The 5-HT1A receptor and recognition memory

Pitsikas, Nikolaos; Tsitsirigou, Stavroula; Zisopoulou, Styliani; Sakellaridis, Nikolaos

doi:10.1016/j.bbr.2004.11.007

Cited by 30 publications

(4 citation statements)

References 48 publications

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“…While no studies have examined the effects of specific receptors targets of mirtazapine in the maintenance of psychostimulant-induced behaviors, a role of the 5-HT 1A receptor (an indirect effect of mirtazapine) in the maintenance of mnemonic processes has been explored. Administration of a 5-HT 1A receptor agonist after training (as mirtazapine was given in the current study) inhibits the maintenance of spatial and fear-conditioned memories [60–62]. Thus, in the current study mirtazapine may have inhibited the maintenance of methamphetamine-induced associative learning via a number of different receptor systems and further studies with repeated administration of selective ligands are needed to determine the receptor(s) responsible for the observed behavioral inhibition by mirtazapine in the current study.…”

Section: Discussionmentioning

confidence: 99%

Repeated mirtazapine nullifies the maintenance of previously established methamphetamine-induced conditioned place preference in rats

Voigt

Mickiewicz

Napier

2011

Behavioural Brain Research

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The atypical antidepressant mirtazapine enhances monoaminergic transmission; thus, mirtazapine therapy may counter the hypo-activation of monoamine systems associated with withdrawal from methamphetamine abuse. Human addiction therapy will likely require chronic administration that is given after brain and behavioral maladaptations are established. To emulate this scenario in rats, we ascertained if acute or repeated mirtazapine treatments could antagonize previously established consequences of repeated methamphetamine. Methamphetamine-induced conditioned place preference (CPP) was used, wherein methamphetamine (1mg/kg, i.p.) was administered in a unique environmental context once-daily for three days interposed by saline injections in an alternate context. Subsequently, mirtazapine (5mg/kg, i.p.) was administered in the home cage either as 10 once-daily injections or a single injection. The expression of CPP was determined in drug-free rats three days after the last mirtazapine injection. Expression of methamphetamine-induced CPP was inhibited by 10 home cage administrations of mirtazapine but not by a single injection of mirtazapine. These findings reveal that mirtazapine can inhibit the maintenance of methamphetamine-induced CPP and that treatment duration and/or treatment timing contributes to this effect of mirtazapine.

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Section: Discussionmentioning

confidence: 99%

Repeated mirtazapine nullifies the maintenance of previously established methamphetamine-induced conditioned place preference in rats

Voigt

Mickiewicz

Napier

2011

Behavioural Brain Research

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“…For example, although low doses of the 5-HT 1A receptor agonist 8-hydroxy-2-(di- n -propylamino)tetralin (8-OH-DPAT) are neutral in terms of their effects on water maze performance (Riekkinen et al, 1994 ), while higher doses of 8-OH-DPAT or the 5-HT 1A receptor agonist buspirone tend to impair water maze performance (Kant et al, 1998 ; Meijer et al, 1998 ). Similarly, 8-OH-DPAT administration impairs performance in novel object recognition (Pitsikas et al, 2005 ) and in putative spatial working memory tasks such as spontaneous alternation (Seibell et al, 2003 ; Ulloa et al, 2004 ). Although it is important to note that there may be sex-dependent effects of 8-OH-DPAT, given that Ulloa et al ( 2004 ) found that this ligand had no effect on spontaneous alternation performance in female rats.…”

Section: Effects Of Selective Serotonin Receptor Mechanisms On Arc Exmentioning

confidence: 99%

“…When administered alone, 5-HT 1A receptor antagonists such as WAY100635 generally have no effect on performance in recognition memory (Pitsikas et al, 2003 , 2005 ), or in autoshaping tasks (Meneses and Hong, 1999 ).…”

Section: Effects Of Selective Serotonin Receptor Mechanisms On Arc Exmentioning

confidence: 99%

A critical evaluation of the activity-regulated cytoskeleton-associated protein (Arc/Arg3.1)'s putative role in regulating dendritic plasticity, cognitive processes, and mood in animal models of depression

Pehrson

Waller

et al. 2015

Front. Neurosci.

