Regulation of NMDA-induced [3H] dopamine release from rat hippocampal slices through sigma-1 binding sites
Introduction
The σ binding sites, originally identified as opiate binding sites, are involved in the action of some neuroleptics (Snyder and Largent, 1989) . The physiological function of σ binding sites and intracellular mechanisms responsible for the pharmacological effects of σ receptor ligands have remained to be determined.
Selective σ ligands have been reported to modulate the N-methyl-d-aspartate (NMDA) response, in vitro and in vivo. Monnet et al. (1990)Monnet et al. 1992aMonnet et al. 1992breported that σ ligands modulate NMDA-induced neuronal activation of CA3 pyramidal neurons and the release of [3H] norepinephrine from hippocampal slices. Sigma ligands have also been found to modulate NMDA-induced intracellular messengers such as cyclic guaninemonophosphate (cGMP) (Ferris et al., 1991) , arachidonic acid (Starr and Werling, 1994) and intracellular Ca2 concentration (Hayashi et al., 1995) . Sigma-1 ligands inhibited [3H] N- [1- (2-thienyl ) cyclohexyl] piperidine (TCP) binding to primary cultured neuronal cells, while σ1 ligands had no apparent effect on [3H] TCP binding to membrane preparations (Yamamoto et al., 1995aYamamoto et al. 1995b) . Moreover, σ1 ligands modulate the MK-801-induced hyperlocomotion in monoamine-depleted mice (Okuyama et al., 1996) . These findings suggest that σ1 binding sites may interact with the NMDA receptor channel complex even though the σ1 binding sites are not the NMDA receptor channel complex itself.
Glutamatergic dysfunction is likely to be involved in the etiology of schizophrenia as well as in dopaminergic hyperactivity (Creese et al., 1976; Toru et al., 1994) . Interactions of σ binding sites with other ionotropic glutamate receptors such as AMPA and kainate have not been fully studied.
We attempted to elucidate the possible involvement of σ binding sites in the regulation by the ionotropic glutamate receptor of the activity of dopaminergic neurons assessing [3H] dopamine release from rat hippocampal slices.
Section snippets
Materials
Male Wistar strain rats, weighing 180–250 g, were used. [3H] Dopamine (S.A. 1.70 and 1.85 TBq\mmol ) was purchased from Amersham, U.K. NMDA and kainate were purchased from Sigma Chemical Co. (St Louis, MO., USA) . α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) was purchased from Research Biochemicals Incorporated (Natick, MA, USA) . N,N-dipropyl-2- [4-methoxy-3- (2-phenylethoxy) phenyl] ethylamine monohydrochloride (NE-100) , 1 (cyclop r o p y l m e t h y l ) -4- (2′- (4″-f l u o r o p
Ionotropic glutamate receptor agonists-induced [3H] dopamine release from rat hippocampal slices
To compare the potency of agonists for ionotropic glutamate receptors in releasing [3H] dopamine from rat hippocampal slices, S1 was determined based on the stimulation induced by 30 μM NMDA and S2 was determined by stimulation of different concentrations of each agonist. NMDA (3–300 μM) , kainate (3–300 μM) or AMPA (3–300 μM) dose-dependently evoked the release of [3H] dopamine from rat hippocampal slices (Fig. 1A) . Among the ionotropic glutamate receptor agonists tested, NMDA was the most
Discussion
We obtained evidence that σ1 ligands modulate the NMDA-induced [3H] dopamine release from rat hippocampal slices.
(+) -Pentazocine, a prototype of the σ1 receptor agonist, inhibited the [3H] dopamine release from rat hippocampal slices elicited by NMDA, while [3H] dopamine release elicited by either AMPA or kainate was not affected. This inhibitory effect of (+) -pentazocine on the NMDA-induced [3H] dopamine release was prevented by σ1 receptor antagonists such as NE-100, DuP734 and XJ448. Thus,
References (28)
- et al.
Eur. J. Pharmacol.
