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Journal articles on the topic 'Eticlopride'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Feng, Xin, Victor M. Henriquez, Judith R. Walters, and Christy L. Ludlow. "Effects of Dopamine D1 and D2 Receptor Antagonists on Laryngeal Neurophysiology in the Rat." Journal of Neurophysiology 102, no. 2 (August 2009): 1193–205. http://dx.doi.org/10.1152/jn.00121.2009.

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Hypophonia is an early symptom in Parkinson's disease (PD) that involves an increase in laryngeal muscle activity, interfering with voice production. Our aim was to use an animal model to better understand the role of different dopamine receptor subtypes in the control of laryngeal neurophysiology. First, we evaluated the combined effects of SCH23390—a D1 receptor antagonist with a D2 receptor antagonist (eticlopride) on laryngeal neurophysiology, and then tested the separate effects of selective receptor antagonists. Thyroarytenoid (TA) and gastrocnemius (GN) muscle activity was measured at rest and while stimulating the internal branch of superior laryngeal nerve to elicit the laryngeal adductor response (LAR) in alpha-chloralose–anesthetized rats. Paired stimuli at different interstimulus intervals between 250 and 5,000 ms measured central conditioning of the LAR. Changes in resting muscle activity, response latency, amplitude, and LAR conditioning after each drug were compared with the saline control. SCH23390 alone increased the resting TA muscle activity ( P < 0.05). With the combined SCH23390 + eticlopride or SCH23390 alone, response latency decreased ( P < 0.01), amplitude increased ( P < 0.01), and the test LAR was reduced at 2,000-ms ISI ( P < 0.01). No LAR changes occurred when eticlopride was administered alone at a low dose and only a tendency to suppress responses was found at a high dose. No changes in GN muscle activity occurred in any of the groups. The results suggest that a loss of stimulation of D1 receptors plays a significant role in laryngeal pathophysiology in PD.

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2

Milanés, M. V., M. T. Marín, and M. L. Laorden. "Effects of morphine withdrawal on catecholaminergic neurons on heart right ventricle; implication of dopamine receptors." Canadian Journal of Physiology and Pharmacology 79, no. 10 (October 1, 2001): 885–91. http://dx.doi.org/10.1139/y01-067.

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The purpose of our study was to examine the effects of D1-and D2-dopamine receptors blockade on the changes in the ventricular content of catecholamines in rats withdrawn from morphine. Rats were given morphine by subcutaneous (sc) implantation of morphine pellets for 5 days. On the eighth day, morphine withdrawal was induced by sc administration of naloxone (1 mg/kg), and rats were killed 30 min later. Pretreatment with SCH 23390 (dopamine D1, D5 receptor antagonist) 15 min prior to naloxone administration suppressed some the behavioural signs of morphine withdrawal, whereas eticlopride (dopamine D2, D3, D4 receptor antagonist) did not. In addition, biochemical analysis indicate that SCH 23390 completely abolished the withdrawal-induced increase in noradrenaline and dopamine turnover in the right ventricle. By contrast, eticlopride did not block the hyperactivity of catecholaminergic neurons in the heart during morphine withdrawal. These data suggest that the hyperactivity of catecholaminergic neurons in the heart during morphine withdrawal is dependent upon D1 dopamine receptor activation. In addition, our results exclude the involvement of D2 dopamine receptors.Key words: morphine withdrawal, right ventricle, catecholaminergic activity.

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3

Masuda, Masao, Setsuko Kanai, and Kyoko Miyasaka. "Inhibitory effect of central dopamine on basal pancreatic secretion in conscious rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 1 (January 1, 1998): G29—G34. http://dx.doi.org/10.1152/ajpgi.1998.274.1.g29.

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We examined the role and the peripheral mechanism of action of central dopamine on basal pancreatic exocrine secretion in conscious rats. Rats were fitted with bile and pancreatic catheters to collect bile and pancreatic juice separately and also with a left lateral brain ventricle and external jugular vein catheters. After 90-min basal collection, the D1- and D2-receptor antagonists (Sch-23390 and eticlopride, respectively) and dopamine were administered into the lateral brain ventricle. Sch-23390 (30, 100, and 300 nmol/rat), but not eticlopride (300 nmol/rat), stimulated pancreatic fluid and protein secretion. Dopamine (30, 100, and 300 nmol/rat) inhibited pancreatic secretion dose dependently. Pretreatment with Sch-23390 prevented the inhibitory effect of dopamine. Intravenously injected Sch-23390 or dopamine had no effect on pancreatic secretion. The inhibitory effect of dopamine was blocked by bretylium, an inhibitor of norepinephrine release, and phentolamine, an α-blocker, but not by vagotomy. The β-antagonist propranolol alone significantly inhibited basal pancreatic secretion, and dopamine did not modify the inhibitory effect of propranolol. The proton pump inhibitor omeprazole partially but not completely reduced the inhibition by dopamine. These results suggest that central dopamine inhibits pancreatic exocrine secretion via D1-like receptors and that the inhibitory effect is mediated via sympathetic nerves, especially α-adrenoceptors.

