U-50488, when they were used together. Discussion: The in silico analysis suggested that, in addition to agonism towards the kappa-opioid receptor, RU-1205 compound exhibits the properties of a p38 MAPK kinase inhibitor, which means it may have a double pharmacological activity. Conclusion: Kappa agonist – compound RU-1205 – is not a trigger of the development of behavioral patterns in animals corresponding to the development of addiction/dysphoria. The mechanism of such an activity may be associated with an inhibitory effect of compound RU-1205 on neuronal p38-MAPK-kinase.

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2

Stuchlik, A., L. Rehakova, L. Rambousek, and K. Vales. "P41 AGONISM ON D2 DOPAMINE RECEPTORS IMPROVES AND D2 ANTAGONISM IMPAIRS SPATIAL COGNITION IN THE ACTIVE ALLOTHETIC PLACE AVOIDANCE TASK." Behavioural Pharmacology 17, no. 5-6 (September 2006): 552. http://dx.doi.org/10.1097/00008877-200609000-00082.

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3

Van Belle, Sarie, Alejandro Estrada, and Anthony Di Fiore. "Kin-biased spatial associations and social interactions in male and female black howler monkeys (Alouatta pigra)." Behaviour 151, no. 14 (2014): 2029–57. http://dx.doi.org/10.1163/1568539x-00003229.

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Kinship has been shown to play a crucial role in shaping the social structure of animal societies. We examined the genetic relationships of adult and sub-adult males () and females () from five social groups of black howler monkeys (Alouatta pigra) at Palenque National Park, Mexico, by genotyping each individual at 21 microsatellite markers. These findings were related to patterns of intragroup spatial associations and affiliative and agonistic interactions recorded over a 28-month period of behavioural observation in the field. We demonstrate that the social structure of this black howler monkey population is dominated by strong social relationships and high degrees of genetic relatedness among females. Female kin had stronger relationships because they were less aggressive to each other than female non-kin. Nevertheless, females resident in the same social group frequently spent time close to one another and affiliated with each other regardless of kinship. Relationships among males from the same social group were based on avoidance and tolerance, as males rarely interacted either affiliatively or agonistically and spent limited time close to one another. Nonetheless, kinship was a significant predictor of agonistic interactions among males, with unrelated or distantly related males engaging in agonism at higher rates than close male kin. Adult males and females rarely co-resided with adult kin from the opposite sex, and they affiliated and spatially associated at rates intermediary to those among females and those among males.

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Sears, Malcolm R. "Epidemiological Trends in Asthma." Canadian Respiratory Journal 3, no. 4 (1996): 261–68. http://dx.doi.org/10.1155/1996/410215.

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Many markers of asthma morbidity have shown substantial increases over the past two decades, including family physician visits, use of anti-asthma medications, emergency room visits and hospital admissions. The reported prevalence of diagnosed asthma and of wheezing has increased, especially in children, with accompanying evidence of increased atopy and increased airway responsiveness. Allergen exposure and parental smoking are significant risk factors for childhood wheezing, whereas the influence of outdoor air pollution is uncertain. Increasing use of beta-agonist treatment, which appears to increase the severity of asthma by increasing early and late responses to allergen, may contribute to increased morbidity and mortality, especially if potent beta-agonists are used. Risk factors for asthma mortality include age, smoking, allergy and airway lability, as well as over-reliance on beta-agonists and poor compliance with other aspects of treatment. Following withdrawal of the potent beta-agonist fenoterol in New Zealand, both hospital admissions and mortality from asthma fell abruptly. Continued patient and physician education, with emphasis on avoidance of risk factors and use of appropriate treatment, should reduce morbidity and mortality from asthma in Canada.

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5

Sato, Tomoaki, Koh-ichi Tanaka, Yoshiko Ohnishi, Masahiro Irifune, and Takashige Nishikawa. "Effect of Donepezil on Group II mGlu Receptor Agonist- or Antagonist-Induced Amnesia on Passive Avoidance in Mice." Neural Plasticity 10, no. 4 (2003): 319–25. http://dx.doi.org/10.1155/np.2003.319.

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We examined the effect of the acetylcholinesterase (ACHE) inhibitor, donepezil hydrocloride (DONP), on group II metabotropic glutamate (mGlu) receptor agonist- or antagonist-induced amnesia in the step-through passive avoidance task in male mice. DCG-IV, a group II mGlu receptor agonist, at dose of 50 ng and LY341495, a group II mGlu receptor antagonist, at dose of 300 ng, significantly attenuated the latency on the step-through task. The subcutaneous injection of DONP at dose of 1 mg/kg 1 hour before passive avoidance performance ameliorated the amnesia induced by DCG-IV and LY341495, whereas donepezil alone did not affect task latency. The results suggest that activation of group II mGlu receptors and disinhibition of the cAMP/PKA signaling pathway (caused by group II mGlu receptor antagonist) have a negative action on step-through passive avoidance memory performance, and that group II mGlu receptors and ACh interact to modulate learning and memory function.

