Observational analysis of the effects of kappa opioid agonists on open field behaviour in the rat

Jackson, Anne; Cooper, Steven J.

doi:10.1007/bf00176854

Cited by 31 publications

(15 citation statements)

References 13 publications

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“…In rodents agonists of k-opioid receptors inhibit locomotion and produce ataxia and sedation (Jackson and Cooper, 1988). k-Opioid-induced effects on motor activity are apparently mediated through the regulation of the mesolimbic and nigrostriatal dopaminergic neurotransmission.…”

Section: Discussionmentioning

confidence: 99%

Big Dynorphin, a Prodynorphin-Derived Peptide Produces NMDA Receptor-Mediated Effects on Memory, Anxiolytic-Like and Locomotor Behavior in Mice

Kuzmin

Madjid

Terenius

et al. 2005

Neuropsychopharmacol

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Effects of big dynorphin (Big Dyn), a prodynorphin-derived peptide consisting of dynorphin A (Dyn A) and dynorphin B (Dyn B) on memory function, anxiety, and locomotor activity were studied in mice and compared to those of Dyn A and Dyn B. All peptides administered i.c.v. increased step-through latency in the passive avoidance test with the maximum effective doses of 2.5, 0.005, and 0.7 nmol/animal, respectively. Effects of Big Dyn were inhibited by MK 801 (0.1 mg/kg), an NMDA ion-channel blocker whereas those of dynorphins A and B were blocked by the k-opioid antagonist nor-binaltorphimine (6 mg/kg). Big Dyn (2.5 nmol) enhanced locomotor activity in the open field test and induced anxiolytic-like behavior both effects blocked by MK 801. No changes in locomotor activity and no signs of anxiolytic-like behavior were produced by dynorphins A and B. Big Dyn (2.5 nmol) increased time spent in the open branches of the elevated plus maze apparatus with no changes in general locomotion. Whereas dynorphins A and B (i.c.v., 0.05 and 7 nmol/animal, respectively) produced analgesia in the hot-plate test Big Dyn did not. Thus, Big Dyn differs from its fragments dynorphins A and B in its unique pattern of memory enhancing, locomotor-and anxiolytic-like effects that are sensitive to the NMDA receptor blockade. The findings suggest that Big Dyn has its own function in the brain different from those of the prodynorphin-derived peptides acting through k-opioid receptors.

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Section: Discussionmentioning

confidence: 99%

Big Dynorphin, a Prodynorphin-Derived Peptide Produces NMDA Receptor-Mediated Effects on Memory, Anxiolytic-Like and Locomotor Behavior in Mice

Kuzmin

Madjid

Terenius

et al. 2005

Neuropsychopharmacol

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“…For litters pretreated on PD 11-15, the test day occurred after 1 abstinence day (i.e., at PD 17). A later test day was not included for this age group, since acute treatment with U-50,488 does not induce locomotor activity after the preweanling period (see Jackson and Cooper 1988;Bolanos et al 1996). On the test day, pretreatment groups were further subdivided with half of the rats receiving a challenge injection of U-50,488 (5 mg/kg, SC), while the other half received saline.…”

Section: Apparatusmentioning

confidence: 99%

Kappa opioid-mediated behavioral sensitization in the preweanling rat: relationship to Fos immunoreactivity