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Major depressive disorder (MDD) is primarily conceptualized as a mood disorder but cognitive dysfunction is also prevalent, and may limit the daily function of MDD patients. Current theories on MDD highlight disturbances in dendritic plasticity in its pathophysiology, which could conceivably play a role in the production of both MDD-related mood and cognitive symptoms. This paper attempts to review the accumulated knowledge on the basic biology of the activity-regulated cytoskeleton-associated protein (Arc or Arg3.1), its effects on neural plasticity, and how these may be related to mood or cognitive dysfunction in animal models of MDD. On a cellular level, Arc plays an important role in modulating dendritic spine density and remodeling. Arc also has a close, bidirectional relationship with postsynaptic glutamate neurotransmission, since it is stimulated by multiple glutamatergic receptor mechanisms but also modulates α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor internalization. The effects on AMPA receptor trafficking are likely related to Arc's ability to modulate phenomena such as long-term potentiation, long-term depression, and synaptic scaling, each of which are important for maintaining proper cognitive function. Chronic stress models of MDD in animals show suppressed Arc expression in the frontal cortex but elevation in the amygdala. Interestingly, cognitive tasks depending on the frontal cortex are generally impaired by chronic stress, while those depending on the amygdala are enhanced, and antidepressant treatments stimulate cortical Arc expression with a timeline that is reminiscent of the treatment efficacy lag observed in the clinic or in preclinical models. However, pharmacological treatments that stimulate regional Arc expression do not universally improve relevant cognitive functions, and this highlights a need to further refine our understanding of Arc on a subcellular and network level.

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“…nNOS and NO inhibits 5-HT uptake (Bryan-Lluka et al, 2004; Chanrion et al, 2007; Harkin et al, 2003; Inan et al, 2004) and the function of 5-HT 1 auto-receptors on raphe neurons (Chiavegatto and Nelson, 2003; Pitsikas et al, 2005). Both effects should increase extracellular 5-HT levels and 5-HT receptor activation.…”

Section: 0 Discussionmentioning

confidence: 99%

Spinal nNOS regulates phrenic motor facilitation by a 5-HT2B receptor- and NADPH oxidase-dependent mechanism

2014

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Acute intermittent hypoxia (AIH) induces phrenic long-term facilitation (pLTF) by a mechanism that requires spinal serotonin (5-HT) receptor activation and NADPH oxidase (NOX) activity. Here, we investigated whether: 1) spinal nitric oxide synthase (NOS) activity is necessary for AIH-induced pLTF; 2) episodic exogenous nitric oxide (NO) is sufficient to elicit phrenic motor facilitation (pMF) without AIH (i.e. pharmacologically); and 3) NO-induced pMF requires spinal 5-HT2B receptor and NOX activation. In anesthetised, mechanically ventilated adult male rats, AIH (3×5min episodes; 10% O2; 5min) elicited a progressive increase in the amplitude of integrated phrenic nerve bursts (i.e. pLTF), which lasted 60 min post-AIH (45.1 ± 8.6% baseline). Pre-treatment with intrathecal (i.t.) injections of a neuronal NOS inhibitor (nNOS-inhibitor-1) near the phrenic motor nucleus attenuated pLTF (14.7 ± 2.5%), whereas an inducible NOS (iNOS) inhibitor (1400W) had no effect (56.3 ± 8.0%). Episodic i.t. injections (3×5μl volume; 5mins) of a NO donor (sodium nitroprusside; SNP) elicited pMF similar in time-course and magnitude (40.4 ± 6.0%, 60 min post-injection) to AIH-induced pLTF. SNP-induced pMF was blocked by a 5-HT2B receptor antagonist (SB206553), a superoxide dismutase mimetic (MnTMPyP), and two NOX inhibitors (apocynin and DPI). Neither pLTF nor pMF were affected by pre-treatment with a PKG inhibitor (KT-5823). Thus, spinal nNOS activity is necessary for AIH-induced pLTF, and episodic spinal NO is sufficient to elicit pMF by a mechanism that requires 5-HT2B receptor activation and NOX-derived ROS formation, which indicates AIH (and NO) elicits spinal respiratory plasticity by a nitrergic-serotonergic mechanism.

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The 5-HT1A receptor and recognition memory

Cited by 30 publications

References 48 publications

Repeated mirtazapine nullifies the maintenance of previously established methamphetamine-induced conditioned place preference in rats

Repeated mirtazapine nullifies the maintenance of previously established methamphetamine-induced conditioned place preference in rats

A critical evaluation of the activity-regulated cytoskeleton-associated protein (Arc/Arg3.1)'s putative role in regulating dendritic plasticity, cognitive processes, and mood in animal models of depression

Spinal nNOS regulates phrenic motor facilitation by a 5-HT2B receptor- and NADPH oxidase-dependent mechanism

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