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6

Zarrindast, M. R., H. Niasari, S. Ahmadi, and B. Shafaghi. "N-methyl-D-aspartate Receptors are Involved in the Effect of Lithium on Passive Avoidance Memory in Mice." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)71083-1.

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In the present study, the effects of intracerebroventricular (i.c.v.) injections of N-methyl-D-aspartate (NMDA) receptor agonist and antagonist on the lithium state-dependent memory have been investigated. For memory assessment, one-trial step-down passive avoidance task was used in adult male NMRI mice. Post-training intraperitoneal (i.p.) administration of lithium (10 mg/kg) impaired the memory of passive avoidance task. Pre-test administration of the same dose of the drug (10 mg/kg) restored impairment of memory by lithium given after training. This is known as state-dependent memory. In addition, pre-test administration of both NMDA receptor agonist (NMDA; 0.01 and 0.1 ng/mouse, i.c.v.) and the non-competitive NMDA receptor antagonist, MK-801 (0.1 and 0.5 mg/mouse, i.c.v) also restored impairment of memory induced by post-training lithium. On the other hand, pre-test co-administration of ineffective dose of NMDA (0.001 ng/mouse, i.c.v.) or MK-801 (0.001 mg/mouse, i.c.v) with lower doses of lithium (1.25, 2.5 and 5 mg/kg, i.p.) increased the restoration of memory by lithium. The results suggest that NMDA receptors are involved, at least partly, in the lithium state-dependent memory of passive avoidance task.

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7

Benetti, Fernando, and Ivan Izquierdo. "Histamine infused into basolateral amygdala enhances memory consolidation of inhibitory avoidance." International Journal of Neuropsychopharmacology 16, no. 7 (August 1, 2013): 1539–45. http://dx.doi.org/10.1017/s1461145712001514.

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Abstract The role of the basolateral amygdala (BLA) in the consolidation of aversive memory is well established. Here we investigate the involvement of the histaminergic system in BLA on this variable. Rats were chronically implanted with bilateral cannulae in the BLA and after recovery were trained in a one-trial step-down inhibitory avoidance task. Immediately after training histaminergic compounds either alone or in combination were infused through the cannulae. Memory was assessed in test sessions carried out 24 h after the training session. Post-training histamine (1–10 nmol; 0.5 µl/side) enhanced consolidation and the histamine H3 receptor antagonist thioperamide (50 nmol; 0.5 µl/side) impaired memory consolidation. The effect was shared by the histamine N-methyltransferase inhibitor SKF-91844 (50 nmol; 0.5 µl/side) as well as by the H3 receptor agonist imetit (10 nmol; 0.5 µl/side). The promnesic action of histamine was unaffected by the H1 receptor antagonist pyrilamine (50 nmol; 0.5 µl/side). The H1 receptor agonist pyridylethylamine (10 nmol; 0.5 µl/side), the H2 agonist dimaprit (10 nmol; 0.5 µl/side) and the H2 antagonist ranitidine (50 nmol; 0.5 µl/side) were ineffective. Histaminergic compounds infused into the BLA had no effect on open-field or elevated plus-maze behaviour. The data show that histamine induces a dose-dependent mnemonic effect in rats and indicate that this reflects a role of endogenous histamine in the BLA mediated by H3 receptors.

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8

Johnson, Jill R., Stephanie R. Pacitto, Jonathan Wong, Elliot W. Archer, Stefan Eirefelt, Anna Miller-Larsson, and Manel Jordana. "Combined budesonide/formoterol therapy in conjunction with allergen avoidance ameliorates house dust mite-induced airway remodeling and dysfunction." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 5 (November 2008): L780—L788. http://dx.doi.org/10.1152/ajplung.90229.2008.

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Allergic asthma is characterized by airway inflammation in response to chronic allergen exposure, resulting in remodeling of the airway wall accompanied by dysfunctional airway physiology. However, a link between the immune-inflammatory response to allergen and changes to airway structure and physiology has not yet been fully elucidated. Moreover, the impact of inhaled corticosteroids and β2-agonists, the primary pharmacotherapy for asthma, on this process has not been completely evaluated. In this study, we employed a murine model of chronic exposure to a common environmental aeroallergen, house dust mite, to recapitulate the phenotype of clinical asthma. By examining the therapeutic effects of corticosteroid/β2-agonist combination therapy with budesonide/formoterol (BUD/FORM) in this model of airway disease, we endeavored to determine the impact of BUD/FORM on lung inflammation, structure, and physiology. BUD/FORM was delivered either while allergen exposure was ongoing (concurrent therapy) or following the cessation of allergen exposure (postexposure therapy). Our results show that airway inflammation was substantially reduced in BUD/FORM-treated mice in the concurrent therapy group, whereas in the postexposure therapy group airway inflammation spontaneously resolved. In contrast, BUD/FORM was most effective in resolving several aspects of airway remodeling and bronchial hyperreactivity when delivered in conjunction with allergen withdrawal. This study demonstrates that although both BUD/FORM therapy and allergen avoidance independently reduce airway inflammation, only BUD/FORM therapy in conjunction with allergen avoidance can effectively reverse airway remodeling and bronchial hyperreactivity induced by chronic allergen exposure.

