Selective serotonin re-uptake inhibition attenuates evoked glutamate release in the dorsal horn of the anaesthetised rat in vivo

Langman, N.J.; Smith, Christopher G.; Whitehead, Kevin J.

doi:10.1016/j.phrs.2005.10.003

Cited by 6 publications

(5 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The addition of a 5-HT uptake blocker to the perfusion fluid is used in some microdialysis experiments to reduce clearance from the extracellular space, thus enhancing the release component of extracellular 5-HT (Adell et al, 2002). On the other hand, low concentrations of 5-HT uptake blockers, such as used in the present study, are without effect on dialysate glutamate in vivo (Langman et al, 2006 ;C. M. T. Queiroz and F. Artigas, unpublished results).…”

Section: Microdialysis Proceduresmentioning

confidence: 73%

Role of different monoamine receptors controlling MK-801-induced release of serotonin and glutamate in the medial prefrontal cortex: relevance for antipsychotic action

López-Gil

Artigas

Adell

2008

Int. J. Neuropsychopharm.

View full text Add to dashboard Cite

Several studies have demonstrated that systemically administered N-methyl-d-aspartate (NMDA) receptor antagonists increase serotonin (5-HT) and glutamate release in the medial prefrontal cortex (mPFC). Previously we showed that the perfusion of clozapine in the mPFC prevented the MK-801-induced increase in extracellular glutamate and 5-HT whereas haloperidol blocked only the effect of MK-801 on glutamate. To study the contribution of different monoaminergic receptors (for which clozapine and haloperidol exhibit distinct affinities) to these effects, here we used in-vivo microdialysis to examine the role of local blockade of dopamine D2, 5-HT2A and alpha1-adrenergic receptors as well as agonism at dopamine D1 and 5-HT1A receptors in the mPFC on the increased efflux of glutamate and 5-HT elicited by MK-801. The results show that M100907 (5-HT2A antagonist), BAY x 3702 (5-HT1A agonist) and prazosin (alpha1-adrenergic antagonist) blocked the MK-801-induced increase of 5-HT and glutamate in the mPFC. However, raclopride, eticlopride (dopamine D2 antagonists) and SKF-38393 (dopamine D1 agonist) were able to prevent the increased efflux of glutamate (but not that of 5-HT) elicited by MK-801. We propose that D2 receptor antagonists and D1 agonists would act predominantly on a subpopulation of GABAergic interneurons of the mPFC, thus leading to an enhanced cortical inhibition that would prevent an excessive glutamatergic transmission. On the other hand, atypical antipsychotic drugs might further act upon 5-HT2A, 5-HT1A and alpha1-adrenoceptors present in pyramidal cells (including those projecting to the dorsal raphe nucleus), which would directly inhibit an excessive excitability of these cells.

show abstract

Section: Microdialysis Proceduresmentioning

confidence: 73%

Role of different monoamine receptors controlling MK-801-induced release of serotonin and glutamate in the medial prefrontal cortex: relevance for antipsychotic action

López-Gil

Artigas

Adell

2008

Int. J. Neuropsychopharm.

View full text Add to dashboard Cite

show abstract

“…The addition of an uptake inhibitor to the perfusion fluid is used in some microdialysis studies to decrease clearance from the extracellular space and magnify the release component of extracellular 5-HT (Adell et al, 2002). On the other hand, low concentrations of 5-HT uptake blockers, such as that used in the present study, are without effect on dialysate glutamate in vivo (Langman et al, 2006;Queiroz and Artigas, unpublished results). Interestingly, voltammetric studies have shown that MK-801 may interact with the serotonin transporter (Iravani et al, 1999;Callado et al, 2000), thereby underscoring the importance of including citalopram in the perfusion fluid.…”

Section: Microdialysis Proceduresmentioning

confidence: 75%

Clozapine and Haloperidol Differently Suppress the MK-801-Increased Glutamatergic and Serotonergic Transmission in the Medial Prefrontal Cortex of the Rat

