The 5‐HT1A receptor agonist 8‐OH‐DPAT prevents prefrontocortical glutamate and serotonin release in response to blockade of cortical NMDA receptors

Calcagno, E.; Carli, M.; Invernizzi, R. W.

doi:10.1111/j.1471-4159.2005.03600.x

Cited by 54Neurotransmitter Receptor Influence on BehaviorNeuroscience and Neuropharmacology ResearchReceptor Mechanisms and Signaling

The 5‐HT1A receptor agonist 8‐OH‐DPAT prevents prefrontocortical glutamate and serotonin release in response to blockade of cortical NMDA receptors

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Calcagno, E., Carli, M., Invernizzi, R. W.·2006·Journal of Neurochemistry

DOI 10.1111/j.1471-4159.2005.03600.x

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Abstract

We studied the role of 5‐HT 1A receptors in controlling the release of glutamate (GLU) in the medial prefrontal cortex (mPFC) of conscious rats with the in vivo microdialysis technique. The effect of the 5‐HT 1A receptor agonist 8‐hydroxy‐2‐(di‐n‐propylamino)tetralin infused in the prefrontal cortex was examined under basal conditions and on the rise of extracellular GLU (+106%) induced by co‐infusion of the competitive N‐methyl‐d‐aspartate receptor antagonist 3‐[(R)‐2‐carboxypiperazin‐4yl]‐propyl‐1‐phosphonic acid (CPP). 8‐OH‐DPAT (0.3 and 3 μ m) had no effect on basal extracellular GLU, but the higher concentration completely abolished the rise of extracellular GLU induced by CPP. CPP also increased extracellular serotonin (5‐HT) in the mPFC (+50%) and this effect was antagonized by 3 μ m 8‐OH‐DPAT which, by itself, had no effect on basal 5‐HT release. The effects of 8‐OH‐DPAT on extracellular GLU and 5‐HT were reversed by the 5‐HT 1A receptor antagonist WAY100 635 (100 μ m), indicating a selective involvement of 5‐HT 1A receptors. WAY100 635 had no effect by itself. These results show that the stimulation of cortical 5‐HT 1A receptors prevents the CPP‐evoked rise of extracellular GLU and 5‐HT and suggest that these effects may contribute to the ability of intracortical 8‐OH‐DPAT to counteract cognitive deficits caused by the blockade of NMDA receptors.

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5-HT1A antagonism with 8-OH-DPAT within the PFC blocks CPP-induced elevations in extracellular glutamate.
“5-HT1A antagonism with 8-OH-DPAT within the PFC was also able to block CPP-induced elevations in extracellular glutamate (Calcagno et al 2006).”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Calcagno et al 2006

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E. Calcagno et al. Journal Compilation Ó 2005 International Society for Neurochemistry, J. Neurochem. (2006) 96, 853-860
Ó 2005 The authors 14714159, 2006, 3, · DOI
Ó 2005 The authors Journal Compilation Ó 2005 International Society for Neurochemistry, J. Neurochem. (2006) 96, 853-860 14714159, 2006, 3, raphe prevents the drug's effect in the frontal cortex. Brain Res. 584, 322-324. · DOI
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Authors: Calcagno, E., Carli, M., & Invernizzi, R. W.
Affiliations: Mario Negri Institute for Pharmacological Research (IT)
Corresponding author: Invernizzi, R. W.
ORCID: Carli, M.
Invernizzi, R. W.
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2006-01-09
Volume: 96
Issue: 3
Pages: 853-860
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1111/j.1471-4159.2005.03600.x
OpenAlex: W2070941417
Cited by: 54
References: 67
Citations by year: 2025: 1 · 2021: 1 · 2019: 1 · 2018: 1 · 2017: 3 · 2016: 2 · 2015: 1 · 2014: 6 · 2013: 6 · 2012: 5
FWCI: 1.39
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Neurochemistry (publishedVersion)
PubMed (publishedVersion)
Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
Funders: Ministero dell’Istruzione, dell’Università e della Ricerca (RBAU01ZS5C)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords: 5-HT1A receptor, 8-OH-DPAT, glutamate release, serotonin release, medial prefrontal cortex, NMDA receptor blockade, CPP, WAY-100635, cognitive impairment, glutamatergic neurotransmission, serotonergic neurotransmission
MeSH terms: Animals, Chromatography, High Pressure Liquid, Dialysis, Dose-Response Relationship, Drug, Drug Interactions, Electrochemistry, Male, Piperazines, Pyridines, Serotonin, Serotonin Antagonists, Receptors, N-Methyl-D-Aspartate, Serotonin Receptor Agonists, 8-Hydroxy-2-(di-n-propylamino)tetralin, Prefrontal Cortex, Excitatory Amino Acid Antagonists, Glutamic Acid, Rats

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The 5‐HT1A receptor agonist 8‐OH‐DPAT prevents prefrontocortical glutamate and serotonin release in response to blockade of cortical NMDA receptors

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