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Regulation of the Fear Network by Mediators of Stress: Norepinephrine Alters the Balance between Cortical and Subcortical Afferent Excitation of the Lateral Amygdala.

Johnson LR, Hou M, Prager EM, Ledoux JE - Front Behav Neurosci (2011)

Bottom Line: The auditory CS reaches the LA subcortically via a direct connection from the auditory thalamus and also from the auditory association cortex itself.In addition binding of NE to β-adrenergic receptors further dissociates sensory processing in the LA.These findings suggest a network mechanism that shifts sensory balance toward the faster but more primitive subcortical input.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry and Program in Neuroscience, Uniformed Services University Bethesda, MD, USA.

ABSTRACT
Pavlovian auditory fear conditioning involves the integration of information about an acoustic conditioned stimulus (CS) and an aversive unconditioned stimulus in the lateral nucleus of the amygdala (LA). The auditory CS reaches the LA subcortically via a direct connection from the auditory thalamus and also from the auditory association cortex itself. How neural modulators, especially those activated during stress, such as norepinephrine (NE), regulate synaptic transmission and plasticity in this network is poorly understood. Here we show that NE inhibits synaptic transmission in both the subcortical and cortical input pathway but that sensory processing is biased toward the subcortical pathway. In addition binding of NE to β-adrenergic receptors further dissociates sensory processing in the LA. These findings suggest a network mechanism that shifts sensory balance toward the faster but more primitive subcortical input.

No MeSH data available.


Related in: MedlinePlus

Norepinephrine decreased the amplitude of the fEPSP in both the Subcortical and the Cortical afferents to the LA. The effect is transient on both pathways. Both pathways show a post-NE rebound response (A). In the presence of PTX, NE decreases the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is transient on both pathways. In contrast, a rebound effect is not observed (B). NE significantly decreased the amplitude of the fEPSP in both the subcortical and the cortical pathways. Moreover, NE significantly decreased the cortical pathway more than the subcortical pathway (C). In the presence of PTX, NE significantly decreased the amplitude of the fEPSP in both the subcortical and the cortical pathways (D). However, in contrast, there was no significant difference in NE induced reduction in amplitude between the cortical and the subcortical pathway.
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Figure 2: Norepinephrine decreased the amplitude of the fEPSP in both the Subcortical and the Cortical afferents to the LA. The effect is transient on both pathways. Both pathways show a post-NE rebound response (A). In the presence of PTX, NE decreases the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is transient on both pathways. In contrast, a rebound effect is not observed (B). NE significantly decreased the amplitude of the fEPSP in both the subcortical and the cortical pathways. Moreover, NE significantly decreased the cortical pathway more than the subcortical pathway (C). In the presence of PTX, NE significantly decreased the amplitude of the fEPSP in both the subcortical and the cortical pathways (D). However, in contrast, there was no significant difference in NE induced reduction in amplitude between the cortical and the subcortical pathway.

Mentions: In the first experiment, we tested the effect of NE itself on the fEPSP in both the cortical and subcortical pathways (Figures 2A,B). NE (20 μM) reduced the amplitude of the evoked fEPSP in both pathways. The effect of NE on fEPSP was rapid (Figure 2A). Thus, after addition of the NE to the superfused ACSF the fEPSP began to decrease in amplitude within 2 min of reaching the brain slice. The reduction in the fEPSP amplitude was maximal in both pathways by 10 min (Figure 2A).


Regulation of the Fear Network by Mediators of Stress: Norepinephrine Alters the Balance between Cortical and Subcortical Afferent Excitation of the Lateral Amygdala.

Johnson LR, Hou M, Prager EM, Ledoux JE - Front Behav Neurosci (2011)

Norepinephrine decreased the amplitude of the fEPSP in both the Subcortical and the Cortical afferents to the LA. The effect is transient on both pathways. Both pathways show a post-NE rebound response (A). In the presence of PTX, NE decreases the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is transient on both pathways. In contrast, a rebound effect is not observed (B). NE significantly decreased the amplitude of the fEPSP in both the subcortical and the cortical pathways. Moreover, NE significantly decreased the cortical pathway more than the subcortical pathway (C). In the presence of PTX, NE significantly decreased the amplitude of the fEPSP in both the subcortical and the cortical pathways (D). However, in contrast, there was no significant difference in NE induced reduction in amplitude between the cortical and the subcortical pathway.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3102213&req=5

Figure 2: Norepinephrine decreased the amplitude of the fEPSP in both the Subcortical and the Cortical afferents to the LA. The effect is transient on both pathways. Both pathways show a post-NE rebound response (A). In the presence of PTX, NE decreases the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is transient on both pathways. In contrast, a rebound effect is not observed (B). NE significantly decreased the amplitude of the fEPSP in both the subcortical and the cortical pathways. Moreover, NE significantly decreased the cortical pathway more than the subcortical pathway (C). In the presence of PTX, NE significantly decreased the amplitude of the fEPSP in both the subcortical and the cortical pathways (D). However, in contrast, there was no significant difference in NE induced reduction in amplitude between the cortical and the subcortical pathway.
Mentions: In the first experiment, we tested the effect of NE itself on the fEPSP in both the cortical and subcortical pathways (Figures 2A,B). NE (20 μM) reduced the amplitude of the evoked fEPSP in both pathways. The effect of NE on fEPSP was rapid (Figure 2A). Thus, after addition of the NE to the superfused ACSF the fEPSP began to decrease in amplitude within 2 min of reaching the brain slice. The reduction in the fEPSP amplitude was maximal in both pathways by 10 min (Figure 2A).

Bottom Line: The auditory CS reaches the LA subcortically via a direct connection from the auditory thalamus and also from the auditory association cortex itself.In addition binding of NE to β-adrenergic receptors further dissociates sensory processing in the LA.These findings suggest a network mechanism that shifts sensory balance toward the faster but more primitive subcortical input.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychiatry and Program in Neuroscience, Uniformed Services University Bethesda, MD, USA.

ABSTRACT
Pavlovian auditory fear conditioning involves the integration of information about an acoustic conditioned stimulus (CS) and an aversive unconditioned stimulus in the lateral nucleus of the amygdala (LA). The auditory CS reaches the LA subcortically via a direct connection from the auditory thalamus and also from the auditory association cortex itself. How neural modulators, especially those activated during stress, such as norepinephrine (NE), regulate synaptic transmission and plasticity in this network is poorly understood. Here we show that NE inhibits synaptic transmission in both the subcortical and cortical input pathway but that sensory processing is biased toward the subcortical pathway. In addition binding of NE to β-adrenergic receptors further dissociates sensory processing in the LA. These findings suggest a network mechanism that shifts sensory balance toward the faster but more primitive subcortical input.

No MeSH data available.


Related in: MedlinePlus