(1990) - et al.
Neurosci. Lett.
(1995) - et al.
Neuropharmacol.
(1996) - et al.
Life Sci
(1994) - et al.
Eur. J. Pharmacol.
(1994) - et al.
LifeSci
(1996) - et al.
Science
(1976) - et al.
J. Neurochem.
(1991) - et al.
J. Neurochem.
(1966) - et al.
J. Pharmacol. Exp. Ther.
(1994)
Eur. J. Pharmacol.
Proc. Natl. Sci. Acad., USA
J. Pharmacol. Exp. Ther.
J. Pharmacol. Exp. Ther.
Cited by (36)
Norepinephrine transporter antagonism prevents dopamine-dependent synaptic plasticity in the mouse dorsal hippocampus
2021, Neuroscience LettersCitation Excerpt :In line with our prior results, the further addition of nisoxetine was still able to diminish the magnitude of strLTP over the last 30 min (Fig. 2C, green traces), reinforcing the finding that NET contributes to DA signaling in dorsal hippocampus. Activation of glutamate receptors, in particular NMDARs, is capable of locally enhancing catecholamine release in hippocampus [28,29]. Expanding on the mechanism of DA release from the NET, we asked if presynaptic NMDARs on LC terminals were involved in our DA-dependent LTP.
Imaging in Parkinson's Disease
2017, International Review of NeurobiologyBrain Imaging of Sigma Receptors
2014, Imaging of the Human Brain in Health and DiseaseN-substituted 8-aminopentacyclo[5.4.0.0<sup>2,6</sup>.0<sup>3,10</sup>. 0<sup>5,9</sup>]undecanes as σ receptor ligands with potential neuroprotective effects
2013, Bioorganic and Medicinal ChemistryCitation Excerpt :However, σ1 receptors are also known to translocate to the plasma membrane, where they regulate voltage-dependent Ca2+ channels and K+ channels.11,12 The ability of σ1 receptors to modulate the activity of several neurotransmitter systems, including those of dopamine (DA),13–15 5-hydroxytryptamine (5-HT),16 and norepinephrine (NE),17,18 has also been demonstrated. The putative σ2 receptor binding site was only recently identified,19 and relatively less is known about the physiological roles of σ2 receptors.
Sigma 1 receptor: A new therapeutic target for pain
2013, European Journal of PharmacologyCitation Excerpt :The synaptic plasticity in the hippocampus is a well established model for learning and memory. σ1 receptor activation in rat hippocampus potentiates glutamate-induced intracellular Ca2+ influx through NMDA receptors by a PKC-dependent mechanism (Monnet et al., 2003) that increases the NMDA receptor response (Hayashi and Su, 2004; Chaki et al., 1998). It was also shown by patch-clamp whole-cell recordings in CA1 pyramidal cells of rat hippocampus that σ1 receptor activation enhances currents through NMDA receptors and long-term potentiation by preventing the opening of small conductance Ca2+-activated K+ channels (Martina et al., 2007).
Synthesis and receptor binding studies of novel 4,4-disubstituted arylalkyl/arylalkylsulfonyl piperazine and piperidine-based derivatives as a new class of σ<inf>1</inf> ligands
2013, European Journal of Medicinal ChemistryCitation Excerpt :With the exception of 30% homology to the yeast enzyme sterol-Δ8/Δ7 isomerase, there are no analogies between σ1 receptors with other mammalian proteins [7,8]. High expressed σ1-Rs in steroid-producing tissues and in CNS suggest their possible roles in neuroendocrine, central neuroactive steroid functions, involvement in psychosis with modulation of synthesis and release of neurotransmitters such as acetylcholine [13] and dopamine [14–16], in modulation of the glutamatergic system with a neuroprotective effect and improvement in learning and memory in animal models of amnesia [17]. Whereas σ1-Rs also plays a key role in modulation of Ca2+ flux [18,19], both subtype receptors are widely over-expressed in many tumor cell lines.