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4

Giuliani, Daniela, and Francesca Ferrari. "Involvement of Dopamine Receptors in the Antipsychotic Profile of (−) Eticlopride." Physiology & Behavior 61, no. 4 (April 1997): 563–67. http://dx.doi.org/10.1016/s0031-9384(96)00503-3.

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5

Wang, Yu, Krisztina Harsanyi, and Stuart C. Mangel. "Endogenous Activation of Dopamine D2 Receptors Regulates Dopamine Release in the Fish Retina." Journal of Neurophysiology 78, no. 1 (July 1, 1997): 439–49. http://dx.doi.org/10.1152/jn.1997.78.1.439.

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Wang, Yu, Krisztina Harsanyi, and Stuart C. Mangel. Endogenous activation of dopamine D2 receptors regulates dopamine release in the fish retina. J. Neurophysiol. 78: 439–449, 1997. In the fish retina, horizontal cell electrical coupling and light responsiveness is regulated by activation of dopamine D1 receptors that are located on the horizontal cells themselves. The effects of dopamine and dopamine D2 receptor agonists and antagonists on cone horizontal cell light responses were studied in in vitro superfused goldfish retinas. Horizontal cell light responses and electrical coupling were assessed by monitoring responses to full-field stimuli and to small, centered (0.4 mm diam) spots of light, respectively. Dopamine (0.2–10 μM) application uncoupled horizontal cells and decreased their responses to full-field stimuli. Application of the D2 antagonist eticlopride (10–50 μM) produced similar effects, whereas quinpirole (0.1–10 μM), a D2 agonist, had the opposite effects. The uncoupling effect of eticlopride was blocked by prior application of SCH23390 (10 μM), a D1 receptor antagonist, and was eliminated after destruction of dopaminergic neurons by prior treatment of the retinas with 6-hydroxydopamine. The effects of these D2 drugs were observed following flickering light stimulation, but were not observed following sustained light stimulation. Application of the D2 antagonists sulpiride (0.5–20 μM) and spiperone (0.25–10 μM) uncoupled horizontal cells when the total concentration of divalent cations (Mg2+ and Ca2+) in the Ringer solution was 1.1 mM. However, when the concentration of divalent cations was 0.2 mM, spiperone had no effect on the horizontal cells and sulpiride increased coupling. In contrast, eticlopride uncoupled the cells and decreased their light responsiveness irrespective of the concentration of divalent cations. The effects of quinpirole also depended on the concentration of divalent cations; its coupling effect was reduced when the divalent cation concentration was increased from 0.2 to 1.0 mM. The results suggest that activation of D2 receptors in the fish retina by endogenous dopamine decreases dopamine release and is greater after flickering compared with sustained light stimulation. These D2 receptors thus function as presynaptic autoreceptors that inhibit dopamine release from dopaminergic cells. In addition, the results also indicate that the effectiveness of some D2 drugs at these receptors is dependent on the concentration of divalent cations.

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6

Li, Wei, William M. Doyon, and John A. Dani. "Quantitative unit classification of ventral tegmental area neurons in vivo." Journal of Neurophysiology 107, no. 10 (May 15, 2012): 2808–20. http://dx.doi.org/10.1152/jn.00575.2011.

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Neurons in the ventral tegmental area (VTA) synthesize several major neurotransmitters, including dopamine (DA), GABA, and glutamate. To classify VTA single-unit neural activity from freely moving rats, we used hierarchical agglomerative clustering and probability distributions as quantitative methods. After many parameters were examined, a firing rate of 10 Hz emerged as a transition frequency between clusters of low-firing and high-firing neurons. To form a subgroup identified as high-firing neurons with GABAergic characteristics, the high-firing classification was sorted by spike duration. To form a subgroup identified as putative DA neurons, the low-firing classification was sorted by DA D2-type receptor pharmacological responses to quinpirole and eticlopride. Putative DA neurons were inhibited by the D2-type receptor agonist quinpirole and returned to near-baseline firing rates or higher following the D2-type receptor antagonist eticlopride. Other unit types showed different responses to these D2-type receptor drugs. A multidimensional comparison of neural properties indicated that these subgroups often clustered independently of each other with minimal overlap. Firing pattern variability reliably distinguished putative DA neurons from other unit types. A combination of phasic burst properties and a low skew in the interspike interval distribution produced a neural population that was comparable to the one sorted by D2 pharmacology. These findings provide a quantitative statistical approach for the classification of VTA neurons in unanesthetized animals.