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9

Martin, Gregory E., Donald J. Rossi, and Michael F. Jarvis. "Adenosine agonists reduce conditioned avoidance responding in the rat." Pharmacology Biochemistry and Behavior 45, no. 4 (August 1993): 951–58. http://dx.doi.org/10.1016/0091-3057(93)90146-k.

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10

BRUCE, K. R., H. STEIGER, N. M. KOERNER, M. ISRAEL, and S. N. YOUNG. "Bulimia nervosa with co-morbid avoidant personality disorder: behavioural characteristics and serotonergic function." Psychological Medicine 34, no. 1 (January 2004): 113–24. http://dx.doi.org/10.1017/s003329170300864x.

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Background. Separate lines of research link lowered serotonin tone to interpersonal submissiveness and bulimia nervosa (BN). We explored the impact of co-morbid avoidant personality disorder (APD), as a proxy for submissiveness, on behavioural inhibition and serotonin function in women with BN.Method. Participants included women with BN with co-morbid APD (BNA+, N=13); women with BN but without APD (BNA−, N=23), and control women with neither BN nor APD (N=23). The women were assessed for psychopathological tendencies and eating disorder symptoms, and participated in a computerized laboratory task that measured behavioural inhibition and disinhibition. Participants also provided blood samples for measurement of serial prolactin responses following oral administration of the partial 5-HT agonist meta-chlorophenylpiperazine (m-CPP).Results. The BNA+ group had higher scores than the other groups on self-report measures of submissiveness, social avoidance, restricted emotional expression, affective instability and self-harming behaviours. Compared with the other groups, the BNA+ group tended to be more inhibited under cues for punishment on the computerized task and to have blunted prolactin response following m-CPP. The bulimic groups did not differ from each other on current eating symptoms or on frequencies of other mental disorders.Conclusions. Findings indicate that women with BN and co-morbid APD may be characterized by interpersonal submissiveness and avoidance, affective instability, self-harm, behavioural inhibition in response to threat and lower sensitivity to serotonergic activation. These findings may indicate common, serotonergic factors, associated with social submissiveness, behavioural inhibition to threat and BN.

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11

Overstreet, David H., Ruth A. Booth, and Donald J. Jenden. "Effects of an irreversible muscarinic agonist (BM123) on avoidance and spontaneous alternation performance." Pharmacology Biochemistry and Behavior 31, no. 2 (October 1988): 337–43. http://dx.doi.org/10.1016/0091-3057(88)90355-3.

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12

Shiri, Mariam, Alireza Komaki, Shahrbanoo Oryan, Masoumeh Taheri, Hamidreza Komaki, and Farshid Etaee. "Effects of cannabinoid and vanilloid receptor agonists and their interaction on learning and memory in rats." Canadian Journal of Physiology and Pharmacology 95, no. 4 (April 2017): 382–87. http://dx.doi.org/10.1139/cjpp-2016-0274.

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Despite previous findings on the effects of cannabinoid and vanilloid systems on learning and memory, the effects of the combined stimulation of these 2 systems on learning and memory have not been studied. Therefore, in this study, we tested the interactive effects of cannabinoid and vanilloid systems on learning and memory in rats by using passive avoidance learning (PAL) tests. Forty male Wistar rats were divided into the following 4 groups: (1) control (DMSO+saline), (2) WIN55,212–2, (3) capsaicin, and (4) WIN55,212–2 + capsaicin. On test day, capsaicin, a vanilloid receptor type 1 (TRPV1) agonist, or WIN55,212–2, a cannabinoid receptor (CB1/CB2) agonist, or both substances were injected intraperitoneally. Compared to the control group, the group treated with capsaicin (TRPV1 agonist) had better scores in the PAL acquisition and retention test, whereas treatment with WIN55,212–2 (CB1/CB2 agonist) decreased the test scores. Capsaicin partly reduced the effects of WIN55,212–2 on PAL and memory. We conclude that the acute administration of a TRPV1 agonist improves the rats’ cognitive performance in PAL tasks and that a vanilloid-related mechanism may underlie the agonistic effect of WIN55,212–2 on learning and memory.

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13

Mahiout, Selma, and Raimo Pohjanvirta. "Aryl hydrocarbon receptor agonists trigger avoidance of novel food in rats." Physiology & Behavior 167 (December 2016): 49–59. http://dx.doi.org/10.1016/j.physbeh.2016.08.033.

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14

Tsuji, Minoru, Hiroshi Takeda, and Teruhiko Matsumiya. "Modulation of Passive Avoidance in Mice by the 5-HT1A Receptor Agonist Flesinoxan: Comparison with the Benzodiazepine Receptor Agonist Diazepam." Neuropsychopharmacology 28, no. 4 (October 3, 2002): 664–74. http://dx.doi.org/10.1038/sj.npp.1300080.

