5-HT7 receptors activate the mitogen activated protein kinase extracellular signal related kinase in cultured rat hippocampal neurons

Errico, Monica; Crozier, Robert A.; Plummer, Mark R.; Cowen, David L.

doi:10.1016/s0306-4522(00)00460-7

Cited by 81 publications

(59 citation statements)

References 26 publications

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“…This result is supported by previous studies in astrocytoma cells showing that serotonin via 5-HT7 receptors can indeed activate p38 MAPK as well as PKC (Lieb et al, 2005). The ability of 5-HT7R to activate the ERK-MAPK pathway has also been demonstrated in cultured neurons expressing endogenous 5-HT7R as well as in cells transiently transfected with 5-HT7R (Errico et al, 2001, Speranza et al, 2013and Speranza et al, 2015. The mechanism by which the 5-HT7 receptors activate ERK1/2 has not been completely elucidated.…”

Section: Mechanismmentioning

confidence: 64%

The 5-HT7 receptor triggers cerebellar long-term synaptic depression via PKC-MAPK

et al. 2016

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The 5-HT7 receptor (5-HT7R) mediates important physiological effects of serotonin, such as memory and emotion, and is emerging as a therapeutic target for the treatment of cognitive disorders and depression. Although previous studies have revealed an expression of 5-HT7R in cerebellum, particularly at Purkinje cells, its functional role and signaling mechanisms have never been described. Using patch-clamp recordings in cerebellar slices of adult mice, we investigated the effects of a selective 5-HT7R agonist, LP-211, on the main plastic site of the cerebellar cortex, the parallel fiber-Purkinje cell synapse. Here we show that 5-HT7R activation induces long-term depression of parallel fiber-Purkinje cell synapse via a postsynaptic mechanism that involves the PKC-MAPK signaling pathway. Moreover, a 5-HT7R antagonist abolished the expression of PF-LTD, produced by pairing parallel fiber stimulation with Purkinje cell depolarization; whereas, application of a 5-HT7R agonist impaired LTP induced by 1 Hz parallel fiber stimulation. Our results indicate for the first time that 5-HT7R exerts a fine regulation of cerebellar bidirectional synaptic plasticity that might be involved in cognitive processes and neuropsychiatric disorders involving the cerebellum

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Section: Mechanismmentioning

confidence: 64%

The 5-HT7 receptor triggers cerebellar long-term synaptic depression via PKC-MAPK

et al. 2016

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“…Three principal MAPKs are expressed in various tissues (p42/44, JNK, and p38 MAPK) [26]. Reports are there demonstrating activation of MAP kinase by 5-HT7 receptors in hippocampal neurons [27] and 5-HT induces cyclooxygenase (COX)-2 by acting on MAPK activation in vascular smooth muscle cells [28]. Therefore, 5-HT can regulate the MAPK system.…”

Section: Discussionmentioning

confidence: 99%

5-Hydroxytryptamine Generates Tonic Inward Currents on Pacemaker Activity of Interstitial Cells of Cajal from Mouse Small Intestine

Shahi

Choi

Zuo

et al. 2011

Korean J Physiol Pharmacol

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“…It has been reported that chronic chemical antidepressant administration increases ERK phosphorylation in the rat hippocampus (Schultz et al, 2001). Studies using primary hippocampal and cerebral cortical cultures have directly shown that serotonin and norepinephrine increase the phosphorylation of ERK via specific receptor subtypes for each monoamine (Errico et al, 2001;Tolbert et al, 2003). Recently, it has also been reported that lithium and valproate, commonly used mood stabilizers for the treatment of manic-depressive illness, increase phospho-ERK in the rat hippocampus and frontal cortex (Einat et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Electroconvulsive Seizures Increase the Expression of MAP Kinase Phosphatases in Limbic Regions of Rat Brain

Kodama

Russell

Duman

2004

Neuropsychopharmacol

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The mitogen-activated protein (MAP) kinase cascades regulate a variety of cellular activities, including cell growth, proliferation, and apoptosis, and are reported to play a role in the actions of antidepressant treatment. There are a number of different classes of protein phosphatases that could influence the MAP kinase cascade. One of these, the MAP kinase phosphatase (MKP) family, is known to play a key role in dephosphorylation of activated MAP kinase. In the present study, we analyzed the expression of the MKP1, MKP2, and MKP3 isoforms in rat brain after electroconvulsive seizure (ECS), considered the most effective treatment for depression. In situ hybridization analysis demonstrates that ECS differentially regulates the expression of the MKP isoforms. Expression of MKP1 mRNA is robustly increased by acute ECS in the major cell layers of the hippocampus, including the dentate gyrus granule cell layer and the CA1 and CA3 pyramidal cell layers. In contrast, MKP2 is induced mainly in the dentate gyrus and MKP3 is preferentially increased in the CA1 and CA3 cell layers. In the prefrontal cortex, all three MKP isoforms are upregulated by acute ECS administration. Chronic ECS resulted in a similar pattern of induction for each of the MKP subtypes, demonstrating that there is little or no desensitization of the response to repeated ECS. The induction of MKP expression serves as negative feedback control for the MAP kinase cascades. Upregulation of MKP expression could dampen the actions of ECS, indicating that blockade of the MKPs could enhance the actions of antidepressant treatment.

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5-HT7 receptors activate the mitogen activated protein kinase extracellular signal related kinase in cultured rat hippocampal neurons

Cited by 81 publications

References 26 publications

The 5-HT7 receptor triggers cerebellar long-term synaptic depression via PKC-MAPK

The 5-HT7 receptor triggers cerebellar long-term synaptic depression via PKC-MAPK

5-Hydroxytryptamine Generates Tonic Inward Currents on Pacemaker Activity of Interstitial Cells of Cajal from Mouse Small Intestine

Electroconvulsive Seizures Increase the Expression of MAP Kinase Phosphatases in Limbic Regions of Rat Brain

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