Possible involvement of CA1 5-HT1B/1D and 5-HT2A/2B/2C receptors in harmaline-induced amnesia

Nasehi, Mohammad; Jamshidi-Mehr, Mehdi; Khakpai, Fatemeh; Zarrindast, Mohammad‐Reza

doi:10.1016/j.pbb.2014.08.007

Cited by 22 publications

(11 citation statements)

References 62 publications

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“…A considerable body of evidence has highlighted the role of harmaline in excitation, euphoria (Rommelspacher et al, 1980), Ca 2+ -homeostasis (Moura et al, 2006), motor tremor (Lamarre and Mercier, 1971), and alteration in associative and motor learning (Du and Harvey, 1997). According to our results, it has been indicated that harmaline impaired memory acquisition (Nasehi et al, 2014;Nasehi et al, 2015;Nasehi et al, 2016), and associative and motor learning (Welsh, 1998). In contrast, some evidence showed that harmaline improved LTM (Moura et al, 2006).…”

Section: Discussionsupporting

confidence: 51%

“…The drugs used in the present study were harmaline (1-methyl-7-methoxy-3,4-dihydro-b-carboline) from Sigma (St. Louis, MO), phaclofen (Sigma, St. Louis, CA, USA) and baclofen (Tocris, UK). The time of injection and doses of the drugs was selected based on our previous studies (Khanegheini et al, 2015;Nasehi et al, 2014;Nasehi et al, 2015;Nasehi et al, 2016). The compounds were tested at doses: harmaline: 1, 2 and 4 mg/kg, phaclofen: 0.001, 0.01, and 0.1 g/mouse, baclofen: 0.001, 0.01, and 0.1 g/mouse.…”

Section: Drugsmentioning

confidence: 99%

“…Moreover, there are reports showing that ␤-carboline alkaloids increase GABA responses in the spinal cord neurons (Skerritt and Macdonald, 1984), and cerebral cortex (Malatynska et al, 1992). In view of (1) the existence of interaction between GABA receptors and harmaline (Malatynska et al, 1992;Skerritt and Macdonald, 1984;Weiss et al, 1995), and (2) the role of hippocampus (Khakpai et al, 2012;Khakpai et al, 2013;Khakpai et al, 2016), harmaline (Nasehi et al, 2014;Nasehi et al, 2015;Nasehi et al, 2016), and GABA receptors (Nakagawa and Takashima, 1997;Shahidi et al, 2008;Yousefi et al, 2012) in learning and memory processes, the aim of the current research was to investigate the effects of harmaline and GABA B receptors on memory consolidation and locomotor activity in the step-down inhibitory avoidance and open field test. In the first set of experiments, the effect of the inhibition and stimulation of GABA B receptors in the CA1 area on memory consolidation was investigated.…”

Section: Introductionmentioning

confidence: 99%

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Possible involvement of the CA1 GABAergic system on harmaline induced memory consolidation deficit

Nasehi

Saadati

Khakpai

et al. 2017

Brain Research Bulletin

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Activation of the GABA receptors inhibit learning and memory processes. The current research was designed to examine the role of dorsal hippocampal (CA1) GABA receptors on harmaline induced memory consolidation deficit in mice. For this purpose, the effects induced by the GABA antagonist phaclofen and the GABA agonist baclofen on memory consolidation were assessed by using the step-down inhibitory avoidance task. Furthermore, the possible involvement of harmaline on GABA receptor's effects was also assessed through using the same behavioral procedure. In a first dose response experiments, post-training intra-CA1 injections of phaclofen did not change while baclofen (0.1μg/mouse) impaired animals' performance in this task, suggesting a modulation of storage of information. Moreover, Post-training intra-peritoneal (i.p.) infusion of harmaline (2 and 5mg/kg) also decreased memory consolidation. Interestingly, phaclofen at the sub-threshold dose (0.001μg/mouse, intra-CA1), successfully antagonized the deficits on memory consolidation induced by the highest doses of harmaline (2 and 4mg/kg, i.p.). On the other hand, non significant dose of baclofenc (0.001μg/mouse, intra-CA1) potentiated impairment of memory consolidation induced by harmaline (2mg/kg, i.p.). In addition in all experiments, locomotor activity did not alter significantly. These results indicate a) that the CA1 GABA receptors are involved in memory consolidation b) that harmaline interact with the CA1 GABA receptors in modulation of memory consolidation.