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15

Kajbaf, F., R. Ahmadi, R. Fatemi Tabatabaie, and E. Safarpoor. "Effect of Intrahippocampal Ghrelin Agonist Administration on Passive Avoidance Learning and Anxiety in Rats." Pakistan Journal of Biological Sciences 15, no. 22 (November 1, 2012): 1063–68. http://dx.doi.org/10.3923/pjbs.2012.1063.1068.

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16

Quartermain, David, Jonathan Clemente, and Anne Shemer. "The 5-HT1A agonist tandospirone disrupts retention but not acquisition of active avoidance learning." Pharmacology Biochemistry and Behavior 48, no. 3 (July 1994): 805–7. http://dx.doi.org/10.1016/0091-3057(94)90350-6.

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17

Samardžić, Janko, Dubravka Švob Štrac, Miljana Obradović, Dejan Oprić, and Dragan I. Obradović. "DMCM, a benzodiazepine site inverse agonist, improves active avoidance and motivation in the rat." Behavioural Brain Research 235, no. 2 (December 2012): 195–99. http://dx.doi.org/10.1016/j.bbr.2012.07.032.

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18

Brioni, Jorge D., and Stephen P. Arneric. "Nicotinic receptor agonists facilitate retention of avoidance training: Participation of dopaminergic mechanisms." Behavioral and Neural Biology 59, no. 1 (January 1993): 57–62. http://dx.doi.org/10.1016/0163-1047(93)91159-k.

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19

NAKAHARA, Noboru, Yoshinori IGA, Fumio MIZOBE, and Gosei KAWANISHI. "Amelioration of Experimental Amnesia (Passive Avoidance Failure) in Rodents by the Selective M1 Agonist AF102B." Japanese Journal of Pharmacology 48, no. 4 (1988): 502–6. http://dx.doi.org/10.1254/jjp.48.502.

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20

Holly, Elizabeth N., Bree Ebrecht, and Adam J. Prus. "The neurotensin-1 receptor agonist PD149163 inhibits conditioned avoidance responding without producing catalepsy in rats." European Neuropsychopharmacology 21, no. 7 (July 2011): 526–31. http://dx.doi.org/10.1016/j.euroneuro.2010.12.004.

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21

Zarrindast, Mohammad Reza, and Bijan Shafaghi. "Effects of adenosine receptor agonists and antagonists on acquisition of passive avoidance learning." European Journal of Pharmacology 256, no. 3 (May 1994): 233–39. http://dx.doi.org/10.1016/0014-2999(94)90548-7.

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22

Viu, E., A. Zapata, J. Capdevila, P. Skolnick, and R. Trullas. "GlycineB Receptor Antagonists and Partial Agonists Prevent Memory Deficits in Inhibitory Avoidance Learning." Neurobiology of Learning and Memory 74, no. 2 (September 2000): 146–60. http://dx.doi.org/10.1006/nlme.1999.3947.

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23

Zang, Kai-Kai, Xiao Xiao, Li-Qiang Chen, Yan Yang, Qi-Lai Cao, Yu-Long Tang, Su-Su Lv, Hong Cao, Ling Zhang, and Yu-Qiu Zhang. "Distinct Function of Estrogen Receptors in the Rodent Anterior Cingulate Cortex in Pain-related Aversion." Anesthesiology 133, no. 1 (April 22, 2020): 165–84. http://dx.doi.org/10.1097/aln.0000000000003324.

