PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 9509494-3 1998 Cocaine induced a significantly greater increase in ACTH in the occasional cocaine users than in the cocaine dependent men (p < .01). Cocaine 0-7 proopiomelanocortin Homo sapiens 52-56 12603818-0 2003 Effect of experimenter-delivered and self-administered cocaine on extracellular beta-endorphin levels in the nucleus accumbens. Cocaine 55-62 proopiomelanocortin Homo sapiens 80-94 12603818-2 2003 Using microdialysis, we studied the effect of cocaine on extracellular levels of beta-endorphin in the nucleus accumbens, a brain region involved in the reinforcing effects of psychostimulant drugs. Cocaine 46-53 proopiomelanocortin Homo sapiens 81-95 12603818-5 2003 The effect of cocaine on beta-endorphin release in the nucleus accumbens was mimicked by a local perfusion of dopamine (5 microm) and was blocked by coadministration of SCH-23390 (10 microm). Cocaine 14-21 proopiomelanocortin Homo sapiens 25-39 12603818-10 2003 We demonstrate an increase in beta-endorphin release in the nucleus accumbens following experimenter-delivered and self-administered cocaine mediated by the local dopaminergic system. Cocaine 133-140 proopiomelanocortin Homo sapiens 30-44 12603818-11 2003 These findings suggest that activation of the beta-endorphin neurons within the arcuate nucleus-nucleus accumbens pathway may be important in the neurobiological mechanisms underlying the behavioral effects of cocaine. Cocaine 210-217 proopiomelanocortin Homo sapiens 46-60 10462091-5 1999 Cocaine produced a mean increase from baseline of 261% for ACTH and 73% for cortisol plasma levels. Cocaine 0-7 proopiomelanocortin Homo sapiens 59-63 11750770-1 2002 Cocaine stimulates the release of adrenocorticotropin hormone (ACTH) and cortisol in both clinical and preclinical studies, but the temporal sequence of cocaine-induced changes in other hormones and affective states is unclear. Cocaine 0-7 proopiomelanocortin Homo sapiens 63-67 11750770-2 2002 The purpose of this study was to analyze the pattern and temporal concordance of cocaine-induced changes in ACTH, cortisol, dihydroepiandrosterone (DHEA), epinephrine, heart rate and subjective reports of euphoria. Cocaine 81-88 proopiomelanocortin Homo sapiens 108-112 11750770-7 2002 Moreover, the increases in euphoria, ACTH, epinephrine and heart rate each were significantly correlated with increases in plasma cocaine levels (P<0.001). Cocaine 130-137 proopiomelanocortin Homo sapiens 37-41 11750770-10 2002 Peak ACTH values were measured at 8.7 (+/-0.8) min after cocaine injection (P<0.01). Cocaine 57-64 proopiomelanocortin Homo sapiens 5-9 11750770-14 2002 The temporal concordance between cocaine-induced stimulation of ACTH, epinephrine and subjective euphoria suggests that these hormonal changes are significant concomitants of the abuse-related effects of cocaine. Cocaine 33-40 proopiomelanocortin Homo sapiens 64-68 11750770-14 2002 The temporal concordance between cocaine-induced stimulation of ACTH, epinephrine and subjective euphoria suggests that these hormonal changes are significant concomitants of the abuse-related effects of cocaine. Cocaine 204-211 proopiomelanocortin Homo sapiens 64-68 11679057-5 2001 All antidepressants, but not saline, cocaine and haloperidol, reduced POMC mRNA expression. Cocaine 37-44 proopiomelanocortin Homo sapiens 70-74 11173167-1 2001 Preclinical and clinical studies have shown that cocaine increases plasma adrenocorticotropin hormone (ACTH) and cortisol. Cocaine 49-56 proopiomelanocortin Homo sapiens 103-107 11173167-7 2001 Similarly, basal and oCRH stimulated ACTH and cortisol levels in cocaine dependent patients did not differ from those in healthy subjects. Cocaine 65-72 proopiomelanocortin Homo sapiens 37-41 9509494-3 1998 Cocaine induced a significantly greater increase