Effect of naloxone and morphine on arcaine-induced state-dependent memory in rats

Mariani, Raquele Kipper; Mello, Carlos Fernando; Rosa, Michelle Melgarejo da; Ceretta, Ana Paula Chiapinotto; Camera, Keli; Rubin, Maribel Antonello

doi:10.1007/s00213-011-2215-6

Cited by 14 publications

(5 citation statements)

References 55 publications

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“…administration of morphine also recovered memory impairment and induced morphine-STD memory retrieval. This finding is in accordance with studies reporting that pre-test morphine can recover the impairment induced by posttraining morphine (Farahmandfar, Naghdi, Karimian, Kadivar, & Zarrindast, 2012;Izquierdo, 1979;Mariani et al, 2011;Rassouli et al, 2010;Zarrindast, Piri, Nasehi, & Ebrahimi-Ghiri, 2012). According to Koob et al (Koob, Le Moal, & Thompson, 2010), as the pre-test application of a drug has effects on memory retrieval, changes in the animal behavior can be attributed to the drug's effects on sensory/motor function; however, in our study, the effect of drugs on animal motor function measured by the open-field test was ruled out.…”

Section: Discussionsupporting

confidence: 93%

Pentylenetetrazol and Morphine Interaction in a State-dependent Memory Model: Role of CREB Signaling

Tavassoli

Ardjmand

2020

Basic Clin. Neurosci. J.

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Introduction: State-dependent (STD) memory is a process, in which the learned information can be optimally retrieved only when the subject is in the state similar to the encoding phase. This phenomenon has been widely studied with morphine. Several studies have reported that Pentylenetetrazole (PTZ) impairs memory in experimental animal models. Due to certain mechanistic interactions between morphine and PTZ, it is hypothesized that PTZ may interfere with the morphine-STD. The cyclic adenosine monophosphate Response Element-Binding (CREB) is considered as the main downstream marker for long-term memory. This study was designed to determine the possible interaction between PTZ and morphine STD and the presumable changes in CREB mRNA. Methods: In an Inhibitory Avoidance (IA) model, posttraining morphine (2.5, 5, and 7.5 mg/ kg-i.p.) was used. The pre-test morphine was evaluated for morphine-induced STD memory. Moreover, the effect of a pre-test PTZ (60 mg/kg-i.p.) was studied along with morphine STD. Locomotion testing was carried out using open-field. Eventually, using real-time-PCR, the CREB mRNA changes in the hippocampus were evaluated. Results: Posttraining MOR (7.5 mg/kg-i.p.) impaired IA memory (P<0.001). The pre-test injection of similar doses of morphine recovered the morphine-induced memory impairment (P<0.001). The pre-test PTZ impaired the IA memory recall (P<0.001); however, the pre-test PTZ along with morphine STD potentiated the morphine-induced STD (P<0.001). Alterations in CREB mRNA were observed in all groups. No difference was seen in the locomotor activity. Conclusion: Presumably, the certain interactive effect of PTZ on morphine-induced STD is mediated through gamma-aminobutyric acid and opioid systems via CREB signaling.

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Section: Discussionsupporting

confidence: 93%

Pentylenetetrazol and Morphine Interaction in a State-dependent Memory Model: Role of CREB Signaling

Tavassoli

Ardjmand

2020

Basic Clin. Neurosci. J.

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“…These data suggest that morphine treatment slightly impaired the consolidation of memory in the honeybees. Our data are in agreement with the results of studies in rodents [7][8][9] .…”

Section: Locomotor Activitysupporting

confidence: 93%

“…For example, in rodents, most studies show that morphine administration before training inhibits the acquisition of memory in paradigms such as active or passive avoidance tasks [1][2][3] and a wide variety of maze tasks [4][5][6] . Other studies report that morphine administration after training impairs memory retrieval in step-down or step-through inhibitory avoidance tasks [7][8][9] . However, some studies show that morphine administration after training or before testing does not alter performance in the step-down inhibitory avoidance test [1] , and administration before testing even facilitates memory retrieval in the passive avoidance task [10] .…”

Section: Introductionmentioning

confidence: 99%

Effects of morphine on associative memory and locomotor activity in the honeybee (Apis mellifera)

Chen

Yao

et al. 2013

Neurosci. Bull.

