The effects of CA1 5HT4 receptors in MK801-induced amnesia and hyperlocomotion

Nasehi, Mohammad; Tabatabaie, Maryam; Khakpai, Fatemeh; Zarrindast, Mohammad‐Reza

doi:10.1016/j.neulet.2014.12.019

Cited by 19 publications

(5 citation statements)

References 40 publications

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“…It has been demonstrated that 5-HT4 receptors are located on the CA1 pyramidal neurons (Andrade and Chaput, 1991; Roychowdhury et al, 1994), and therefore they provide a regulatory mechanism by which 5-HT may bidirectionally modulate the responsiveness of individual pyramidal cells. Our findings are in agreement with other behavioral data in which RS67333 or RS23597 impaired memory when they were microinjected into the CA1 region (Nasehi et al, 2015e), CA3 region (Nasehi et al, 2015c), or basolateral amygdala (Chegini et al, 2014). In contrast, some pharmacological evidence indicates that 5-HT4 receptors (BIMU1 or BIMU8) may improve learning and memory (Bockaert, Claeysen, et al, 2004; Meneses, 1999).…”

Section: Discussionsupporting

confidence: 93%

Modulation of cannabinoid signaling by hippocampal 5-HT4 serotonergic system in fear conditioning

et al. 2016

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Behavioral studies have suggested a key role for the cannabinoid system in the modulation of conditioned fear memory. Likewise, much of the literature has revealed that the serotonergic system affects Pavlovian fear conditioning and extinction. A high level of functional overlap between the serotonin and cannabinoid systems has also been reported. To clarify the interaction between the hippocampal serotonin (5-HT4) receptor and the cannabinoid CB1 receptor in the acquisition of fear memory, the effects of 5-HT4 agents, arachidonylcyclopropylamide (ACPA; CB1 receptor agonist), and the combined use of these drugs on fear learning were studied in a fear conditioning task in adult male NMRI mice. Pre-training intraperitoneal administration of ACPA (0.1 mg/kg) decreased the percentage of freezing time in both context- and tone-dependent fear conditions, suggesting impairment of the acquisition of fear memory. Pre-training, intra-hippocampal (CA1) microinjection of RS67333, a 5-HT4 receptor agonist, at doses of 0.1 and 0.2 or 0.2 µg/mouse impaired contextual and tone fear memory, respectively. A subthreshold dose of RS67333 (0.005 µg/mouse) did not alter the ACPA response in either condition. Moreover, intra-CA1 microinjection of RS23597 as a 5-HT4 receptor antagonist did not alter context-dependent fear memory acquisition, but it did impair tone-dependent fear memory acquisition. However, a subthreshold dose of the RS23597 (0.01 µg/mouse) potentiated ACPA-induced fear memory impairment in both conditions. Therefore, we suggest that the blockade of hippocampal 5-HT4 serotonergic system modulates cannabinoid signaling induced by the activation of CB1 receptors in conditioned fear.

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Section: Discussionsupporting

confidence: 93%

Modulation of cannabinoid signaling by hippocampal 5-HT4 serotonergic system in fear conditioning

et al. 2016

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“…Certainly, forgetting as therapeutic targets for dysfunctional memory it has been little explored. As above mentioned, similar results, including pharmacological and neurobiological changes to those reported in autoshaping have been described in other memory behavioral tasks (for review see King et al, 2008 ; Marcos et al, 2008 ; Da Silva Costa-Aze et al, 2012 ; Reichel et al, 2012 ; Woods et al, 2012 ; Haahr et al, 2013 ; Freret et al, 2014 ; Nasehi et al, 2014b ; Seyedabadi et al, 2014 ; Subramaniyan et al, 2014 ; Wilkinson et al, 2014 ; Delotterie et al, 2015 ; Sase et al, 2015 ; Westrich et al, 2015 ).…”

Section: Memory Tasks and Molecular Changessupporting

confidence: 69%

Serotonin, neural markers, and memory

Meneses¹

2015

Front. Pharmacol.

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Diverse neuropsychiatric disorders present dysfunctional memory and no effective treatment exits for them; likely as result of the absence of neural markers associated to memory. Neurotransmitter systems and signaling pathways have been implicated in memory and dysfunctional memory; however, their role is poorly understood. Hence, neural markers and cerebral functions and dysfunctions are revised. To our knowledge no previous systematic works have been published addressing these issues. The interactions among behavioral tasks, control groups and molecular changes and/or pharmacological effects are mentioned. Neurotransmitter receptors and signaling pathways, during normal and abnormally functioning memory with an emphasis on the behavioral aspects of memory are revised. With focus on serotonin, since as it is a well characterized neurotransmitter, with multiple pharmacological tools, and well characterized downstream signaling in mammals' species. 5-HT1A, 5-HT4, 5-HT5, 5-HT6, and 5-HT7 receptors as well as SERT (serotonin transporter) seem to be useful neural markers and/or therapeutic targets. Certainly, if the mentioned evidence is replicated, then the translatability from preclinical and clinical studies to neural changes might be confirmed. Hypothesis and theories might provide appropriate limits and perspectives of evidence.

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“…Regarding the effects of NMDAR antagonists on motor function, it is known that MK-801 induces hyperlocomotion [64]. Additionally, MK801 and amantadine attenuate catalepsy induced by dopamine depletion after reserpine and haloperidol administration [18,65,66].…”

Section: Discussionmentioning

confidence: 99%