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7

Bernstein, Seth N., and Richard J. Beninger. "Turning in Rats Following Intraaccumbens Shell Injections of Amphetamine or Eticlopride." Pharmacology Biochemistry and Behavior 65, no. 2 (February 2000): 203–7. http://dx.doi.org/10.1016/s0091-3057(99)00194-x.

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8

Dong, Zhanglei, Bingwu Huang, Chenchen Jiang, Jiangfan Chen, Han Lin, Qingquan Lian, and Binbin Wu. "The Adenosine A2A Receptor Activation in Nucleus Accumbens Suppress Cue-Induced Reinstatement of Propofol Self-administration in Rats." Neurochemical Research 46, no. 5 (February 22, 2021): 1081–91. http://dx.doi.org/10.1007/s11064-021-03238-9.

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AbstractPropofol has shown strong addictive properties in rats and humans. Adenosine A2A receptors (A2AR) in the nucleus accumbens (NAc) modulate dopamine signal and addictive behaviors such as cocaine- and amphetamine-induced self-administration. However, whether A2AR can modulate propofol addiction remains unknown. AAV-shA2AR was intra-NAc injected 3 weeks before the propofol self-administration training to test the impacts of NAc A2AR on establishing the self-administration model with fixed ratio 1 (FR1) schedule. Thereafter, the rats were withdrawal from propofol for 14 days and tested cue-induced reinstatement of propofol seeking behavior on day 15. The propofol withdrawal rats received one of the doses of CGS21680 (A2AR agonist, 2.5–10.0 ng/site), MSX-3 (A2AR antagonist, 5.0–20.0 μg/site) or eticlopride (D2 receptor (D2R) antagonist, 0.75–3.0 μg/site) or vehicle via intra-NAc injection before relapse behavior test. The numbers of active and inactive nose-poke response were recorded. Focal knockdown A2AR by shA2AR did not affect the acquisition of propofol self-administration behavior, but enhance cue-induced reinstatement of propofol self-administration compared with the AAV-shCTRLgroup. Pharmacological activation of the A2AR by CGS21680 (≥ 5.0 ng/site) attenuated cue-induced reinstatement of propofol self-administration behavior. Similarly, pharmacological blockade of D2R by eticlopride (0.75–3.0 μg/site) attenuated propofol seeking behavior. These effects were reversed by the administration of MSX-3 (5.0–20.0 μg/site). The A2AR- and D2R-mediated effects on propofol relapse were not confounded by the learning process, and motor activity as the sucrose self-administration and locomotor activity were not affected by all the treatments. This study provides genetic and pharmacological evidence that NAc A2AR activation suppresses cue-induced propofol relapse in rats, possibly by interacting with D2R.

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9

WATANABE, Kiyoko, Toshimitsu FUKUMURA, Shigeaki SASAKI, Minoru MAEDA, and Shuzo TAKEHARA. "New Fluorine-Substituted Analogue of Eticlopride with High Affinity toward Dopamine D2 Receptors." CHEMICAL & PHARMACEUTICAL BULLETIN 39, no. 12 (1991): 3211–14. http://dx.doi.org/10.1248/cpb.39.3211.

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10

Kmieciak-Kołada, K., J. Pawłowski, E. Obuchowicz, and Z. S. Herman. "Eticlopride modifies the food intake by its influence on neuropeptide Y in the hypothalamus." Pharmacological Research 31 (January 1995): 105. http://dx.doi.org/10.1016/1043-6618(95)86681-7.

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11

Ferrari, F., and D. Giuliani. "Effects of (-)eticlopride and 7-OH-DPAT on the tail-suspension test in mice." Journal of Psychopharmacology 11, no. 4 (July 1997): 339–44. http://dx.doi.org/10.1177/026988119701100409.

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12

Ferrari, F., and D. Giuliani. "Influence of eticlopride on cocaine- and DA D2 agonist-induced behavioral effects in rats." Pharmacology Biochemistry and Behavior 53, no. 3 (March 1996): 525–30. http://dx.doi.org/10.1016/0091-3057(95)02045-4.

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13

Saran, Anil, and Evans Coutinho. "Quantum mechanical calculations on dopamine D2-receptor antagonists: Conformation of remoxipride, eticlopride and NCQ 115." Proceedings / Indian Academy of Sciences 106, no. 2 (April 1994): 149–61. http://dx.doi.org/10.1007/bf02840739.

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14

Koerber, Jonathon, David Goodman, Jesse L. Barnes, and Jeffrey W. Grimm. "The dopamine D2 antagonist eticlopride accelerates extinction and delays reacquisition of food self-administration in rats." Behavioural Pharmacology 24, no. 8 (December 2013): 633–39. http://dx.doi.org/10.1097/fbp.0000000000000002.

