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Mohammadreza Zarrindast - One of the best experts on this subject based on the ideXlab platform.

  • influence of intracerebral administration of no agents in dorsal hippocampus ca1 on cannabinoid state dependent Memory in the step down passive avoidance test
    Physiology & Behavior, 2010
    Co-Authors: Mohammad Nasehi, Morteza Piri, Nida Jamaliraeufy, Mohammadreza Zarrindast
    Abstract:

    Abstract In the present study, the effects of nitric oxide agents on WIN55, 212-2 induced State-Dependent Memory of passive avoidance task were examined in mice. One-trial step-down paradigm was used for the assessment of Memory retention in adult male NMRI mice. Post-training intra-CA1 administration of CB1 and CB2 receptor agonists, WIN55, 212-2 (0.25, 0.5 and 1 µg/mouse), dose-dependently decreased Memory retrieval. The Memory impairment induced by post-training administration of WIN55, 212-2 (1 µg/mouse) was restored by pre-test administration of the same dose of the drug (1 μg/mouse, intra-CA1), showing the WIN55, 212-2 State-Dependent Memory. Single intra-CA1 administration of l -arginine (0.3, 1 and 3 µg/mouse) or L-NAME (0.3, 1 and 3 µg/mouse), 5 min pre-test could not alter Memory retrieval. On the other hand, in the animals in which retrieval was impaired due to post-training administration of WIN55, 212-2 (1 µg/mouse), pre-test intra-CA1 administration of l -arginine (1 and 3 µg/mouse), but not L-NAME (0.3, 1 and 3 µg/mouse) 24 h after training restored Memory retrieval. Also, in the animals which received both post-training (1 µg/mouse) and pre-test injections of WIN55, 212-2 (1 µg/mouse), the injection of L-NAME (3 µg/mouse, intra-CA1), 2 min before pre-test administration decreased retrieval. Furthermore, in the animals under the influence of post-training administration of WIN55, 212-2 (1 µg/mouse), pre-test co-administration of non-effective doses of WIN55, 212-2 (0.25 µg/mouse) and l -arginine (0.3 and 1 µg/mouse), increased the restoration of Memory by pre-test WIN55, 212-2. These findings may demonstrate the involvement of NO in State-Dependent Memory induced by intra-CA1 administration of WIN55, 212-2.

  • involvement of dorsal hippocampal α adrenergic receptors in the effect of scopolamine on Memory retrieval in inhibitory avoidance task
    Neurobiology of Learning and Memory, 2010
    Co-Authors: N S Azami, Morteza Piri, Shahrbano Oryan, Mehrdad Jahanshahi, Vahab Babapour, Mohammadreza Zarrindast
    Abstract:

    The present study evaluated the possible role of alpha-adrenergic receptors of the dorsal hippocampus on scopolamine-induced amnesia and scopolamine State-Dependent Memory in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulae in the CA1 regions of the dorsal hippocampus, trained in a step-through type inhibitory avoidance task, and tested 24h after training to measure step-through latency. Results indicate that post-training or pre-test intra-CA1 administration of scopolamine (1 and 2 microg/rat) dose-dependently reduced the step-through latency, showing an amnestic response. Amnesia produced by post-training scopolamine (2 microg/rat) was reversed by pre-test administration of the scopolamine that is due to a State-Dependent effect. Interestingly, pre-test intra-CA1 microinjection of alpha1-adrenergic agonist, phenylephrine (1 and 2 microg/rat) or alpha2-adrenergic agonist, clonidine improved post-training scopolamine (2 microg/rat)-induced retrieval impairment. Furthermore, pre-test intra-CA1 microinjection of phenylephrine (0.25, 0.5 and 1 microg/rat) or clonidine (0.25, 0.5 and 1 microg/rat) with an ineffective dose of scopolamine (0.25 microg/rat), synergistically improved Memory performance impaired by post-training scopolamine. On the other hand, pre-test injection of alpha1-receptors antagonist prazosin (1 and 2 microg/rat) or alpha2-receptors antagonist yohimbine (1 and 2 microg/rat) prevented the restoration of Memory by pre-test scopolamine. It is important to note that pre-test intra-CA1 administration of the same doses of prazosin or yohimbine, alone did not affect Memory retrieval. These results suggest that alpha1- and alpha2-adrenergic receptors of the dorsal hippocampal CA1 regions may play an important role in scopolamine-induced amnesia and scopolamine State-Dependent Memory.

