Role of the central amygdala GABA-A receptors in morphine state-dependent memory

Rassouli, Yassaman; Rezayof, Ameneh; Zarrindast, Mohammad‐Reza

doi:10.1016/j.lfs.2010.04.006

Cited by 24 publications

(17 citation statements)

References 47 publications

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“…In line with previous reports our results demonstrated that morphine dose-dependently decreased rats' performances in the acquisition and retrieval in the passive avoidance task [25,26] and the Morris water maze [27]. The adrenergic system may be involved in this phenomenon [28].…”

Section: Discussionsupporting

confidence: 92%

The Possible Role of Medial Prefrontal Cortex Beta-1-Adrenoceptors in Morphine-Induced Amnesia

Torkaman-Boutorabi

Hashemi-Hezaveh²,

Sheidadoust³

et al. 2014

Pharmacology

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The prelimbic region of the medial prefrontal cortex (mPFC) in the brain is crucial for memory. Norepinephrine elicits an important influence on mPFC functions. The stimulation of β-adrenoceptors (β-ARs) may play a critical role in the consolidation of long-term memory. The present study examines the possible role of β₁-ARs located in the mPFC on morphine-induced amnesia in rats. The animals were bilaterally implanted with chronic cannulas in the mPFC, trained in a step-through-type passive avoidance task and tested 24 h after training to measure step-through latency. Our present results indicated that posttraining intraperitoneal administration of morphine (2.5, 5 and 7.5 mg/kg) dose-dependently reduced the step-through latency. Different doses of xamoterol (0.01, 0.1 and 1 µg/rat) have shown no significant change in the step-through latency, but posttraining intra-mPFC microinjection of atenolol (0.2 and 0.4 µg/rat) had an amnesic effect. Moreover, atenolol-caused amnesia was reversed by an ineffective dose of xamoterol (0.1 µg/rat). On the other hand, coadministration of an ineffective dose of atenolol (0.1 µg/rat) with an ineffective dose of morphine (2.5 mg/kg) induced an amnesic effect. Meanwhile, xamoterol had no effect on morphine-induced amnesia. These results suggest that β₁-ARs of the prelimbic region in the mPFC may play an important role in morphine-induced amnesia.

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Section: Discussionsupporting

confidence: 92%

The Possible Role of Medial Prefrontal Cortex Beta-1-Adrenoceptors in Morphine-Induced Amnesia

Torkaman-Boutorabi

Hashemi-Hezaveh²,

Sheidadoust³

et al. 2014

Pharmacology

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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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“…It is well known that the drugs of abuse such as morphine or ethanol produce this kind of learning. For example, post-training (Rezayof et al, 2008) or pre-test administration (Farahmandfar et al, 2012) of morphine as a μ-opioid receptor agonist impaired memory retrieval which can be reversed by pre-test administration of the drug (Rassouli et al, 2010) in different animal learning models. The administration of ethanol which mainly targets the GABA-A and NMDA receptors (Peoples and Weight, 1999) per se induces an amnesic effect (Sanday et al, 2013;Nash and Takarangi, 2011) and produces SDM (For review see Koek, 2011).…”

Section: Introductionmentioning

confidence: 99%

Basolateral amygdala CB1 cannabinoid receptors are involved in cross state-dependent memory retrieval between morphine and ethanol

Ofogh¹,

Rezayof²,

Sardari³

et al. 2016

Pharmacology Biochemistry and Behavior

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Role of the central amygdala GABA-A receptors in morphine state-dependent memory

Cited by 24 publications

References 47 publications

The Possible Role of Medial Prefrontal Cortex Beta-1-Adrenoceptors in Morphine-Induced Amnesia

The Possible Role of Medial Prefrontal Cortex Beta-1-Adrenoceptors in Morphine-Induced Amnesia

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

Basolateral amygdala CB1 cannabinoid receptors are involved in cross state-dependent memory retrieval between morphine and ethanol

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