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Section: Discussionsupporting

confidence: 51%

Section: Drugsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Possible involvement of the CA1 GABAergic system on harmaline induced memory consolidation deficit

Nasehi

Saadati

Khakpai

et al. 2017

Brain Research Bulletin

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“…However, different from a partial attenuation of the late-phase hyperactivity by Lu AF21934, a positive allosteric modulator of metabotropic glutamate receptor 4 (mGlu4) [41], the present study showed a complete attenuation of the early-phase hypoactivity by 5-HT 1A receptor antagonist WAY-100635 (Figure 4). While harmaline interacts with various receptors [41–43], the contribution of 5-HT 1A receptor to mouse home-cage activity may be explained by the facts that harmaline acts as a 5-HT 1A receptor agonist [28, 42, 44], and harmaline-mediated inhibition of MAO-A leads to a remarkable increase of 5-HT level in central nervous system where 5-HT itself exhibits a higher affinity to 5-HT 1A receptor than other 5-HT receptors [25, 45, 46]. In addition, the critical role of 5-HT 1A receptor in hypoactivity, different from the transient hyperactivity caused by handling and injection stresses (Figure 1), is in agreement with previous findings on the importance of 5-HT 1A receptor in the control of locomotor activities in rats [47].…”

Section: Discussionmentioning

confidence: 99%

Modification of 5-methoxy-N,N-dimethyltryptamine-induced hyperactivity by monoamine oxidase A inhibitor harmaline in mice and the underlying serotonergic mechanisms

Jiang

Shen

2016

Pharmacological Reports

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Background 5-Methoxy-N,N-dimethyltryptamine (5-MeO-DMT) and harmaline are indolealkylamine (IAA) drugs often abused together. Our recent studies have revealed the significant effects of co-administered harmaline, a monoamine oxidase inhibitor (MAOI), on 5-MeO-DMT pharmacokinetics and thermoregulation. This study was to delineate the impact of harmaline and 5-MeO-DMT on home-cage activity in mouse models, as well as the contribution of serotonin (5-HT) receptors. Methods Home-cage activities of individual animals were monitored automatically in the home cages following implantation of telemetry transmitters and administration of various doses of IAA drugs and 5-HT receptor antagonists. Area under the effect curve (AUEC) of mouse activity values were calculated by trapezoidal rule. Results High dose of harmaline (15 mg/kg, ip) alone caused an early-phase (0–45 min) hypoactivity in mice that was fully attenuated by 5-HT1A receptor antagonist WAY-100635, whereas a late-phase (45–180 min) hyperactivity that was reduced by 5-HT2A receptor antagonist MDL-100907. 5-MeO-DMT (10 and 20 mg/kg, ip) alone induced biphasic effects, an early-phase (0–45 min) hypoactivity that was completely attenuated by WAY-100635, and a late-phase (45–180 min) hyperactivity that was fully suppressed by MDL-100907. Interestingly, co-administration of MAOI harmaline (2–15 mg/kg) with a subthreshold dose of 5-MeO-DMT (2 mg/kg) induced excessive hyperactivities at late phase (45–180 min) that could be abolished by either WAY-100635 or MDL-100907. Conclusions Co-administration of MAOI with 5-MeO-DMT provokes excessive late-phase hyperactivity, which involves the activation of both 5-HT1A and 5-HT2A receptors.

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“…The injector cannula was attached to a 2.5 μl Hamilton syringe via a polyethylene tubing. Injection time was 60 s, followed by an additional 60 s to facilitate diffusion of the drug from the tip of the injection cannula (Nasehi et al, 2013;Nasehi et al, 2014).…”

Section: Drugs and Injectionsmentioning

confidence: 99%

The hippocampal NMDA receptors may be involved in acquisition, but not expression of ACPA-induced place preference

Nasehi

Sharaf-Dolgari

Ebrahimi-Ghiri

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Possible involvement of CA1 5-HT1B/1D and 5-HT2A/2B/2C receptors in harmaline-induced amnesia

Cited by 22 publications

References 62 publications

Possible involvement of the CA1 GABAergic system on harmaline induced memory consolidation deficit

Possible involvement of the CA1 GABAergic system on harmaline induced memory consolidation deficit

Modification of 5-methoxy-N,N-dimethyltryptamine-induced hyperactivity by monoamine oxidase A inhibitor harmaline in mice and the underlying serotonergic mechanisms

The hippocampal NMDA receptors may be involved in acquisition, but not expression of ACPA-induced place preference

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