  • involvement of dorsal hippocampal nicotinic receptors in the effect of morphine on Memory retrieval in passive avoidance task
    European Journal of Pharmacology, 2008
    Co-Authors: Lotfollah Khajehpour, Ameneh Rezayof, Mohammadreza Zarrindast
    Abstract:

    Abstract The present study evaluated the possible role of nicotinic acetylcholine receptors of the dorsal hippocampus on morphine-induced amnesia and morphine State-Dependent Memory in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulas in the CA1 regions of the dorsal hippocampi, trained in a step-through type passive avoidance task, and tested 24 h after training to measure step-through latency. Results indicate that post-training subcutaneous (s.c.) administration of morphine (2.5–7.5 mg/kg) dose-dependently reduced the step-through latency, showing an amnestic response. Post-training intra-CA1 microinjection of nicotine (0.5–1 μg/rat) decreased significantly the amnesia induced by post-training morphine (7.5 mg/kg). Moreover, co-treatment of mecamylamine (0.5 and 1 μg/rat, intra-CA1) with an ineffective dose of morphine (2.5 mg/kg), immediately after training, caused inhibition of Memory retrieval. On the other hand, amnesia produced by post-training morphine (7.5 mg/kg) was reversed by pre-test administration of the opioid that is due to a State-Dependent effect. Interestingly, pre-test intra-CA1 microinjection of nicotine (0.25 and 0.5 μg/rat) improved post-training morphine (7.5 mg/kg)-induced retrieval impairment. Moreover, pre-test administration of the same doses of nicotine in combination with a lower dose of morphine (0.5 mg/kg), which had no effects alone, synergistically improved Memory performance impaired by post-training morphine. Pre-test injection of mecamylamine (0.5–2 μg/rat) prevented the restoration of Memory by pre-test morphine. It is important to note that post-training or pre-test intra-CA1 administration of the same doses of nicotine or mecamylamine, alone did not affect Memory retrieval. These results suggest that nicotinic acetylcholine receptors of the hippocampal CA1 regions may play an important role in morphine-induced amnesia and morphine State-Dependent Memory.

  • nitric oxide modulates state dependency induced by lithium in an inhibitory avoidance task in mice
    Behavioural Pharmacology, 2007
    Co-Authors: Mohammadreza Zarrindast, Manizheh Mardaneh Shendy, Shamseddin Ahmadi
    Abstract:

    The effect of intracerebroventricular (i.c.v.) injections of L-arginine, a nitric oxide (NO) precursor and L-NAME, an inhibitor of NO synthase, on retrieval of State-Dependent Memory induced by LiCl (lithium) was investigated. A one-trial step-down inhibitory avoidance task was used for Memory assessment in adult male NMRI mice. Intraperitoneal administration of lithium (10 mg/kg), immediately after training, impaired Memory on the test day. Pretest administration of different doses of lithium (5, 10 and 20 mg/kg) reversed the impairment of Memory caused by posttraining lithium (10 mg/kg). In addition, pretest administration of L-arginine (0.001, 0.01 and 0.1 microg/mouse, i.c.v.) or L-NAME (0.001, 0.01 and 0.1 microg/mouse, i.c.v.) also reversed amnesia induced by posttraining lithium. Furthermore, pretest coadministration with lithium of a dose of L-arginine (0.0001 microg/mouse, i.c.v.) or L-NAME (0.0001 microg/mouse, i.c.v.) that had no effects when administered alone, increased the effect of lithium on retrieval of inhibitory avoidance Memory. The results suggest that NO may have a modulatory role on State-Dependent retrieval of inhibitory avoidance Memory induced by lithium.

  • influence of intracerebroventricular administration of dopaminergic drugs on morphine state dependent Memory in the step down passive avoidance test
    Neurobiology of Learning and Memory, 2006
    Co-Authors: Mohammadreza Zarrindast, Azita Khalilzadeh, Soheila Fazlitabaei, Maryam Bananej, Ali Haerirohani, Ameneh Rezayof
    Abstract:

    Abstract The effects of dopaminergic drugs on morphine State-Dependent Memory of passive avoidance task were examined in mice. Pre-training administration of morphine (5 mg/kg) led to State-Dependent learning with impaired Memory retrieval on the test day which was reversed by pre-test administration of the same dose of the opiate. The pre-test intracerebroventricular (i.c.v.) administration of the dopamine D 1 receptor agonist (SKF38393), dopamine D2 receptor agonist (quinpirole) and dopamine D2 receptor antagonist (sulpiride) not only reversed the effect of pre-training morphine treatment, but also increased this action of the drug. Furthermore, the pre-test i.c.v. administration of dopamine D 1 receptor antagonist (SCH23390) prevented the restoration of Memory by morphine. In conclusion, the morphine-induced recovery of Memory, on the test day, seems to be induced, at least in part, through dopamine receptors.