et al. 1998

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When given acutely, drugs that stimulate kappa opioid receptors (e.g., U-50,488) enhance the locomotor activity of preweanling rats and induce regional increases in Fos immunoreactivity (IR). In contrast, the effects of chronic treatment with kappa opioid agonists are unknown. The purpose of the present study was two-fold: first, to determine whether repeated treatment with a kappa opioid agonist would sensitize the locomotor activity of preweanling rats and, second, to determine whether changes in Fos IR correspond with the occurrence of locomotor sensitization. To test these hypotheses, rats were injected with U-50,488 (5 mg/kg, s.c.) or saline on either postnatal days (PD) 5-9 or PD 11-15. For rats pretreated on PD 5-9, a test day injection of U-50,488 or saline was given after either 1 or 7 abstinence days (i.e., at PD 11 or PD 17). For rats pretreated on PD 11-15, a test day injection of U-50,488 or saline was given after 1 abstinence day (i.e., at PD 17). In two additional experiments, the acute and chronic effects of U-50,488 treatment were assessed in adult rats. As expected, repeated treatment with U-50,488 produced locomotor sensitization at both PD 11 and PD 17, but only when the test day occurred 1, and not 7, days after cessation of drug pretreatment. Thus, the persistence of the sensitized response was very brief. Test day treatment with U-50,488 stimulated Fos IR in various brain regions of the preweanling rat, including the medial striatum, nucleus accumbens, lateral habenula, and septal area. Chronic treatment with U-50,488 depressed Fos expression in a number of brain regions (relative to acutely treated rats); however, these changes in Fos IR did not necessarily coincide with the occurrence of behavioral sensitization. Repeated treatment with U-50,488 did not produce locomotor sensitization in adult rats, so Fos IR was not assessed in this age group. Therefore, while acute treatment with U-50,488 both increased locomotor activity and stimulated Fos IR in preweanling rats, chronic U-50,488 treatment produced behavioral changes that did not correspond with Fos expression.

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“…For example, the kappa opioid agonist U-50,488 reduces basal rates of locomotor activity and rearing, while attenuating cocaine-induced locomotion and place preference conditioning (Ukai and Kameyama 1985;Jackson and Cooper 1988;Suzuki et al 1992;Crawford et al 1995). The U-50,488-induced suppression of DA-mediated behaviors may be due to actions in either the mesolimbic or nigrostriatal pathways.…”

Section: Introductionmentioning

confidence: 95%

Kappa opioid mediated locomotor activity in the preweanling rat: role of pre- and postsynaptic dopamine receptors

et al. 1997

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Treatment with a non-selective DA receptor agonist (i.e., NPA) has previously been shown to attenuate the kappa opioid mediated locomotor activity of preweanling rats. The purpose of the present study was to determine whether stimulation of D1-like or D2-like receptors is responsible for this behavioral effect and whether the critical DA receptors are located pre- or postsynaptically. To assess these questions, 17-day-old rats were injected with saline, the D2/D3 agonist quinpirole (0.1, 0.3, or 1.0 mg/kg, i.p.), or the D1 agonist SKF 38393 (7.5, 15, or 30 mg/kg, i.p.), 20 min after receiving the kappa opioid agonist U-50,488 (5 mg/kg, s.c.) or saline. Results showed that the locomotor activating effects of U-50,488 were blocked by the D2/D3, but not the D1, receptor agonist. To dissociate the effects of DA autoreceptors and postsynaptic receptors, 17-day-old rats were given alpha-methyl-DL-p-tyrosine (AMPT reduces endogenous DA stores) prior to U-50,488 or amphetamine (1.5 mg/kg, s.c.) treatment. Interestingly, AMPT (which reduced DA levels by more than 80%) fully attenuated amphetamine-induced locomotor activity, while having little effect on U-50,488-induced locomotion. In addition, quinpirole blocked the locomotor activating effects of U-50,488 in rats acutely depleted of DA. When considered together, these results indicate that kappa opioid stimulation enhances locomotor activity regardless of presynaptic DA levels. Similarly, quinpirole appears to attenuate U-50,488-induced locomotor activity by stimulating postsynaptic D2-like receptors, since the D2/D3 agonist inhibited kappa opioid mediated behavior independent of endogenous DA levels.

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Observational analysis of the effects of kappa opioid agonists on open field behaviour in the rat

Cited by 31 publications

References 13 publications

Big Dynorphin, a Prodynorphin-Derived Peptide Produces NMDA Receptor-Mediated Effects on Memory, Anxiolytic-Like and Locomotor Behavior in Mice

Big Dynorphin, a Prodynorphin-Derived Peptide Produces NMDA Receptor-Mediated Effects on Memory, Anxiolytic-Like and Locomotor Behavior in Mice

Kappa opioid-mediated behavioral sensitization in the preweanling rat: relationship to Fos immunoreactivity

Kappa opioid mediated locomotor activity in the preweanling rat: role of pre- and postsynaptic dopamine receptors

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