Neurosteroid enhances glutamate release in rat prelimbic cortex via activation of α1-adrenergic and σ1 receptors

Dong, Yi; Fu, Yingmei; Sun, Jianli; Zhu, Yi‐Chun; Sun, Feng-Yan; Zheng, Ping

doi:10.1007/s00018-005-5004-8

Cited by 31 publications

(38 citation statements)

References 39 publications

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“…Loss of function in the fronto-cortical system, involved in the cognitive control of conflict and in the regulation of emotional processes (Kalivas and Volkow, 2005;Perry et al, 2011;Robbins et al, 2008), has been postulated to be responsible for the poor decisionmaking and heightened incentive salience of reward in drug addiction, compulsive eating, and obesity (Boeka and Lokken, 2011;Koob and Volkow, 2010;Volkow et al, 2008). A heightened fronto-cortical Sig-R activity may be responsible for an increase in glutamate release (Dong et al, 2005(Dong et al, , 2007, which, speculatively, may in turn promote compulsiveness for the highly palatable diet and diminished cognitive control Volkow, 2005, 2011;Melendez and Kalivas, 2003;Melendez et al, 2005). Circles show brain regions that were punched out: anterior cingulate cortex (ACC), prefrontal cortex (PFC), insular cortex (IC), dorsal striatum (DS), and nucleus accumbens (NAcc).…”

Section: Discussionmentioning

confidence: 99%

Antagonism of Sigma-1 Receptors Blocks Compulsive-Like Eating

Cottone

Wang

Park

et al. 2012

Neuropsychopharmacol

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Binge eating disorder is an addiction-like disorder characterized by episodes of rapid and excessive food consumption within discrete periods of time which occur compulsively despite negative consequences. This study was aimed at determining whether antagonism of Sigma-1 receptors (Sig-1Rs) blocked compulsive-like binge eating. We trained male wistar rats to obtain a sugary, highly palatable diet (Palatable group) or a regular chow diet (Chow control group), for 1 h a day under fixed ratio 1 operant conditioning. Following intake stabilization, we evaluated the effects of the selective Sig-1R antagonist BD-1063 on food responding. Using a light/dark conflict test, we also tested whether BD-1063 could block the time spent and the food eaten in an aversive, open compartment, where the palatable diet was offered. Furthermore, we measured Sig-1R mRNA and protein expression in several brain areas of the two groups, 24 h after the last binge session. Palatable rats rapidly developed binge-like eating, escalating the 1 h intake by four times, and doubling the eating rate and the regularity of food responding, compared to Chow rats. BD-1063 dose-dependently reduced binge-like eating and the regularity of food responding, and blocked the increased eating rate in Palatable rats. In the light/dark conflict test, BD-1063 antagonized the increased time spent in the aversive compartment and the increased intake of the palatable diet, without affecting motor activity. Finally, Palatable rats showed reduced Sig-1R mRNA expression in prefrontal and anterior cingulate cortices, and a two-fold increase in Sig-1R protein expression in anterior cingulate cortex compared to control Chow rats. These findings suggest that the Sig-1R system may contribute to the neurobiological adaptations driving compulsive-like eating, opening new avenues of investigation towards pharmacologically treating binge eating disorder. Neuropsychopharmacology (2012Neuropsychopharmacology ( ) 37, 2593Neuropsychopharmacology ( -2604 doi:10.1038/npp.2012 published online 20 June 2012 Keywords: binge eating disorder; food intake; eating disorders; addiction; palatability; risk-taking behavior INTRODUCTIONBinge eating disorder is a deadly disease that affects approximately 15 million people in the United States (Hudson et al, 2007) and very frequently occurs comorbidly with obesity, diabetes, cardiovascular diseases, and certain psychiatric conditions, such as anxiety and depression (APA, 2000;Javaras et al, 2008;Wilfley et al, 2011;Yanovski, 2003). Binge eating episodes are characterized by excessive, rapid, and compulsive consumption of highly palatable foods (eg, food rich in sugars and/or fats) within short periods of time, and are followed by food restriction (APA, 2000;Avena et al, 2008;Corwin, 2006). The cyclic binge/restriction pattern of consumption of highly palatable foods has raised the question of whether binge eating disorder can be considered an addiction-'like' disorder; however, the debate remains open (Corwin and Grigson, 2009). An effective ...

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Section: Discussionmentioning

confidence: 99%

Antagonism of Sigma-1 Receptors Blocks Compulsive-Like Eating

Cottone

Wang

Park

et al. 2012

Neuropsychopharmacol

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“…Numerous s 1 protein activators including ( + )-SKF-10 047, ( + )-pentazocine, SA4503, or PRE-084 attenuated Ab 25-35 -induced learning impairments (Maurice et al, 1998;Meunier et al, 2006). Indeed, activation of the s 1 protein rapidly results in amplification of Ca 2 + mobilization from intracellular stores, facilitating Ca 2 + -dependent intracellular pathways and activation of intracellular kinases (Morin-Surun et al, 1999;Hayashi and Su, 2001;Dong et al, 2005). In turn, s 1 protein activators increase hippocampus glutamatergic transmission by facilitating glutamate release, activation of glutamate receptors and long-term potentiation (Monnet et al, 1992;Dong et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, activation of the s 1 protein rapidly results in amplification of Ca 2 + mobilization from intracellular stores, facilitating Ca 2 + -dependent intracellular pathways and activation of intracellular kinases (Morin-Surun et al, 1999;Hayashi and Su, 2001;Dong et al, 2005). In turn, s 1 protein activators increase hippocampus glutamatergic transmission by facilitating glutamate release, activation of glutamate receptors and long-term potentiation (Monnet et al, 1992;Dong et al, 2005). They may also directly facilitate cholinergic neurotransmission by inducing acetylcholine release in the Figure 5 Morphological analysis of astrocytic reaction using GFAP immunolabeling in Ab 25-35 -treated mice.…”