Majid Jafarisabet - One of the best experts on this subject based on the ideXlab platform.

  • nitric oxide in the dorsal hippocampal area is involved on muscimol state dependent Memory in the step down passive avoidance test
    Pharmacology Biochemistry and Behavior, 2014
    Co-Authors: Majid Jafarisabet, Mohammadamin Khodadadnejad, Saeed Ghoraba, Ramin Ataee
    Abstract:

    Abstract In the present study, the effects of intra-dorsal hippocampal (intra-CA1) injections of nitric oxide (NO) agents on muscimol State-Dependent Memory were examined in mice. A single-trial step-down passive avoidance task was used for the assessment of Memory retrieval in adult male NMRI mice. Post-training intra-CA1 administration of a GABA A receptor agonist, muscimol (0.05 and 0.1 μg/mouse) dose dependently induced impairment of Memory retention. Pre-test injection of muscimol (0.05 and 0.1 μg/mouse) induced State-Dependent retrieval of the Memory acquired under post-training muscimol (0.1 μg/mouse, intra-CA1) influence. Pre-test injection of a NO precursor, l -arginine (1 and 2 μg/mouse, intra-CA1) improved Memory retention, although the low dose of the drug (0.5 μg/mouse) did not affect Memory retention. Pre-test injection of an inhibitor of NO-synthase, l -NAME (0.5 and 1 μg/mouse, intra-CA1) impaired Memory retention, although the low dose of the drug (0.25 μg/mouse) did not affect Memory retention. In other series of experiments, pre-test intra-CA1 injection of l -arginine (0.25 and 0.5 μg/mouse) 5 min before the administration of muscimol (0.1 μg/mouse, intra-CA1) dose dependently inhibited muscimol State-Dependent Memory. Pre-test intra-CA1 administration of l -arginine (0.125, 0.25 and 0.5 μg/mouse) by itself cannot affect Memory retention. Pre-test intra-CA1 injection of l -NAME (0.25 μg/mouse, intra-CA1) reversed the Memory impairment induced by post-training administration of muscimol (0.1 μg/mouse, intra-CA1). Moreover, pre-test administration of l -NAME (0.125 and 0.25 μg/mouse, intra-CA1) with an ineffective dose of muscimol (0.025 μg/mouse, intra-CA1) significantly restored the retrieval and induced muscimol State-Dependent Memory. Pre-test intra-CA1 administration of l -NAME (0.0625, 0.125 and 0.25 μg/mouse) by itself cannot affect Memory retention. It may be suggested that the nitric oxide in the dorsal hippocampal area play an important role in muscimol State-Dependent Memory.

  • involvement of dorsal hippocampal muscarinic cholinergic receptors on muscimol state dependent Memory of passive avoidance in mice
    Life Sciences, 2011
    Co-Authors: Majid Jafarisabet
    Abstract:

    Abstract Aims In the present study, the effects of bilateral intra-dorsal hippocampal (intra-CA1) injections of cholinergic agents on muscimol State-Dependent Memory were examined in mice. Main methods A single-trial step-down passive avoidance task was used for the assessment of Memory retention in adult male NMRI mice. Key findings Pre-training intra-CA1 administration of a GABA-A receptor agonist, muscimol (0.05 and 0.1 μg/mouse) dose dependently induced impairment of Memory retention. Pre-test injection of muscimol (0.05 and 0.1 μg/mouse, intra-CA1) induced State-Dependent retrieval of the Memory acquired under pre-training muscimol (0.1 μg/mouse, intra-CA1) influence. Pre-test intra-CA1 injection of an acetylcholinesterase inhibitor, physostigmine (0.5 and 1 μg/mouse, intra-CA1) reversed the Memory impairment induced by pre-training administration of muscimol (0.1 μg/mouse, intra-CA1). Moreover, pre-test administration of physostigmine (0.5 and 1 μg/mouse, intra-CA1) with an ineffective dose of muscimol (0.025 μg/mouse, intra-CA1) significantly restored the retrieval and induced muscimol State-Dependent Memory. Pre-test intra-CA1 administration of physostigmine (0.25, 0.5 and 1 μg/mouse) by itself cannot affect Memory retention. Pre-test intra-CA1 injection of the muscarinic receptor antagonist, atropine (1 and 2 μg/mouse) 5 min before the administration of muscimol (0.1 μg/mouse, intra-CA1) dose dependently inhibited muscimol State-Dependent Memory. Pre-test intra-CA1 administration of atropine (0.5, 1 and 2 μg/mouse) by itself cannot affect Memory retention. Significance The results suggest that muscarinic cholinergic mechanism of the CA1 may influence muscimol State-Dependent Memory.