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15

Ferrari, F., and D. Giuliani. "Influence of the DA D2 antagonist (−) eticlopride on cocaine-induced hypermotility and sexual excitement in rat." Pharmacological Research 31 (January 1995): 30. http://dx.doi.org/10.1016/1043-6618(95)86380-x.

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16

Obiol-Pardo, Cristian, Laura López, Manuel Pastor, and Jana Selent. "Progress in the structural prediction of G protein-coupled receptors: D3 receptor in complex with eticlopride." Proteins: Structure, Function, and Bioinformatics 79, no. 6 (April 12, 2011): 1695–703. http://dx.doi.org/10.1002/prot.23021.

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17

Ferrari, Francesca, and Daniela Giuliani. "Behavioural assessment in rats of the antipsychotic potential of the potent dopamine D2 receptor antagonist, (-)eticlopride." Pharmacological Research 31, no. 5 (May 1995): 261–67. http://dx.doi.org/10.1016/1043-6618(95)80030-1.

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18

Awenowicz, Patrick W., and Linda L. Porter. "Local Application of Dopamine Inhibits Pyramidal Tract Neuron Activity in the Rodent Motor Cortex." Journal of Neurophysiology 88, no. 6 (December 1, 2002): 3439–51. http://dx.doi.org/10.1152/jn.00078.2002.

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Cortical neurons respond in a variety of ways to locally applied dopamine, perhaps because of the activation of different receptors within or among subpopulations of cells. This study was conducted to assess the effects of dopamine and the receptor subtypes that mediate the responses of a specific population of neurons, the pyramidal tract neurons (PTNs) in the rodent motor cortex. The specific subfamilies of dopamine receptors expressed by PTNs also were determined. PTNs were identified by antidromic stimulation in intact animals. Extracellular recordings of their spontaneous activity and glutamate-induced excitation were performed with multi-barrel pipettes to allow simultaneous recording and iontophoresis of several drugs. Prolonged (30 s) application of dopamine caused a progressive, nonlinear decrease in spontaneous firing rates for nearly all PTNs, with significant reductions from baseline spontaneous activity (71% of baseline levels) occurring between 20 and 30 s of iontophoresis. The D1 selective (SCH23390) and the D2 selective (eticlopride) antagonists were both effective in blocking dopamine-induced inhibition in nearly all PTNs. Mean firing levels were maintained within 3% of baseline levels during co-application of the D1 antagonist with dopamine and within 11% of baseline levels during co-application of the D2 antagonist and dopamine. SCH23390 was ineffective however, in 2 of 16 PTNs, and eticlopride was ineffective in 3 PTNs. The dopamine blockade by both antagonists in most neurons, along with the selective blockade by one, but not the other antagonist in a few neurons indicate that the overall population of PTNs exhibits a heterogeneous expression of dopamine receptors. The firing rate of PTNs was significantly enhanced by iontophoresis of glutamate (mean = 141% of baseline levels). These increases were attenuated significantly (mean= 98% of baseline) by co-application with dopamine in all PTNs, indicating dopaminergic interactions with glutamate transmission. The expression of dopamine receptors was studied with dual-labeling techniques. PTNs were identified by retrograde labeling with fast blue and the D1a, D2, or D5 receptor proteins were stained immunohistochemically. Some, but not all PTNs, showed labeling for D1a, D2, or D5 receptors. The D1a and D2 receptor immunoreactivity was observed primarily in the somata of PTNs, whereas D5 immunoreactivity extended well into the apical dendrites of PTNs. In accordance with findings of D1 and D2 receptor antagonism of dopamine's actions, the identification of three DA receptor subtypes on PTNs suggests that dopamine can directly modulate PTN activity through one or more receptor subtypes.

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19

FUKUMURA, Toshimitsu, Hideki DOHMOTO, Minoru MAEDA, Etsuko FUKUZAWA, and Masaharu KOJIMA. "Synthesis and in vitro affinity for dopamine D-2 receptor of N-fluorine-substituted analogs of eticlopride." CHEMICAL & PHARMACEUTICAL BULLETIN 38, no. 6 (1990): 1740–42. http://dx.doi.org/10.1248/cpb.38.1740.

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20

Schenk, Susan, and Dave Gittings. "Effects of SCH 23390 and eticlopride on cocaine-seeking produced by cocaine and WIN 35,428 in rats." Psychopharmacology 168, no. 1-2 (November 5, 2002): 118–23. http://dx.doi.org/10.1007/s00213-002-1276-y.

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21

Rocca, Jeffery F., Joshua G. Lister, and Richard J. Beninger. "Spiroperidol, but not eticlopride or aripiprazole, produces gradual increases in descent latencies in the bar test in rats." Behavioural Pharmacology 28, no. 1 (February 2017): 30–36. http://dx.doi.org/10.1097/fbp.0000000000000264.