in ACTH in the occasional cocaine users than in the cocaine dependent men (p < .01). Cocaine 75-82 proopiomelanocortin Homo sapiens 52-56 8596268-5 1996 FINDINGS: Cocaine cues significantly increased anxiety, ACTH, cortisol, and HVA. Cocaine 10-17 proopiomelanocortin Homo sapiens 56-60 9506757-1 1998 The purpose of this study was to determine the covariance between plasma cocaine and ACTH pharmacokinetics. Cocaine 73-80 proopiomelanocortin Homo sapiens 85-89 9506757-5 1998 ACTH increases were significantly correlated (P < 0.0001) with increases in plasma cocaine levels (r = 0.67; r2 = 0.44). Cocaine 86-93 proopiomelanocortin Homo sapiens 0-4 9506757-8 1998 The area under the curve for plasma cocaine was 6463 +/- 1070 ng/min x mL, and the area under the curve for ACTH was 1873 +/- 188 pmol/min x L. The mean half-life for plasma cocaine was 46.7 +/- 4.0 min, and that for ACTH was 35.8 +/- 5.1 min. Cocaine 174-181 proopiomelanocortin Homo sapiens 217-221 1338055-1 1992 In order to establish possible alterations in the hypothalamic pituitary-adrenal axis and in ACTH-related opioids in cocaine addicts, plasma ACTH, cortisol and beta-endorphin levels were measured throughout the day in 9 cocaine addicts [age: 27 +/- 5 years (mean +/- SE); weight: 72 +/- 6.1 kg, duration of cocaine addiction: at least 2 years] on the day of their admission to a recovery community for drug abusers (first test) and after 15 days of abstinence (second test). Cocaine 117-124 proopiomelanocortin Homo sapiens 93-97 7932162-0 1994 Cocaine effects on pulsatile secretion of ACTH in men. Cocaine 0-7 proopiomelanocortin Homo sapiens 42-46 7932162-1 1994 The effects of cocaine on pulsatile secretion of adrenocorticotropic hormone (ACTH) in men were studied under controlled clinical research ward conditions. Cocaine 15-22 proopiomelanocortin Homo sapiens 49-76 7932162-11 1994 Mean ACTH valley levels (P < .02) and mean valley nadir (P < .02) were also significantly increased after cocaine administration. Cocaine 112-119 proopiomelanocortin Homo sapiens 5-9 7984271-7 1994 The ACTH responses to d-fenfluramine and 8-OH-DPAT were inhibited in cocaine pretreated rats. Cocaine 69-76 proopiomelanocortin Homo sapiens 4-8 7984271-11 1994 Cocaine-induced deficits in the ACTH response to 5-HT releasers may reflect 5-HT1A receptor subsensitivity, but presynaptic deficits cannot be excluded. Cocaine 0-7 proopiomelanocortin Homo sapiens 32-36 1331401-17 1992 Cocaine-induced increases in plasma ACTH levels may be due to its effects on dopaminergic systems which modulate corticotropin-releasing factor release in brain. Cocaine 0-7 proopiomelanocortin Homo sapiens 36-40 1329800-0 1992 Buprenorphine attenuates the effects of cocaine on adrenocorticotropin (ACTH) secretion and mood states in man. Cocaine 40-47 proopiomelanocortin Homo sapiens 72-76 1329800-1 1992 Adrenocorticotropin (ACTH) levels in plasma increased rapidly to 105% above baseline within 5 minutes after intravenous injection of cocaine (30 mg) in cocaine-dependent men. Cocaine 133-140 proopiomelanocortin Homo sapiens 21-25 1329800-1 1992 Adrenocorticotropin (ACTH) levels in plasma increased rapidly to 105% above baseline within 5 minutes after intravenous injection of cocaine (30 mg) in cocaine-dependent men. Cocaine 152-159 proopiomelanocortin Homo sapiens 21-25 1329800-2 1992 The time course of ACTH stimulation paralleled increases in plasma cocaine levels and self-reports of salient drug effects on mood states and did not occur after placebo administration. Cocaine 67-74 proopiomelanocortin Homo sapiens 19-23 1329800-3 1992 An opioid mixed agonist-antagonist, buprenorphine (4 mg/day sublingually), suppressed the acute cocaine-induced stimulation of both ACTH and euphoria. Cocaine 96-103 proopiomelanocortin Homo sapiens 132-136 1338055-10 1992 During the first