  • muscimol state dependent Memory involvement of dorsal hippocampal μ opioid receptors
    Behavioural Brain Research, 2009
    Co-Authors: Majid Jafarisabet, Iman Jannatdastjerdi
    Abstract:

    Abstract In the present study, the effects of subcutaneous (s.c.) injections of morphine, a μ-opioid receptor agonist and intra-dorsal hippocampal (intra-CA1) injections of naloxone, a μ-opioid receptor antagonist on muscimol State-Dependent Memory were examined in mice. A single-trial step-down passive avoidance task was used for the assessment of Memory retention in adult male NMRI mice. Pre-training intra-CA1 administration of a GABAA receptor agonist, muscimol (0.025, 0.05, 0.1 and 0.2 μg/mouse) dose dependently induced impairment of Memory retention. Pre-test injection of muscimol (0.05, 0.1 and 0.2 μg/mouse, intra-CA1) induced State-Dependent retrieval of the Memory acquired under pre-training muscimol (0.1 μg/mouse, intra-CA1) influence. Pre-test injection of morphine (0.5 and 1 mg/kg, s.c.) 30 min before the administration of muscimol (0.1 μg/mouse, intra-CA1) dose dependently inhibited muscimol State-Dependent Memory. Pre-test intra-CA1 injection of naloxone (0.1 and 0.2 μg/mouse, intra-CA1) improved pre-training muscimol (0.1 μg/mouse)-induced retrieval impairment. Moreover, pre-test administration of naloxone (0.1 and 0.2 μg/mouse, intra-CA1) with an ineffective dose of muscimol (0.025 μg/mouse) significantly restored the retrieval and induced muscimol State-Dependent Memory. These findings implicate the involvement of a dorsal hippocampal μ-opioid receptor mechanism in muscimol State-Dependent Memory.

Soheila Fazlitabaei - One of the best experts on this subject based on the ideXlab platform.

  • influence of intracerebroventricular administration of dopaminergic drugs on morphine state dependent Memory in the step down passive avoidance test
    Neurobiology of Learning and Memory, 2006
    Co-Authors: Mohammadreza Zarrindast, Azita Khalilzadeh, Soheila Fazlitabaei, Maryam Bananej, Ali Haerirohani, Ameneh Rezayof
    Abstract:

    Abstract The effects of dopaminergic drugs on morphine State-Dependent Memory of passive avoidance task were examined in mice. Pre-training administration of morphine (5 mg/kg) led to State-Dependent learning with impaired Memory retrieval on the test day which was reversed by pre-test administration of the same dose of the opiate. The pre-test intracerebroventricular (i.c.v.) administration of the dopamine D 1 receptor agonist (SKF38393), dopamine D2 receptor agonist (quinpirole) and dopamine D2 receptor antagonist (sulpiride) not only reversed the effect of pre-training morphine treatment, but also increased this action of the drug. Furthermore, the pre-test i.c.v. administration of dopamine D 1 receptor antagonist (SCH23390) prevented the restoration of Memory by morphine. In conclusion, the morphine-induced recovery of Memory, on the test day, seems to be induced, at least in part, through dopamine receptors.