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Background Brain-derived estrogen is implicated in pain-related aversion; however, which estrogen receptors mediate this effect remains unclear. This study hypothesized that the different estrogen receptors in the rostral anterior cingulate cortex play distinct roles in pain-related aversion. Methods Formalin-induced conditioned place avoidance and place escape/avoidance paradigms were used to evaluate pain-related aversion in rodents. Immunohistochemistry and Western blotting were used to detect estrogen receptor expression. Patch-clamp recordings were used to examine N-methyl-d-aspartate–mediated excitatory postsynaptic currents in rostral anterior cingulate cortex slices. Results The administration of the estrogen receptor-β antagonist 4-(2-phenyl-5,7-bis [trifluoromethyl] pyrazolo [1,5-a] pyrimidin-3-yl) phenol (PHTPP) or the G protein–coupled estrogen receptor-1 antagonist (3aS*,4R*,9bR*)-4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-3H-cyclopenta [c] quinolone (G15) but not the estrogen receptor-α antagonist 1,3-bis (4-hydroxyphenyl)-4-methyl-5-[4-(2-piperidinylethoxy) phenol]-1H-pyrazole dihydrochloride (MPP) into the rostral anterior cingulate cortex blocked pain-related aversion in rats (avoidance score, mean ± SD: 1,3-bis [4-hydroxyphenyl]-4-methyl-5-(4-[2-piperidinylethoxy] phenol)-1H-pyrazole dihydrochloride (MPP): 47.0 ± 18.9%, 4-(2-phenyl-5,7-bis [trifluoromethyl] pyrazolo [1,5-a] pyrimidin-3-yl) phenol (PHTPP): −7.4 ± 20.6%, and [3aS*,4R*,9bR*]-4-[6-bromo-1,3-benzodioxol-5-yl]-3a,4,5,9b-3H-cyclopenta [c] quinolone (G15): −4.6 ± 17.0% vs. vehicle: 46.5 ± 12.2%; n = 7 to 9; P < 0.0001). Consistently, estrogen receptor-β knockdown but not estrogen receptor-α knockdown by short-hairpin RNA also inhibited pain-related aversion in mice (avoidance score, mean ± SD: estrogen receptor-α–short-hairpin RNA: 26.0 ± 7.1% and estrogen receptor-β–short-hairpin RNA: 6.3 ± 13.4% vs. control short-hairpin RNA: 29.1 ± 9.1%; n = 7 to 10; P < 0.0001). Furthermore, the direct administration of the estrogen receptor-β agonist 2,3-bis (4-hydroxyphenyl)-propionitrile (DPN) or the G protein–coupled estrogen receptor-1 agonist (±)-1-([3aR*,4S*,9bS*]-4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta [c]quinolin-8-yl)-ethanone (G1) into the rostral anterior cingulate cortex resulted in conditioned place avoidance (avoidance score, mean ± SD: 2,3-bis (4-hydroxyphenyl)-propionitrile (DPN): 35.3 ± 9.5% and (±)-1-([3aR*,4S*,9bS*]-4-(6-bromo-1,3-benzodioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta [c]quinolin-8-yl)-ethanone (G1): 43.5 ± 22.8% vs. vehicle: 0.3 ± 14.9%; n = 8; P < 0.0001) but did not affect mechanical or thermal sensitivity. The activation of the estrogen receptor-β/protein kinase A or G protein–coupled estrogen receptor-1/protein kinase B pathway elicited the long-term potentiation of N-methyl-d-aspartate–mediated excitatory postsynaptic currents. Conclusions These findings indicate that estrogen receptor-β and G protein–coupled estrogen receptor-1 but not estrogen receptor-α in the rostral anterior cingulate cortex contribute to pain-related aversion by modulating N-methyl-d-aspartate receptor–mediated excitatory synaptic transmission. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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Senda, Toshihiko, Kiyoshi Matsuno, Tetsuya Kobayashi, and Shiro Mita. "Reduction of the Scopolamine-Induced Impairment of Passive-Avoidance Performance by σ Receptor Agonist in Mice." Physiology & Behavior 61, no. 2 (February 1997): 257–64. http://dx.doi.org/10.1016/s0031-9384(96)00447-7.

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Nakahara, Noboru, Yoshinori Iqa, Fumio Mizobe, and Gosei Kawanishi. "Beneficial effects of a selective M1-agonist AF102B on experimental amnesia models in a passive avoidance task." Japanese Journal of Pharmacology 49 (1989): 271. http://dx.doi.org/10.1016/s0021-5198(19)56649-5.

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26

Parent, Marise B., and Paul E. Gold. "Intra-septal infusions of glucose potentiate inhibitory avoidance deficits when co-infused with the GABA agonist muscimol." Brain Research 745, no. 1-2 (January 1997): 317–20. http://dx.doi.org/10.1016/s0006-8993(96)01206-1.

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27

Jha, Gautam Gopalji, and Engle Jeff. "Suppression of testosterone production using abiraterone acetate (AA) with or without androgen deprivation therapy (ADT) in metastatic castration resistant prostate cancer (mCRPC)." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): 5049. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.5049.

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5049 Background: Patients with metastatic prostate cancer (mPC) are treated with lifelong ADT even after progression and every treatment for mPC has been tested only in the setting of androgen deprivation. Androgen synthesis inhibitor AA which inhibits synthesis of androgen that later get converted to testosterone has been studied and approved only alongside ADT similar to all other agents that have no or limited activity on testosterone suppression. We reviewed the ability of AA to sufficiently suppress testosterone levels as compared to AA plus ADT and its potential impact on cost savings. Methods: This retrospective study included consecutive patients with mCRPC treated with AA alone or in combination with ADT (in absence of orchiectomy) who had been followed with serial testosterone values on therapy. A cost analysis was performed to determine the cost avoidance by omitting leuprolide injections while on AA. The cost avoidance was calculated by multiplying the total number of injections by the wholesale acquisition cost of $5252.86 for a three month leuprolide injection. Results: Of 57 patients included in the final analysis, 36 received AA plus ADT, 10 received AA alone, and 11 started off with AA plus ADT before transitioning to AA alone. Testosterone levels were drawn 235 times. Testosterone was undetectable (below < 2 ng/dl) in both arms, 134 of 152 in combination arm and 86 of 99 in the AA alone arm. The median testosterone concentration when detectable was 3 ng/dL in AA alone and 3.5 ng/dL in AA plus ADT. None in the combination arm and only one testosterone value in AA arm had testosterone > than 30 ng/dl. The mean duration of AA use in this study was close to one year, and the total duration of therapy was approximately 61 years which could result in elimination of 244 leuprolide administrations and approximately $1.29 million in total cost savings. Conclusions: AA alone is able to effectively suppress testosterone synthesis in patients with prostate cancer. ADT with GnRH agonist or antagonist can be safely withheld while on therapy with AA and testosterone values followed to confirm adequate androgen suppression. This has acquired new significance after studies in patients with hormone sensitive disease where median duration of treatment was 33 months which could translate to an avoidable expense of $55.5 million for 960 patients in ‘STAMPEDE’ study and $34.5 million in ‘LATITUDE’ study from leuprolide administration in combination arm.