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22

Martelle, Jennifer L., and Michael A. Nader. "A Review of the Discovery, Pharmacological Characterization, and Behavioral Effects of the Dopamine D2-Like Receptor Antagonist Eticlopride." CNS Neuroscience & Therapeutics 14, no. 3 (September 2008): 248–62. http://dx.doi.org/10.1111/j.1755-5949.2008.00047.x.

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23

Rogers, Robert D., Adeline Wong, Chris McKinnon, and Catharine A. Winstanley. "Systemic Administration of 8-OH-DPAT and Eticlopride, but not SCH23390, Alters Loss-Chasing Behavior in the Rat." Neuropsychopharmacology 38, no. 6 (January 7, 2013): 1094–104. http://dx.doi.org/10.1038/npp.2013.8.

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24

Areola, Oluwasanmi O., and Arun L. Jadhav. "Low-level lead exposure modulates effects of quinpirole and eticlopride on response rates in a fixed-interval schedule." Pharmacology Biochemistry and Behavior 69, no. 1-2 (May 2001): 151–56. http://dx.doi.org/10.1016/s0091-3057(01)00526-3.

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25

Fowler, S. C., and Jiing-Ren Liou. "Haloperidol, raclopride, and eticlopride induce microcatalepsy during operant performance in rats, but clozapine and SCH 23390 do not." Psychopharmacology 140, no. 1 (November 9, 1998): 81–90. http://dx.doi.org/10.1007/s002130050742.

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26

Stiles, Lucy, Yiwen Zheng, Cynthia L. Darlington, and Paul F. Smith. "The effects of the D2 dopamine receptor antagonist, eticlopride, on attention following bilateral vestibular deafferentation in the rat." Neuroscience Letters 506, no. 2 (January 2012): 193–97. http://dx.doi.org/10.1016/j.neulet.2011.11.003.

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27

Brown, Russell W., Kimberly N. Thompson, Ivy A. Click, Razaria A. C. Best, Stephanie K. Thacker, and Marla K. Perna. "The effects of eticlopride on Morris water task performance in male and female rats neonatally treated with quinpirole." Psychopharmacology 180, no. 2 (February 5, 2005): 234–40. http://dx.doi.org/10.1007/s00213-005-2148-z.

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28

Highgate, Quenten, Afnan Al Abadey, and Susan Schenk. "Repeated eticlopride administration increases dopamine D2 receptor expression and restores behavioral flexibility disrupted by methamphetamine exposure to male rats." Behavioural Brain Research 435 (October 2022): 114064. http://dx.doi.org/10.1016/j.bbr.2022.114064.

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29

Vargo, J. M., and J. F. Marshall. "Reduced eticlopride-induced fos expression in caudate–putamen and globus pallidus after unilateral frontal cortex injury: relation to neglect." Neuroscience 76, no. 4 (January 1997): 1083–95. http://dx.doi.org/10.1016/s0306-4522(96)00414-9.

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30

Blokland, A., A. Sik, and C. Lieben. "Evaluation of DOI, 8-OH-DPAT, eticlopride and amphetamine on impulsive responding in a reaction time task in rats." Behavioural Pharmacology 16, no. 2 (March 2005): 93–100. http://dx.doi.org/10.1097/00008877-200503000-00004.

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31

Adams, Amy C., and Kristen A. Keefe. "Degree of immediate early gene induction in striatum by eticlopride determines sensitivity to N-methyl-d-aspartate receptor blockade." Brain Research 885, no. 2 (December 2000): 201–7. http://dx.doi.org/10.1016/s0006-8993(00)02941-3.

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32

Soto, Paul L., David K. Grandy, Steven R. Hursh, and Jonathan L. Katz. "Behavioral economics of food reinforcement and the effects of prefeeding, extinction, and eticlopride in dopamine D2 receptor mutant mice." Psychopharmacology 215, no. 4 (February 2, 2011): 775–84. http://dx.doi.org/10.1007/s00213-011-2173-z.

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33

MAEDA, Minoru, Shigeki SASAKI, Toshimitsu FUKUMURA, Etsuko FUKUZAWA, Kiyoko WATANABE, Masaharu KOJIMA, Takashi TAHARA, Kouji MASUDA, and Yuichi ICHIYA. "Positron-Emitting N-(18F)Fluoroalkyl and (18F)Fluoropyrrolidinyl Analogues of Eticlopride as Potential in Vivo Radioligands for Dopamine D2 Receptors." CHEMICAL & PHARMACEUTICAL BULLETIN 40, no. 7 (1992): 1793–98. http://dx.doi.org/10.1248/cpb.40.1793.

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34

Areola, Oluwasanmi O., and Arun L. Jadhav. "Responsiveness of extracellular dopamine in the nucleus accumbens to systemic quinpirole and eticlopride is modulated by low-level lead exposure." Environmental Toxicology and Pharmacology 19, no. 2 (February 2005): 323–28. http://dx.doi.org/10.1016/j.etap.2004.08.009.