  • influence of morphine or apomorphine induced sensitization on histamine state dependent learning in the step down passive avoidance test
    Behavioural Brain Research, 2006
    Co-Authors: Mohammadreza Zarrindast, Azita Khalilzadeh, Nazanin Malekmohammadi, Soheila Fazlitabaei
    Abstract:

    Effects of morphine- or apomorphine-induced sensitization on histamine State-Dependent Memory of passive avoidance task were examined in mice. Pre-training intracerebroventricular (i.c.v.) administration of histamine (20 μg/mouse) decreased the learning of a one-trial passive avoidance task. Pre-test administration of histamine (10 and 20 μg/mouse) reversed amnesia induced by pre-training of histamine, with maximum response at 20 μg/mouse. Pre-training histamine-induced amnesia was also reversed in morphine- or apomorphine-sensitized mice that had previously received once daily injections of morphine (20 and 30 mg/kg) or apomorphine (0.5 and 1 mg/kg) for 3 days. The reversion of histamine-induced amnesia in morphine-sensitized mice was decreased by once daily administration of naloxone (0.5 and 1 mg/kg), SCH 23390 (0.05 and 0.1 mg/kg) or sulpiride (25, 50 and 100 mg/kg) prior to injection of morphine (30 mg/kg/day, 3 days). Furthermore, once daily administration of sulpiride (50 and 100 mg/kg) but not SCH 23390 (0.01, 0.05 and 0.1 mg/kg) prior to apomorphine (1 mg/kg, for 3 days) decreased the reversion of pre-training histamine-induced amnesia by apomorphine. The results suggest that apomorphine or morphine sensitization affects the impairment of Memory induced by histamine and thus it is postulated that opioid and dopamine receptors may play an important role in this effect.

  • influence of intracerebroventricular administration of cannabinergic drugs on morphine state dependent Memory in the step down passive avoidance test
    Behavioural Pharmacology, 2006
    Co-Authors: Katayoun Kangarluhaghighi, Azita Khalilzadeh, Soheila Fazlitabaei
    Abstract:

    The effects of cannabinergic drugs on morphine State-Dependent Memory of passive avoidance task were examined in mice. Pre-training (0.25, 0.5 and 5 mg/kg) and post-training (5 mg/kg) administration of morphine impaired Memory retrieval on the test day. Impairment of Memory retrieval by morphine (5 mg/kg) on the test day was reversed by pre-test administration of the same dose of the opioid. The pre-test intracerebroventricular administration of the cannabinoid CB1/CB2 receptor agonist (WIN55,212-2) (0.75 and 1 microg/mouse) not only mimicked the effect of pre-test morphine treatment, but also increased this action of the opioid. Furthermore, the pre-test intracerebroventricular administration of CB1 receptor antagonist (AM251) (20 and 100 ng/mouse) prevented the restoration of Memory by morphine. Pre-training administration of WIN55,212-2 (1 microg/mouse) led to State-Dependent learning with impaired Memory retrieval on the test day as well, which was reversed by pre-test administration of the drug (0.5, 0.75 and 1 microg/mouse) or morphine (1 and 5 mg/kg). Restoration of impairment induced by WIN55,212-2 was decreased by both the opioid receptor antagonists, naloxone (0.01 microg/mouse) and AM251 (20 and 100 ng/mouse). In conclusion, the improvement of Memory retrieval by morphine treatment on the test day seems to be induced, at least in part, by the cannabinoid CB1 receptors.

Ramin Ataee - One of the best experts on this subject based on the ideXlab platform.

  • nitric oxide in the dorsal hippocampal area is involved on muscimol state dependent Memory in the step down passive avoidance test
    Pharmacology Biochemistry and Behavior, 2014
    Co-Authors: Majid Jafarisabet, Mohammadamin Khodadadnejad, Saeed Ghoraba, Ramin Ataee
    Abstract:

    Abstract In the present study, the effects of intra-dorsal hippocampal (intra-CA1) injections of nitric oxide (NO) agents on muscimol State-Dependent Memory were examined in mice. A single-trial step-down passive avoidance task was used for the assessment of Memory retrieval in adult male NMRI mice. Post-training intra-CA1 administration of a GABA A receptor agonist, muscimol (0.05 and 0.1 μg/mouse) dose dependently induced impairment of Memory retention. Pre-test injection of muscimol (0.05 and 0.1 μg/mouse) induced State-Dependent retrieval of the Memory acquired under post-training muscimol (0.1 μg/mouse, intra-CA1) influence. Pre-test injection of a NO precursor, l -arginine (1 and 2 μg/mouse, intra-CA1) improved Memory retention, although the low dose of the drug (0.5 μg/mouse) did not affect Memory retention. Pre-test injection of an inhibitor of NO-synthase, l -NAME (0.5 and 1 μg/mouse, intra-CA1) impaired Memory retention, although the low dose of the drug (0.25 μg/mouse) did not affect Memory retention. In other series of experiments, pre-test intra-CA1 injection of l -arginine (0.25 and 0.5 μg/mouse) 5 min before the administration of muscimol (0.1 μg/mouse, intra-CA1) dose dependently inhibited muscimol State-Dependent Memory. Pre-test intra-CA1 administration of l -arginine (0.125, 0.25 and 0.5 μg/mouse) by itself cannot affect Memory retention. Pre-test intra-CA1 injection of l -NAME (0.25 μg/mouse, intra-CA1) reversed the Memory impairment induced by post-training administration of muscimol (0.1 μg/mouse, intra-CA1). Moreover, pre-test administration of l -NAME (0.125 and 0.25 μg/mouse, intra-CA1) with an ineffective dose of muscimol (0.025 μg/mouse, intra-CA1) significantly restored the retrieval and induced muscimol State-Dependent Memory. Pre-test intra-CA1 administration of l -NAME (0.0625, 0.125 and 0.25 μg/mouse) by itself cannot affect Memory retention. It may be suggested that the nitric oxide in the dorsal hippocampal area play an important role in muscimol State-Dependent Memory.