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Jafari-Sabet, Majid, Hamed Mofidi, and Mohammad-Sadegh Attarian-Khosroshahi. "NMDA receptors in the dorsal hippocampal area are involved in tramadol state-dependent memory of passive avoidance learning in mice." Canadian Journal of Physiology and Pharmacology 96, no. 1 (January 2018): 45–50. http://dx.doi.org/10.1139/cjpp-2017-0228.

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The precise neurobiological mechanisms of tramadol abuse underlying the cognitive function are still unknown. The aim of the present study was to examine the possible effects of intra-CA1 injections of N-methyl-d-aspartate (NMDA), a glutamate NMDA receptor (NMDAR) agonist, and d,l-2-amino-5-phosphonopentanoic acid (DL-AP5), a competitive NMDAR antagonist, on tramadol state-dependent memory. A single-trial step-down passive avoidance task was used for the assessment of memory retrieval in adult male NMRI mice. Post-training i.p. administration of an atypical μ-opioid receptor agonist, tramadol (2.5 and 5 mg/kg), dose-dependently induced impairment of memory retention. Pre-test injection of tramadol (2.5 and 5 mg/kg) induced state-dependent retrieval of the memory acquired under post-training administration of tramadol (5 mg/kg) influence. Pre-test intra-CA1 injection of NMDA (10−5 and 10−4 μg/mouse) 5 min before the administration of tramadol (5 mg/kg, i.p.) dose-dependently inhibited tramadol state-dependent memory. Pre-test intra-CA1 injection of DL-AP5 (0.25 and 0.5 μg/mouse) reversed the memory impairment induced by post-training administration of tramadol (5 mg/kg). Pre-test administration of DL-AP5 (0.25 and 0.5 μg/mouse) with an ineffective dose of tramadol (1.25 mg/kg) restored the retrieval and induced tramadol state-dependent memory. It can be concluded that dorsal hippocampal NMDAR mechanisms play an important role in the modulation of tramadol state-dependent memory.

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Ukai, Makoto, Yoshiko Watanabe, and Tsutomu Kameyama. "Endomorphins 1 and 2, endogenous μ-opioid receptor agonists, impair passive avoidance learning in mice." European Journal of Pharmacology 421, no. 2 (June 2001): 115–19. http://dx.doi.org/10.1016/s0014-2999(01)01009-3.

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Ensler, K., C. N. Ryan, and J. L. Evenden. "Effects of repeated treatment with 5-HT1A agonists on active avoidance responding in the rat." Psychopharmacology 112, no. 1 (August 1993): 45–54. http://dx.doi.org/10.1007/bf02247362.

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McElroy, John F., Jay J. Stimmel, and James M. O'Donnell. "Effects of centrally acting beta adrenergic agonists on discrete trial conditioned avoidance behavior in rats." Psychopharmacology 97, no. 1 (January 1989): 108–14. http://dx.doi.org/10.1007/bf00443423.

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Fernando, A., G. Urcelay, A. Mar, A. Dickinson, and T. Robbins. "Free-Operant Avoidance Behavior by Rats after Reinforcer Revaluation Using Opioid Agonists and D-Amphetamine." Journal of Neuroscience 34, no. 18 (April 30, 2014): 6286–93. http://dx.doi.org/10.1523/jneurosci.4146-13.2014.

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Yamashita, Paula SM, Daiane S. Rosa, Christopher A. Lowry, and Helio Zangrossi. "Serotonin actions within the prelimbic cortex induce anxiolysis mediated by serotonin 1a receptors." Journal of Psychopharmacology 33, no. 1 (December 19, 2018): 3–11. http://dx.doi.org/10.1177/0269881118817384.

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Background: Serotonin plays an important role in the regulation of anxiety, acting through complex modulatory mechanisms within distinct brain structures. Serotonin can act through complex negative feedback mechanisms controlling the neuronal activity of serotonergic circuits and downstream physiologic and behavioral responses. Administration of serotonin or the serotonin 1A receptor agonist, (±)-8-hydroxy-2-(dipropylamino)tetralin (8-OH-DPAT), into the prefrontal cortex, inhibits anxiety-like responses. The prelimbic area of the prefrontal cortex regulates serotonergic neurons within the dorsal raphe nucleus and is involved in modulating anxiety-like behavioral responses. Aims: This study aimed to investigate the serotonergic role within the prelimbic area on anxiety- and panic-related defensive behavioral responses. Methods: We investigated the effects of serotonin within the prelimbic area on inhibitory avoidance and escape behaviors in the elevated T-maze. We also extended the investigation to serotonin 1A, 2A, and 2C receptors. Results: Intra-prelimbic area injection of serotonin or 8-OH-DPAT induced anxiolytic effects without affecting escape behaviors. Previous administration of the serotonin 1A receptor antagonist, WAY-100635, into the prelimbic area counteracted the anxiolytic effects of serotonin. Neither the serotonin 2A nor the serotonin 2C receptor preferential agonists, (±)-2,5-dimethoxy-4-iodoamphetamine (DOI) and 6-chloro-2-(1-piperazinyl) pyrazine (MK-212), respectively, affected behavioral responses in the elevated T-maze. Conclusion: Facilitation of serotonergic signaling within the prelimbic area of rats induced an anxiolytic effect in the elevated T-maze test, which was mediated by local serotonin 1A receptors. This inhibition of anxiety-like defensive behavioral responses may be mediated by prelimbic area projections to neural systems controlling anxiety, such as the dorsal raphe nucleus or basolateral amygdala.