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Morphine can modulate the processes underlying memory in vertebrates. However, studies have shown various modulations by morphine: positive, negative and even neutral. The honeybee is a potential platform for evaluating the effects of drugs, especially addictive drugs, on the nervous system. However, the involvement of morphine in learning and memory in insects or other invertebrates is poorly understood. The current work evaluated whether morphine affects memory acquisition, consolidation and retrieval in honeybees, using the proboscis extension response (PER) paradigm. We demonstrated that morphine treatment (5 μg/bee) before training decreased the percentage of correct PERs and the response latency related to aversive rather than rewarding odors when tested after 1 or 24 h. Morphine treatment after training also caused a decrease in this latency when tested after 24 h. Meanwhile, morphine treatment reduced the ambulation distance when tested after 30 min. Our findings suggest that morphine impairs the acquisition of short-and long-term associative memory and slightly disrupts the consolidation of long-term memory in honeybees. These negative effects cannot be explained by reduced locomotion but by impaired memory associated with aversion.

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“…For example, a neuromodulatory receptor antagonist could impair retrieval if given shortly before testing, but it might have no effect on retrieval if given shortly before both training and testing because the extent of signaling by the neuromodulator during memory formation would be similar to that during retrieval. Such roles and effects are referred to as “state‐dependent” (Jafari‐Sabet and Jannat‐Dastjerdi, ; Ardjmand et al, ; Mariani et al, ), and they reflect a conditional rather than an absolute role in retrieval. Additional, more specific roles for neuromodulators in retrieval may also occur, and these will be discussed when considering roles for the individual neuromodulatory systems below.…”

Section: Introductionmentioning

confidence: 99%

Neuromodulatory signaling in hippocampus‐dependent memory retrieval

Thomas

2015

Hippocampus

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Considerable advances have been made toward understanding the molecular signaling events that underlie memory acquisition and consolidation. In contrast, less is known about memory retrieval, despite its necessity for utilizing learned information. This review focuses on neuromodulatory and intracellular signaling events that underlie memory retrieval mediated by the hippocampus, for which the most information is currently available. Among neuromodulators, adrenergic signaling is required for the retrieval of various types of hippocampus-dependent memory. Although they contribute to acquisition and/or consolidation, cholinergic and dopaminergic signaling are generally not required for retrieval. Interestingly, while not required for retrieval, serotonergic and opioid signaling may actually constrain memory retrieval. Roles for histamine and non-opioid neuropeptides are currently unclear but possible. A critical effector of adrenergic signaling in retrieval is reduction of the slow afterhyperpolarization mediated by β1 receptors, cyclic AMP, protein kinase A, Epac, and possibly ERK. In contrast, stress and glucocorticoids impair retrieval by decreasing cyclic AMP, mediated in part by the activation of β2 -adrenergic receptors. Clinically, alterations in neuromodulatory signaling and in memory retrieval occur in Alzheimer's disease, Down syndrome, depression, and post-traumatic stress disorder, and recent evidence has begun to link changes in neuromodulatory signaling with effects on memory retrieval.

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Effect of naloxone and morphine on arcaine-induced state-dependent memory in rats

Abstract: These results suggest that state dependency induced by arcaine involves the opioid system.

Cited by 14 publications

References 55 publications

Pentylenetetrazol and Morphine Interaction in a State-dependent Memory Model: Role of CREB Signaling

Pentylenetetrazol and Morphine Interaction in a State-dependent Memory Model: Role of CREB Signaling

Effects of morphine on associative memory and locomotor activity in the honeybee (Apis mellifera)

Neuromodulatory signaling in hippocampus‐dependent memory retrieval

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