Ameneh Rezayof - One of the best experts on this subject based on the ideXlab platform.

  • involvement of dorsal hippocampal nicotinic receptors in the effect of morphine on Memory retrieval in passive avoidance task
    European Journal of Pharmacology, 2008
    Co-Authors: Lotfollah Khajehpour, Ameneh Rezayof, Mohammadreza Zarrindast
    Abstract:

    Abstract The present study evaluated the possible role of nicotinic acetylcholine receptors of the dorsal hippocampus on morphine-induced amnesia and morphine State-Dependent Memory in adult male Wistar rats. The animals were bilaterally implanted with chronic cannulas in the CA1 regions of the dorsal hippocampi, trained in a step-through type passive avoidance task, and tested 24 h after training to measure step-through latency. Results indicate that post-training subcutaneous (s.c.) administration of morphine (2.5–7.5 mg/kg) dose-dependently reduced the step-through latency, showing an amnestic response. Post-training intra-CA1 microinjection of nicotine (0.5–1 μg/rat) decreased significantly the amnesia induced by post-training morphine (7.5 mg/kg). Moreover, co-treatment of mecamylamine (0.5 and 1 μg/rat, intra-CA1) with an ineffective dose of morphine (2.5 mg/kg), immediately after training, caused inhibition of Memory retrieval. On the other hand, amnesia produced by post-training morphine (7.5 mg/kg) was reversed by pre-test administration of the opioid that is due to a State-Dependent effect. Interestingly, pre-test intra-CA1 microinjection of nicotine (0.25 and 0.5 μg/rat) improved post-training morphine (7.5 mg/kg)-induced retrieval impairment. Moreover, pre-test administration of the same doses of nicotine in combination with a lower dose of morphine (0.5 mg/kg), which had no effects alone, synergistically improved Memory performance impaired by post-training morphine. Pre-test injection of mecamylamine (0.5–2 μg/rat) prevented the restoration of Memory by pre-test morphine. It is important to note that post-training or pre-test intra-CA1 administration of the same doses of nicotine or mecamylamine, alone did not affect Memory retrieval. These results suggest that nicotinic acetylcholine receptors of the hippocampal CA1 regions may play an important role in morphine-induced amnesia and morphine State-Dependent Memory.

  • influence of intracerebroventricular administration of dopaminergic drugs on morphine state dependent Memory in the step down passive avoidance test
    Neurobiology of Learning and Memory, 2006
    Co-Authors: Mohammadreza Zarrindast, Azita Khalilzadeh, Soheila Fazlitabaei, Maryam Bananej, Ali Haerirohani, Ameneh Rezayof
    Abstract:

    Abstract The effects of dopaminergic drugs on morphine State-Dependent Memory of passive avoidance task were examined in mice. Pre-training administration of morphine (5 mg/kg) led to State-Dependent learning with impaired Memory retrieval on the test day which was reversed by pre-test administration of the same dose of the opiate. The pre-test intracerebroventricular (i.c.v.) administration of the dopamine D 1 receptor agonist (SKF38393), dopamine D2 receptor agonist (quinpirole) and dopamine D2 receptor antagonist (sulpiride) not only reversed the effect of pre-training morphine treatment, but also increased this action of the drug. Furthermore, the pre-test i.c.v. administration of dopamine D 1 receptor antagonist (SCH23390) prevented the restoration of Memory by morphine. In conclusion, the morphine-induced recovery of Memory, on the test day, seems to be induced, at least in part, through dopamine receptors.