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35

Bernardi, Danilo Magnani, Juliana Pelissari Marchi, Cintia de Souza Alferes Araújo, Vanessa Rodrigues do Nascimento, Diego de Souza Lima, Samantha Wietzikoski, Marcelo Machado Ferro, et al. "Dopamine docking studies of biologically active metabolites from Curcuma longa L." Research, Society and Development 10, no. 7 (July 2, 2021): e59910716992. http://dx.doi.org/10.33448/rsd-v10i7.16992.

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The dopaminergic system is involved in a wide range of neuropsychiatric and neurodegenerative disorders. The lack of receptor subtype specificity is related to several pharmacological side effects that are observed during therapy among parkinsonian and schizophrenic patients. It is of paramount importance to search for new compounds that act on dopamine receptors with therapeutic potential, higher clinical effectiveness, and fewer adverse effects. In the present study, we performed a molecular docking study of D2, D3, and D4 receptor interactions with 92 metabolites from Curcuma longa using an in silico approach. We sought to identify compounds for possible drug development. A virtual library of compounds was built using molecules that were identified in the phytochemical characterization of C. longa. Protocols that were validated by redocking were applied to a virtual scan of this library using the Autodock-v4.2.3, Autodock Vina, and Molegro-v6.0 Virtual Docker programs, with four repetitions each. The three-dimensional structures of D2, D3, and D4 receptors in complex with risperidone, eticlopride, and nemonapride were obtained from the Protein Data Bank. Four compounds—stigmasterol, β-sitosterol, cholest-5-en-3-one, and cholestan-3-ol,2-methylene-(3β, 5α)—were the most likely to bind D2, D3, and D4 dopamine receptors, suggesting their potential for possible drug development.

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36

Johnson, Rebecca A., Stephen M. Johnson, and Gordon S. Mitchell. "Catecholaminergic modulation of respiratory rhythm in an in vitro turtle brain stem preparation." Journal of Applied Physiology 85, no. 1 (July 1, 1998): 105–14. http://dx.doi.org/10.1152/jappl.1998.85.1.105.

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An in vitro brain stem preparation from adult turtles was used to determine effects of dopamine (DA) and norepinephrine (NE) on the pattern of respiratory motor output recorded from hypoglossal nerve roots (XII). Bath-applied DA (10–200 μM) increased the frequency of respiratory bursts (peaks) from 0.9 ± 0.2 to 2.4 ± 0.3 (SE) peaks/min, resulting in a 99 ± 9% increase in neural minute activity. R[+]-SCH-23390 (10 μM, D1 antagonist) and eticlopride (20 μM, D2 antagonist) attenuated the DA-mediated increase in peak frequency by 52 and 59%, respectively. On the other hand, the DA-receptor agonists apomorphine (D1, D2), quinelorane (D2), and SKF-38393 (D1) had no effect on peak frequency. Prazosin, an α1-adrenergic antagonist (250 nM) abolished the DA-mediated frequency increase. Although NE (10–200 μM) and phenylephrine (10–200 μM, α1-adrenergic agonist) increased peak frequency from 0.5 ± 0.1 to 1.2 ± 0.3 peaks/min and from 0.6 ± 0.1 to 1.0 ± 0.2 peaks/min, respectively, these effects were not as large as that with DA alone. The data suggest that both dopaminergic and adrenergic receptor activation in the brain stem increase respiratory frequency in turtles, but the DA receptor-mediated increase is dependent on coactivation of α1-adrenergic receptors.

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37

Stoilova, Vanya V., Sina A. Wette, and Maik C. Stüttgen. "A Free-Operant Reward-Tracking Paradigm to Study Neural Mechanisms and Neurochemical Modulation of Adaptive Behavior in Rats." International Journal of Molecular Sciences 20, no. 12 (June 25, 2019): 3098. http://dx.doi.org/10.3390/ijms20123098.

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The ability to respond flexibly to changing environmental circumstances is a hallmark of goal-directed behavior, and compromised flexibility is associated with a wide range of psychiatric conditions in humans, such as addiction and stress-related disorders. To identify neural circuits and transmitter systems implicated in the provision of cognitive flexibility, suitable animal paradigms are needed. Ideally, such models should be easy to implement, allow for rapid task acquisition, provide multiple behavioral readouts, and permit combination with physiological and pharmacological testing and manipulation. Here, we describe a paradigm meeting these requirements and employ it to investigate the neural substrates and neurochemical modulation of adaptive behavior. Water-restricted rats learned to emit operant responses for positive reinforcement (water reward) within minutes in a free-operant conditioning environment. Without further training, animals were able to track changes in the reward schedule. Given prior evidence that the medial prefrontal cortex (mPFC) and the dopaminergic system are required for flexible behavior, we aimed to assess both in more detail. Silencing of mPFC compromised flexible behavior when avoidance of punishment was required. Systemic injections of the D2-receptor agonist quinpirole and the D2-receptor antagonist eticlopride had complex, differential impacts on reward seeking and adaptive behavior.

