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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

The β agonist isoproterenol (ISO) increased the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is not transient on both pathways, inducing a long lasting response (A). In the presence of PTX, ISO increases the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is not transient on both pathways, inducing a long lasting response (B). ISO significantly increases the amplitude of the fEPSP in both the subcortical and the cortical pathways. Moreover, ISO significantly increased the cortical pathway more than the subcortical pathway (C). In the presence of PTX, ISO significantly increased the amplitude of the fEPSP in both the subcortical and the cortical pathways (D). However, in contrast, there was no significant increase in ISO induced potentiation of amplitude between the cortical and the subcortical pathway.
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Figure 3: The β agonist isoproterenol (ISO) increased the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is not transient on both pathways, inducing a long lasting response (A). In the presence of PTX, ISO increases the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is not transient on both pathways, inducing a long lasting response (B). ISO significantly increases the amplitude of the fEPSP in both the subcortical and the cortical pathways. Moreover, ISO significantly increased the cortical pathway more than the subcortical pathway (C). In the presence of PTX, ISO significantly increased the amplitude of the fEPSP in both the subcortical and the cortical pathways (D). However, in contrast, there was no significant increase in ISO induced potentiation of amplitude between the cortical and the subcortical pathway.

Mentions: In the third experiment we directly compared the effects of the β adrenergic receptor agonist isoproterenol (ISO) on the fEPSP recorded in LA after stimulation of the cortical and subcortical pathways (Figures 3A,B). Prior to drug treatment, fEPSPs in both pathways were reduced to 50% of maximum and stable recordings established as above. ISO (15 μM) increased the amplitude of the evoked fEPSP in both pathways (Figure 3A). Like NE, the effect of ISO on the fEPSP was rapid. After the addition of the drug, the fEPSPs increased in amplitude within 2 min of reaching the brain slice. The increase in the fEPSP amplitude reach maximum in both pathways in less than 10 min (Figure 3A).


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)

The β agonist isoproterenol (ISO) increased the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is not transient on both pathways, inducing a long lasting response (A). In the presence of PTX, ISO increases the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is not transient on both pathways, inducing a long lasting response (B). ISO significantly increases the amplitude of the fEPSP in both the subcortical and the cortical pathways. Moreover, ISO significantly increased the cortical pathway more than the subcortical pathway (C). In the presence of PTX, ISO significantly increased the amplitude of the fEPSP in both the subcortical and the cortical pathways (D). However, in contrast, there was no significant increase in ISO induced potentiation of 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 3: The β agonist isoproterenol (ISO) increased the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is not transient on both pathways, inducing a long lasting response (A). In the presence of PTX, ISO increases the amplitude of the fEPSP in both the subcortical and the cortical afferents to the LA. The effect is not transient on both pathways, inducing a long lasting response (B). ISO significantly increases the amplitude of the fEPSP in both the subcortical and the cortical pathways. Moreover, ISO significantly increased the cortical pathway more than the subcortical pathway (C). In the presence of PTX, ISO significantly increased the amplitude of the fEPSP in both the subcortical and the cortical pathways (D). However, in contrast, there was no significant increase in ISO induced potentiation of amplitude between the cortical and the subcortical pathway.
Mentions: In the third experiment we directly compared the effects of the β adrenergic receptor agonist isoproterenol (ISO) on the fEPSP recorded in LA after stimulation of the cortical and subcortical pathways (Figures 3A,B). Prior to drug treatment, fEPSPs in both pathways were reduced to 50% of maximum and stable recordings established as above. ISO (15 μM) increased the amplitude of the evoked fEPSP in both pathways (Figure 3A). Like NE, the effect of ISO on the fEPSP was rapid. After the addition of the drug, the fEPSPs increased in amplitude within 2 min of reaching the brain slice. The increase in the fEPSP amplitude reach maximum in both pathways in less than 10 min (Figure 3A).

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