López-Gil

Babot

Amargós-Bosch

et al. 2007

Neuropsychopharmacol

170

162

View full text Add to dashboard Cite

The administration of noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists such as phencyclidine and ketamine has been shown to increase the extracellular concentration of glutamate and serotonin (5-HT) in the medial prefrontal cortex (mPFC). In the present work, we used in vivo microdialysis to examine the effects of the more potent noncompetitive NMDA receptor antagonist, MK-801, on the efflux of glutamate and 5-HT in the mPFC, and whether the MK-801-induced changes in the cortical efflux of both transmitters could be blocked by clozapine and haloperidol given systemically or intra-mPFC. The systemic, but not the local administration of MK-801, induced an increased efflux of 5-HT and glutamate, which suggests that the NMDA receptors responsible for these effects are located outside the mPFC, possibly in GABAergic neurons that tonically inhibit glutamatergic inputs to the mPFC. The MK-801-induced increases of extracellular glutamate and 5-HT were dependent on nerve impulse and the activation of mPFC AMPA/ kainate receptors as they were blocked by tetrodotoxin and NBQX, respectively. Clozapine and haloperidol blocked the MK-801-induced increase in glutamate, whereas only clozapine was able to block the increased efflux of 5-HT. The local effects of clozapine and haloperidol paralleled those observed after systemic administration, which emphasizes the relevance of the mPFC as a site of action of these antipsychotic drugs in offsetting the neurochemical effects of MK-801. The ability of clozapine to block excessive cortical 5-HT efflux elicited by MK-801 might be related to the superior efficacy of this drug in treating negative/cognitive symptoms of schizophrenia.

show abstract

“…Indirect evidence in animal models or in vitro systems suggests that SSRIs may influence glutamatergic neurotransmission, though the mechanism is not known (Langman et al, 2006;Matrisciano et al, 2008;Shioda et al, 2004;Svenningsson et al, 2007). For example, an in vitro model of neurogenesis suggests synergy between SSRIs and glutamate receptor (mGluR2 and 3) agonists (Matrisciano et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Genetic and Clinical Predictors of Sexual Dysfunction in Citalopram-Treated Depressed Patients

Perlis

Laje

Smoller

et al. 2009

Neuropsychopharmacol

View full text Add to dashboard Cite

Sexual dysfunction is a major contributor to treatment discontinuation and nonadherence among patients treated with selective serotonin reuptake inhibitors (SSRIs). The mechanisms by which depressive symptoms in general, as well as SSRI exposure in particular, may worsen sexual function are not known. We examined genetic polymorphisms, including those of the serotonin and glutamate systems, for association with erectile dysfunction, anorgasmia, and decreased libido during citalopram treatment. Clinical data were drawn from a nested case-control cohort derived from the STAR*D study, a multicenter, prospective, effectiveness trial in outpatients with nonpsychotic major depressive disorder (MDD). Self-reports of erectile dysfunction, decreased libido, or difficulty achieving orgasm based on the Patient-Rated Inventory of Side Effects were examined among Caucasian subjects (n ¼ 1473) for whom DNA and adverse effect measures were available, and who were treated openly with citalopram for up to 14 weeks. Of 1473 participants, 799 (54%) reported decreased libido; 525 (36%) reported difficulty achieving orgasm. Of 574 men, 211 (37%) reported erectile dysfunction. Using a set-based test for association, single nucleotide polymorphisms in glutamatergic genes were associated with decreased libido (GRIA3; GRIK2), difficulty achieving orgasm (GRIA1), and difficulty achieving erection (GRIN3A) (experiment-wide permuted po0.05 for each). Evidence of association persisted after adjustment for baseline clinical and sociodemographic differences. Likewise, evidence of association was similar when the cohort was limited to those who did not report a given adverse event at the first post-baseline visit (ie, those whose adverse events were known to be treatment emergent). These hypothesis-generating analyses suggest the potential for glutamatergic treatment targets for sexual dysfunction during major depressive episodes.

show abstract

Selective serotonin re-uptake inhibition attenuates evoked glutamate release in the dorsal horn of the anaesthetised rat in vivo

Cited by 6 publications

References 44 publications

Role of different monoamine receptors controlling MK-801-induced release of serotonin and glutamate in the medial prefrontal cortex: relevance for antipsychotic action

Role of different monoamine receptors controlling MK-801-induced release of serotonin and glutamate in the medial prefrontal cortex: relevance for antipsychotic action

Clozapine and Haloperidol Differently Suppress the MK-801-Increased Glutamatergic and Serotonergic Transmission in the Medial Prefrontal Cortex of the Rat

Genetic and Clinical Predictors of Sexual Dysfunction in Citalopram-Treated Depressed Patients

Contact Info

Product

Resources

About