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Shaik, Anver Basha, Comfort A. Boateng, Francisco O. Battiti, Alessandro Bonifazi, Jianjing Cao, Li Chen, Rezvan Chitsazi, et al. "Structure Activity Relationships for a Series of Eticlopride-Based Dopamine D₂/D₃ Receptor Bitopic Ligands." Journal of Medicinal Chemistry 64, no. 20 (October 12, 2021): 15313–33. http://dx.doi.org/10.1021/acs.jmedchem.1c01353.

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Claytor, Renee, Joshua A. Lile, and Michael A. Nader. "The effects of eticlopride and the selective D3-antagonist PNU 99194-A on food- and cocaine-maintained responding in rhesus monkeys." Pharmacology Biochemistry and Behavior 83, no. 3 (March 2006): 456–64. http://dx.doi.org/10.1016/j.pbb.2006.03.007.

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Piggins, Hugh, and Zulifiquar Merali. "The effects of concurrent D-1 and D-2 dopamine receptor blockade with sch 23390 and eticlopride, on bombesin-induced behaviours." Progress in Neuro-Psychopharmacology and Biological Psychiatry 13, no. 3-4 (January 1989): 583–94. http://dx.doi.org/10.1016/0278-5846(89)90150-4.

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LaHoste, G. J., and J. F. Marshall. "Chronic eticlopride and dopamine denervation induce equal nonadditive increases in striatal D2 receptor density: Autoradiographic evidence against the dual mechanism hypothesis." Neuroscience 41, no. 2-3 (January 1991): 473–81. http://dx.doi.org/10.1016/0306-4522(91)90342-l.

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Köhler, Christer, Håkan Hall, and Lars Gawell. "Regional in vivo binding of the substituted benzamide [3H]eticlopride in the rat brain: Evidence for selective labelling of dopamine receptors." European Journal of Pharmacology 120, no. 2 (January 1986): 217–26. http://dx.doi.org/10.1016/0014-2999(86)90543-1.

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Soto, Paul L., David K. Grandy, Steven R. Hursh, and Jonathan L. Katz. "Erratum to: Behavioral economics of food reinforcement and the effects of prefeeding, extinction, and eticlopride in dopamine D2 receptor mutant mice." Psychopharmacology 232, no. 9 (March 28, 2015): 1669. http://dx.doi.org/10.1007/s00213-015-3918-x.

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Paudel, Pradeep, Su Hui Seong, Sangwook Wu, Suhyun Park, Hyun Ah Jung, and Jae Sue Choi. "Eckol as a Potential Therapeutic against Neurodegenerative Diseases Targeting Dopamine D3/D4 Receptors." Marine Drugs 17, no. 2 (February 10, 2019): 108. http://dx.doi.org/10.3390/md17020108.

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The G protein-coupled receptor (GPCR) family of proteins comprises signaling proteins that mediate cellular responses to various hormones and neurotransmitters, and serves as a prime target for drug discovery. Towards our goal of discovering secondary metabolites from natural sources that can function as neuronal drugs, we evaluated the modulatory effect of eckol on various GPCRs via cell-based functional assays. In addition, we conducted in silico predictions to obtain molecular insights into the functional effects of eckol. Functional assays revealed that eckol had a concentration-dependent agonist effect on dopamine D3 and D4 receptors. The half maximal effective concentration (EC50) of eckol for the dopamine D3 and D4 receptors was 48.62 ± 3.21 and 42.55 ± 2.54 µM, respectively, while the EC50 values of dopamine as a reference agonist for these two receptors were 2.9 and 3.3 nM, respectively. In silico studies revealed that a low binding energy in addition to hydrophilic, hydrophobic, π–alkyl, and π–π T-shaped interactions are potential mechanisms by which eckol binds to the dopamine receptors to exert its agonist effects. Molecular dynamics (MD) simulation revealed that Phe346 of the dopamine receptors is important for binding of eckol, similar to eticlopride and dopamine. Our results collectively suggest that eckol is a potential D3/D4 agonist for the management of neurodegenerative diseases, such as Parkinson’s disease.

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Sloley, B. D., V. L. Trudeau, J. G. Dulka, and R. E. Peter. "Selective depletion of dopamine in the goldfish pituitary caused by domperidone." Canadian Journal of Physiology and Pharmacology 69, no. 6 (June 1, 1991): 776–81. http://dx.doi.org/10.1139/y91-116.