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Sanna, Fabrizio, Maria Giuseppa Corda, Maria Rosaria Melis, Maria Antonietta Piludu, Stefan Löber, Harald Hübner, Peter Gmeiner, Antonio Argiolas, and Osvaldo Giorgi. "Dopamine agonist-induced penile erection and yawning: A comparative study in outbred Roman high- and low-avoidance rats." Pharmacology Biochemistry and Behavior 109 (August 2013): 59–66. http://dx.doi.org/10.1016/j.pbb.2013.05.002.

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Jafari-Sabet, Majid, Mohammad-Reza Zarrindast, Mehdi Rezayat, Ameneh Rezayof, and Bijan Djahanguiri. "The influence of NMDA receptor agonist and antagonist on morphine state-dependent memory of passive avoidance in mice." Life Sciences 78, no. 2 (November 2005): 157–63. http://dx.doi.org/10.1016/j.lfs.2005.04.040.

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Suzuki, Masanori, Takashi Yamaguchi, Yukiko Ozawa, Akihiko Iwai, and Minoru Yamamoto. "Effect of YM796, a novel muscarinic agonist, on the impairment of passive avoidance response in senescence-accelerated mice." Pharmacology Biochemistry and Behavior 51, no. 4 (August 1995): 623–26. http://dx.doi.org/10.1016/0091-3057(94)00425-i.

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Lin, Chao, Ren-Yi Liu, and Yu-Cang Du. "Cysteinyl methyl ester of AVP(4–8), a potent agonist on the maintenance of passive avoidance in rats." Peptides 11, no. 4 (July 1990): 633–39. http://dx.doi.org/10.1016/0196-9781(90)90172-2.

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Elías, P. "Chronic aerial exposure to glucorticoids or beta-agonists affects avoidance learning and exploratory motivation in rats." Behavioural Brain Research 149, no. 1 (February 4, 2004): 95–105. http://dx.doi.org/10.1016/s0166-4328(03)00222-5.

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Haraguchi, Hirofumi, and Hisashi Kuribara. "Behavioral Effects of Adenosine Agonists: Evaluation by Punishment, Discrete Shuttle Avoidance and Activity Tests in Mice." Japanese Journal of Pharmacology 55, no. 3 (1991): 303–10. http://dx.doi.org/10.1016/s0021-5198(19)39931-7.

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Haraguchi, Hirofumi, and Hisashi Kuribara. "Behavioral effects of adenosine agonists: Evaluation by punishment, discrete shuttle avoidance and activity tests in mice." Japanese Journal of Pharmacology 55, no. 3 (1991): 303–10. http://dx.doi.org/10.1254/jjp.55.303.

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Khavandgar, S. "The Effects of Adenosine Receptor Agonists and Antagonists on Morphine State-Dependent Memory of Passive Avoidance." Neurobiology of Learning and Memory 78, no. 2 (September 2002): 390–405. http://dx.doi.org/10.1006/nlme.2002.4071.

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42

Kruk-Slomka, Marta, Anna Boguszewska-Czubara, Tomasz Slomka, Barbara Budzynska, and Grazyna Biala. "Correlations between the Memory-Related Behavior and the Level of Oxidative Stress Biomarkers in the Mice Brain, Provoked by an Acute Administration of CB Receptor Ligands." Neural Plasticity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/9815092.

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The endocannabinoid system, through cannabinoid (CB) receptors, is involved in memory-related responses, as well as in processes that may affect cognition, like oxidative stress processes. The purpose of the experiments was to investigate the impact of CB1 and CB2 receptor ligands on the long-term memory stages in male Swiss mice, using the passive avoidance (PA) test, as well as the influence of these compounds on the level of oxidative stress biomarkers in the mice brain. A single injection of a selective CB1 receptor antagonist, AM 251, improved long-term memory acquisition and consolidation in the PA test in mice, while a mixed CB1/CB2 receptor agonist WIN 55,212-2 impaired both stages of cognition. Additionally, JWH 133, a selective CB2 receptor agonist, and AM 630, a competitive CB2 receptor antagonist, significantly improved memory. Additionally, an acute administration of the highest used doses of JWH 133, WIN 55,212-2, and AM 630, but not AM 251, increased total antioxidant capacity (TAC) in the brain. In turn, the processes of lipids peroxidation, expressed as the concentration of malondialdehyde (MDA), were more advanced in case of AM 251. Thus, some changes in the PA performance may be connected with the level of oxidative stress in the brain.