test, cocaine addicts showed higher plasma ACTH, cortisol and beta-endorphin levels than normal controls at all examined time points. Cocaine 23-30 proopiomelanocortin Homo sapiens 60-64 1338055-10 1992 During the first test, cocaine addicts showed higher plasma ACTH, cortisol and beta-endorphin levels than normal controls at all examined time points. Cocaine 23-30 proopiomelanocortin Homo sapiens 79-93 2189049-4 1990 The indirect effects of cocaine on the immune system could be mediated by ACTH, beta-endorphin and corticosterone. Cocaine 24-31 proopiomelanocortin Homo sapiens 74-78 1336674-2 1992 Cocaine has been shown to alter circulating levels of the neurotransmitters, dopamine, norepinephrine, epinephrine, as well as the hypothalamic-pituitary-adrenal axis hormones corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH), and cortisol. Cocaine 0-7 proopiomelanocortin Homo sapiens 214-241 1336674-2 1992 Cocaine has been shown to alter circulating levels of the neurotransmitters, dopamine, norepinephrine, epinephrine, as well as the hypothalamic-pituitary-adrenal axis hormones corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH), and cortisol. Cocaine 0-7 proopiomelanocortin Homo sapiens 243-247 2189049-4 1990 The indirect effects of cocaine on the immune system could be mediated by ACTH, beta-endorphin and corticosterone. Cocaine 24-31 proopiomelanocortin Homo sapiens 80-94 18848957-6 2009 Cocaine stimulated ACTH, cortisol, and LH, whereas cocaine+nalbuphine in combination produced a smaller increase in ACTH, and decreased cortisol and LH. Cocaine 0-7 proopiomelanocortin Homo sapiens 19-23 18848957-6 2009 Cocaine stimulated ACTH, cortisol, and LH, whereas cocaine+nalbuphine in combination produced a smaller increase in ACTH, and decreased cortisol and LH. Cocaine 51-58 proopiomelanocortin Homo sapiens 116-120 18848957-7 2009 Thus it appears that nalbuphine attenuated cocaine"s effects on ACTH, cortisol, and LH. Cocaine 43-50 proopiomelanocortin Homo sapiens 64-68 18674556-3 2008 However, cocaine dose produced a greater increase in high and a more prolonged increase in plasma ACTH, while cocaine cue produced a decline in skin temperature. Cocaine 9-16 proopiomelanocortin Homo sapiens 98-102 33716662-3 2021 Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART). Cocaine 365-372 proopiomelanocortin Homo sapiens 331-352 33716662-3 2021 Changes in these signaling pathways would control phosphorylation of transcription factors cAMP response-element binding protein (CREB), forkhead box01 (FoxO1), and brain homeobox transcription factor (BSX) leading to food intake inhibition through changes in the expression of neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opio melanocortin (POMC), and cocaine and amphetamine-related transcript (CART). Cocaine 365-372 proopiomelanocortin Homo sapiens 354-358 20570051-5 2010 Post hoc analysis indicated the early life stress/non-cocaine dependent individuals exhibited significantly higher levels of ACTH as compared to the early life stress/cocaine-dependent group. Cocaine 54-61 proopiomelanocortin Homo sapiens 125-129 20004523-9 2010 On the CUE task, in contrast, female cocaine-dependent subjects had a more blunted ACTH response than did the other three groups (p=0.02). Cocaine 37-44 proopiomelanocortin Homo sapiens 83-87 17904221-8 2009 RESULTS: Cocaine addicted individuals in general showed significantly lower HVA, and higher PRL, ACTH and cortisol basal levels respect to controls. Cocaine 9-16 proopiomelanocortin Homo sapiens 97-101 30290413-5 2008 The best characterized pathways are the orexigenic neuropeptide Y/Agouti-related protein and the anorexigenic pro-opiomelanocortin/cocaine- and amphetamine-related transcript neurons in the arcuate nucleus of the hypothalamus. Cocaine 131-138 proopiomelanocortin Homo sapiens 110-130