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The effects of the dopamine type-2 receptor (D-2) antagonist domperidone on pituitary and brain amine concentrations and serum gonadotropin levels in the goldfish were investigated. Domperidone caused a long-lasting, dose-dependent depletion of dopamine in the goldfish pituitary. Pituitary concentrations of 5-hydroxytryptamine (5HT) were unaffected by domperidone treatment. Concentrations of noradenaline, dopamine, and 5HT in the hypothalamus and telencephalon were also unaffected by domperidone treatment. In contrast to the goldfish, dopamine levels in both mouse pituitary and hypothalamus were unaffected by domperidone treatment. The depletion of dopamine was observed in both sexually regressed and recrudescent male and female fish, but elevation of serum gonadotropin levels in response to domperidone treatment occurred only in sexually recrudescent fish. Treatment of sexually recrudescent fish with the D-2 antagonists pimozide, (−)-sulpiride and eticlopride and the dopamine type-1 (D-1) antagonists SKF 83566 and SCH 23390 failed to elicit a depletion of pituitary dopamine or elevation of serum gonadotropin. Treatment of sexually recrudescent fish with domperidone, α-methyl-p-tyrosine or carbidopa elicited comparable depletions of pituitary dopamine and elevations of serum gonadotropin. The results suggest that in addition to D-2 receptor antagonist activity, domperidone has some other neuropharmacological action on dopaminergic neurones in the goldfish pituitary.Key words: domperidone, dopamine, noradrenaline, 5-hydroxytryptamine, pituitary, hypothalamus, telencephalon, gonadotropin, goldfish.

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Hall, Håkan, Christer Köhler, and Lars Gawell. "Some in vitro receptor binding properties of [3H]eticlopride, a novel substituted benzamide, selective for dopamine-D2 receptors in the rat brain." European Journal of Pharmacology 111, no. 2 (May 1985): 191–99. http://dx.doi.org/10.1016/0014-2999(85)90756-3.

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Brown, Russell W., Michael T. Bardo, Derek D. Mace, Scott B. Phillips, and Philipp J. Kraemer. "d-amphetamine facilitation of Morris water task performance is blocked by eticlopride and correlated with increased dopamine synthesis in the prefrontal cortex." Behavioural Brain Research 114, no. 1-2 (September 2000): 135–43. http://dx.doi.org/10.1016/s0166-4328(00)00225-4.

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Harrison, Amanda, Fabrizio Gasparini, and Athina Markou. "Nicotine potentiation of brain stimulation reward reversed by DHβE and SCH 23390, but not by eticlopride, LY 314582 or MPEP in rats." Psychopharmacology 160, no. 1 (February 1, 2002): 56–66. http://dx.doi.org/10.1007/s00213-001-0953-6.

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Ferrari, F., and D. Giuliani. "The selective D2 dopamine receptor antagonist eticlopride counteracts the ejaculatio praecox induced by the selective D2 dopamine agonist SND 919 in the rat." Life Sciences 55, no. 14 (January 1994): 1155–62. http://dx.doi.org/10.1016/0024-3205(94)00244-4.

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Bandyopadhyay, Susanta, Carlos Gonzalez-Islas, and John J. Hablitz. "Dopamine Enhances Spatiotemporal Spread of Activity in Rat Prefrontal Cortex." Journal of Neurophysiology 93, no. 2 (February 2005): 864–72. http://dx.doi.org/10.1152/jn.00922.2004.

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Dopaminergic modulation of prefrontal cortex (PFC) is important for neuronal integration in this brain region known to be involved in cognition and working memory. Because of the complexity and heterogeneity of the effect of dopamine on synaptic transmission across layers of the neocortex, dopamine's net effect on local circuits in PFC is difficult to predict. We have combined whole cell patch-clamp recording and voltage-sensitive dye imaging to examine the effect of dopamine on the excitability of local excitatory circuits in rat PFC in vitro. Whole cell voltage-clamp recording from visually identified layer II/III pyramidal neurons in rat brain slices revealed that, in the presence of bicuculline (10 μM), bath-applied dopamine (30–60 μM) increased the amplitude of excitatory postsynaptic currents (EPSCs) evoked by weak intracortical stimulus. The effect was mimicked by the selective D1 receptor agonist SKF 81297 (1 μM). Increasing stimulation resulted in epileptiform discharges. SKF 81297 (1 μM) significantly lowered the threshold stimulus required for generating epileptiform discharges to 83% of control. In the imaging experiments, bath application of dopamine or SKF 81297 enhanced the spatiotemporal spread of activity in response to weak stimulation and previously subthreshold stimulation resulted in epileptiform activity that spread across the whole cortex. These effects could be blocked by the selective D1 receptor antagonist SCH 23390 (10 μM) but not by the D2 receptor antagonist eticlopride (5 μM). These results indicate that dopamine, by a D1 receptor–mediated mechanism, enhances spatiotemporal spread of synaptic activity and lowers the threshold for epileptiform activity in local excitatory circuits within PFC.

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