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Rasmussen, Thøger, Anders Fink-Jensen, Per Sauerberg, Michael D. B. Swedberg, Christian Thomsen, Malcolm J. Sheardown, Lone Jeppesen, et al. "The muscarinic receptor agonist BuTAC, a novel potential antipsychotic, does not impair learning and memory in mouse passive avoidance." Schizophrenia Research 49, no. 1-2 (April 2001): 193–201. http://dx.doi.org/10.1016/s0920-9964(00)00129-8.

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Wang, Xiaqing, Meng Sun, Lu Gan, and Weihai Chen. "MK212, a 5-hydroxytryptamine 2C receptor agonist, inhibits conditioned avoidance responses independent of blocking endogenous dopamine release in rats." Progress in Neuro-Psychopharmacology and Biological Psychiatry 89 (March 2019): 16–22. http://dx.doi.org/10.1016/j.pnpbp.2018.08.022.

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45

Ohyama, Mitsuko, Yukiko Ozawa, Takashi Yamaguchi, Koichiro Takahashi, and Minoru Yamamoto. "Effects of a new Ml muscarinic agonist, YM796, on impairment of passive avoidance task in mice with acetylcholine hypofunction." Japanese Journal of Pharmacology 61 (1993): 93. http://dx.doi.org/10.1016/s0021-5198(19)51282-3.

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Makoto, Ukai, Nakayama Shinobu, Hamada Tami, and Kameyama Tsutomu. "Discriminative stimulus properties of the mixed agonist-antagonist pentazocine in the rat using two-choice discrete-trial avoidance paradigm." Pharmacology Biochemistry and Behavior 33, no. 2 (June 1989): 355–59. http://dx.doi.org/10.1016/0091-3057(89)90513-3.

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47

Charlier, Yana, Christian Brabant, Maria Elisa Serrano, Yves Lamberty, and Ezio Tirelli. "The prototypical histamine H3 receptor inverse agonist thioperamide improves multiple aspects of memory processing in an inhibitory avoidance task." Behavioural Brain Research 253 (September 2013): 121–27. http://dx.doi.org/10.1016/j.bbr.2013.07.016.

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48

Carli, Miriana, Salvatore Tranchina, and Rosario Samanin. "8-Hydroxy-2-(di-n-propylamino)tetralin, a 5-HT1A receptor agonist, impairs performance in a passive avoidance task." European Journal of Pharmacology 211, no. 2 (February 1992): 227–34. http://dx.doi.org/10.1016/0014-2999(92)90533-a.

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49

Jerusalinsky, Diana, Carlos Cerveñansky, Roger Walz, Marino Bianchin, and Iván Izquierdo. "A peptide muscarinic toxin from the Green Mamba venom shows agonist-like action in an inhibitory avoidance learning task." European Journal of Pharmacology 240, no. 1 (August 1993): 103–5. http://dx.doi.org/10.1016/0014-2999(93)90554-u.

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50

Silva, Marcelina Jasmine, Zhanette Coffee, Chong Ho Yu, and Marc O. Martel. "Anxiety and Fear Avoidance Beliefs and Behavior May Be Significant Risk Factors for Chronic Opioid Analgesic Therapy Reliance for Patients with Chronic Pain—Results from a Preliminary Study." Pain Medicine 22, no. 9 (February 17, 2021): 2106–16. http://dx.doi.org/10.1093/pm/pnab069.

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Abstract Objective To describe differences between patients with chronic, non-cancer pain (CNCP) who were successfully able to cease full mu agonist chronic opioid analgesic therapy (COAT), and those who exhibited refractory COAT reliance, among those who participated in a multidisciplinary program designed for COAT cessation. Design A retrospective review of electronic medical records (EMR) data was organized for preliminary analysis. Setting A multicenter private practice specializing in CNCP, which received patient referrals from the surrounding geographical area of primary and specialty care offices in Northern California. Subjects Data from 109 patients with CNCP who participated in a multidisciplinary program to cease COAT between the dates of October 2017 to December 2019 were examined. Methods EMR data, pre-COAT cessation, of oral morphine milligram equivalence (MME) and validated questionnaire responses assessing anxiety and fear-based beliefs and behavior, as well as opioid misuse, were extracted and compared between those who successfully ceased COAT and those who did not. Results Patients who were unsuccessful at COAT cessation reported significantly higher Fear Avoidance Beliefs Questionnaire (FAB) scores. No significant differences were found based on incoming MME amounts, Current Opioid Misuse Measure (COMM) or Tampa Scale of Kinesiophobia (TSK) scores. Pain Catastrophizing Scale (PCS) scores showed a split pattern with unclear significance. Conclusions Results suggest that fear avoidance beliefs and behavior, as measured by the FAB, play a significant role in refractory COAT reliance for patients with CNCP.

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