α2‐Adrenoreceptor activation inhibits LTP and LTD in the basolateral amygdala: involvement of Gi/o‐protein‐mediated modulation of Ca2+‐channels and inwardly rectifying K+‐channels in LTD
Abstract
Activation of adrenoreceptors modulates synaptic transmission in the basolateral amygdala. Here, we investigated the effects of alpha2-adrenoreceptor activation on long-term depression and long-term potentiation in an in vitro slice preparation of the mouse basolateral amygdala. Field potentials and excitatory postsynaptic currents were evoked in the basolateral amygdala by stimulating the lateral amygdala. Norepinephrine (20 micro m) reduced synaptic transmission and completely blocked the induction of long-term potentiation and long-term depression. The alpha2-adrenoreceptor antagonist yohimbine (2 micro m) reversed this effect. The alpha2-adrenoreceptor agonist clonidine (10 micro m) mimicked the effects of norepinephrine. The Gi/o-protein inhibitor pertussis toxin (5 micro g/mL) reversed the effect of clonidine. Long-term depression was blocked in the presence of omega-conotoxin GVIA, but not omega-agatoxin IVA. Clonidine inhibited voltage-activated Ca2+ currents mediated via N- or P/Q-type Ca2+-channels. The inhibitory action of clonidine on long-term depression was reversed when inwardly rectifying K+-channels were blocked by Ba2+ (300 micro m). The present data suggest that alpha2-adrenoreceptor activation impairs the induction of long-term depression in the basolateral amygdala by a Gi/o-protein-mediated inhibition of presynaptic N-type Ca2+-channels and activation of inwardly-rectifying K+-channels.
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Stimulation of α2A-ARs weakens amygdala function.
“Stimulation of α2A-ARs weakens amygdala function99, reduces stress-induced dopamine release in the PFC100 and reduces the tonic firing of locus coeruleus neurons and thus reduces norepinephrine release87,101.”
From Stress weakens prefrontal networks: molecular insults to higher cognition (2015) · cites this paper as [99]
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- Authors
- DeBock, F., Kurz, J., Azad, S. C., Parsons, C. G., Hapfelmeier, G., Zieglgänsberger, W., & Rammes, G.
- Affiliations
- TUM Klinikum (DE)
- Max Planck Institute of Psychiatry (DE)
- Merz (Germany) (DE)
- Corresponding author
- Rammes, G.
- Venue
- European Journal of Neuroscience
- Publisher
- Wiley
- Published
- 2003-04
- Volume
- 17
- Issue
- 7
- Pages
- 1411-1424
- ISSN
- 0953-816X (ISSN-L)
- 1460-9568
- OpenAlex
- W2151504418
- Cited by
- 81
- References
- 63
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 4 · 2022: 1 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 1 · 2016: 6 · 2015: 5 · 2014: 4 · 2013: 2 · 2012: 3
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Journal of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- alpha2-adrenoceptors, long-term potentiation, long-term depression, basolateral amygdala, Gi/o proteins, norepinephrine, clonidine, yohimbine, pertussis toxin, omega-conotoxin GVIA, omega-agatoxin IVA, N-type calcium channels, P/Q-type calcium channels, inwardly rectifying potassium channels, presynaptic inhibition, synaptic transmission, lateral amygdala
- MeSH terms
- Adenylyl Cyclase Inhibitors, Adrenergic alpha-Agonists, Adrenergic alpha-Antagonists, Amygdala, Animals, Barium, Cadmium, Calcium Channel Blockers, Clonidine, Electric Stimulation, Enzyme Inhibitors, Colforsin, Imines, Isoquinolines, Membrane Potentials, Norepinephrine, Piperazines, Pyridines, Serotonin Antagonists, Sulfonamides, Yohimbine, 3',5'-Cyclic-AMP Phosphodiesterases, Calcium Channels, Long-Term Potentiation, Receptors, Adrenergic, alpha-2, Patch-Clamp Techniques, Excitatory Postsynaptic Potentials, omega-Agatoxin IVA, omega-Conotoxins, Heterotrimeric GTP-Binding Proteins, Potassium Channels, Inwardly Rectifying, Potassium Channel Blockers, Long-Term Synaptic Depression, Pertussis Toxin, Mice, Cyclic Nucleotide Phosphodiesterases, Type 4, In Vitro Techniques
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