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Cited by 172Memory and Neural MechanismsNeuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on Behavior

Regulation of conditioned responses of basolateral amygdala neurons

GRACE, A, ROSENKRANZ, J·2002·Physiology & Behavior
DOI 10.1016/s0031-9384(02)00909-5
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Abstract

The basolateral amygdala (BLA) is a component of a system that drives and modulates affective behavior. Some forms of affective behavior are regulated by the prefrontal cortex (PFC) and enhanced by dopamine (DA). By using intracellular and extracellular electrophysiological techniques in anesthetized rats, our studies attempt to uncover cellular mechanisms that allow for regulation of affect by PFC-induced inhibition of BLA output and plasticity, as well as mechanisms by which DA enhances affective behavior via modulation of BLA neuronal excitability, afferent input and plasticity. We have found that stimulation of medial PFC (mPFC) results in a profound inhibition of BLA output, manifest as a suppression of spontaneous, intracellular current-driven or sensory cortical afferent-driven spike firing of BLA projection neurons. This inhibition is mediated by excitation of GABAergic interneurons of the BLA. Activation of DA receptors attenuates this inhibitory action of the mPFC, while enhancing other (i.e., sensory-related) inputs by increases in postsynaptic excitability of BLA projection neurons. Furthermore, Pavlovian conditioning procedures that pair an odor with a footshock result in enhanced odor-evoked postsynaptic potentials. This plasticity of odor-evoked responses is blocked by antagonism of DA receptors and by stimulation of mPFC. Our data indicate that the mPFC exerts regulatory control over BLA via suppression of spontaneous and sensory-driven activity, as well as BLA plasticity. Activation of DA receptors suppresses the inhibitory influence of the mPFC, allowing sensory-driven BLA activity and plasticity. Functionally, in the presence of high DA levels, which suppresses mPFC-evoked inhibition, one source of affective control will be dampened. Furthermore, sensory-related inputs will be further enhanced by the increased excitability of BLA neurons. This situation is expected to maximize affective responses to sensory stimuli, as well as plasticity.

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  • The mPFC exerts powerful feedforward inhibition over the baseline activity of BLA principal neurons in vivo.

    “the mPFC has been demonstrated to exert powerful feedforward inhibition over the baseline activity of BLA principal neurons in vivo116”

    From Resolving the neural circuits of anxiety (2015) · cites this paper as [116]

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Authors
GRACE, A., & ROSENKRANZ, J.
Affiliations
University of Pittsburgh (US)
Corresponding author
GRACE, A
ORCID
Venue
Physiology & Behavior
Publisher
Elsevier BV
Published
2002-12
Volume
77
Issue
4-5
Pages
489-493
ISSN
0031-9384 (ISSN-L)
DOI
10.1016/s0031-9384(02)00909-5
OpenAlex
W2075329358
Cited by
172
References
35
Citations by year
2026: 2 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 4 · 2021: 6 · 2020: 7 · 2019: 4 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 13 · 2014: 7 · 2013: 10 · 2012: 15
FWCI
3.17
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Physiology & Behavior (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
basolateral amygdala, medial prefrontal cortex, dopamine receptors, classical conditioning, fear conditioning, GABAergic interneurons, neuronal excitability, synaptic plasticity, emotional behavior, projection neurons, odor-evoked responses
MeSH terms
Amygdala, Animals, Conditioning, Operant, Dopamine, Humans, Neuronal Plasticity, Neurons, Neurons, Afferent, Schizophrenia, Prefrontal Cortex

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