Section: Discussionmentioning

confidence: 99%

Antiamnesic and Neuroprotective Effects of the Aminotetrahydrofuran Derivative ANAVEX1-41 Against Amyloid β25–35-Induced Toxicity in Mice

Villard

Espallergues

Keller

et al. 2008

Neuropsychopharmacol

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The antiamnesic and neuroprotective activities of the new aminotetrahydrofuran derivative tetrahydro-N,N-dimethyl-5,5-diphenyl-3-furanmethanamine hydrochloride (ANAVEX1-41), a nonselective muscarinic receptor ligand and s 1 protein activator, were examined in mice injected intracerebroventricularly with amyloid b [25][26][27][28][29][30][31][32][33][34][35] ) peptide (9 nmol). Ab 25-35 impaired significantly spontaneous alternation performance, a spatial working memory, and passive avoidance response. When ANAVEX1-41 (1-1000 mg/kg i.p.) was administered 7 days after Ab 25-35 , ie, 20 min before the behavioral tests, it significantly reversed the Ab 25-35 -induced deficits, the most active doses being in the 3-100 mg/kg range. When the compound was preadministered 20 min before Ab 25-35 , ie, 7 days before the tests, it prevented the learning impairments at 30-100 mg/kg. Morphological analysis of corticolimbic structures showed that Ab 25-35 induced a significant cell loss in the CA1 pyramidal cell layer of the hippocampus that was prevented by ANAVEX1-41 (100 mg/kg). Increased number of glial fibrillary acidic protein immunopositive cells in the retrosplenial cortex or throughout the hippocampus revealed an Ab 25-35 -induced inflammation that was prevented by ANAVEX1-41. The drug also prevented the parameters of Ab 25-35 -induced oxidative stress measured in hippocampus extracts, ie, the increases in lipid peroxidation and protein nitration. ANAVEX1-41, however, failed to prevent Ab 25-35 -induced caspase-9 expression. The compound also blocked the Ab 25-35 -induced caspase-3 expression, a marker of apoptosis. Both the muscarinic antagonist scopolamine and the s 1 protein inactivator BD1047 prevented the beneficial effects of ANAVEX1-41 (30 or 100 mg/kg) against Ab 25-35 -induced learning impairments, suggesting that muscarinic and s 1 targets are involved in the drug effect. A synergic effect could indeed account for the very low active doses measured in vivo. These data outline the therapeutic potential of ANAVEX1-41 as a neuroprotective agent in Alzheimer's disease.

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“…The effect of PREGS in the prelimbic cortex appears to be mediated via alpha-1 adrenergic and sigma-1 receptors, whereas the effect in the hippocampus is dependent on sigma-1 receptors only. Intracellular calcium released from the endoplasmatic reticulum plays a key role in the enhancement of glutamate release [24]. DHEA-S, another neurosteroid with sigma-1 receptor agonist action, also enhances the spontaneous release of glutamate in prelimbic cortex and hippocampus.…”

Section: Modulation Of Glutamate Release By Sigma-1 Agonistsmentioning

confidence: 99%

The cholinergic system, sigma-1 receptors and cognition

Waarde

Ramakrishnan

Rybczynska

et al. 2011

Behavioural Brain Research

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a b s t r a c tThis article provides an overview of present knowledge regarding the relationship between the cholinergic system and sigma-1 receptors, and discusses potential applications of sigma-1 receptor agonists in the treatment of memory deficits and cognitive disorders. Sigma-1 receptors, initially considered as a subtype of the opioid family, are unique ligand-regulated molecular chaperones in the endoplasmatic reticulum playing a modulatory role in intracellular calcium signaling and in the activity of several neurotransmitter systems, particularly the cholinergic and glutamatergic pathways. Several central nervous system (CNS) drugs show high to moderate affinities for sigma-1 receptors, including acetylcholinesterase inhibitors (donepezil), antipsychotics (haloperidol, rimcazole), selective serotonin reuptake inhibitors (fluvoxamine, sertraline) and monoamine oxidase inhibitors (clorgyline). These compounds can influence cognitive functions both via their primary targets and by activating sigma-1 receptors in the CNS. Sigma-1 agonists show powerful anti-amnesic and neuroprotective effects in a large variety of animal models of cognitive dysfunction involving, among others (i) pharmacologic target blockade (with muscarinic or NMDA receptor antagonists or p-chloroamphetamine); (ii) selective lesioning of cholinergic neurons; (iii) CNS administration of ␤-amyloid peptides; (iv) aging-induced memory loss, both in normal and senescentaccelerated rodents; (v) neurodegeneration induced by toxic compounds (CO, trimethyltin, cocaine), and (vi) prenatal restraint stress.

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Neurosteroid enhances glutamate release in rat prelimbic cortex via activation of α1-adrenergic and σ1 receptors

Cited by 31 publications

References 39 publications

Antagonism of Sigma-1 Receptors Blocks Compulsive-Like Eating

Antagonism of Sigma-1 Receptors Blocks Compulsive-Like Eating

Antiamnesic and Neuroprotective Effects of the Aminotetrahydrofuran Derivative ANAVEX1-41 Against Amyloid β25–35-Induced Toxicity in Mice

The cholinergic system, sigma-1 receptors and cognition

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