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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

Comparison across experiments confirms the dependence on GABAA receptors for the differential actions of NE and the β agonist isoproterenol (ISO) in the subcortical and cortical pathways. Additional comparison of subcortical and cortical pathways across different experiments supports the finding that the cortical pathway is differently regulated by NE and ISO. The GABAA antagonist (PTX) reduces the reduction on the amplitude of fEPSPs in both the cortical and subcortical pathways in response to NE (A). Second, there was more reduction in the cortical pathway than the subcortical (A). In the presence of PTX the potentiation of the cortical pathway by ISO was reduced (B). Together these data suggest that inhibiting GABAA transmission contributes to a significant change in the cortical fEPSPs response to NE and ISO but not to the subcortical fEPSP.
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Figure 4: Comparison across experiments confirms the dependence on GABAA receptors for the differential actions of NE and the β agonist isoproterenol (ISO) in the subcortical and cortical pathways. Additional comparison of subcortical and cortical pathways across different experiments supports the finding that the cortical pathway is differently regulated by NE and ISO. The GABAA antagonist (PTX) reduces the reduction on the amplitude of fEPSPs in both the cortical and subcortical pathways in response to NE (A). Second, there was more reduction in the cortical pathway than the subcortical (A). In the presence of PTX the potentiation of the cortical pathway by ISO was reduced (B). Together these data suggest that inhibiting GABAA transmission contributes to a significant change in the cortical fEPSPs response to NE and ISO but not to the subcortical fEPSP.

Mentions: We directly compared the fEPSP responses across experimental groups in order to obtain a comparison of how GABAA affected NE and ISO responses in the cortical and subcortical pathways. To do this we compared the experiments with and without GABAA inhibition (blocked with PTX) as a single experiment and first asked if there was a main effect as a result of PTX being present. Second, we again compared across experiments and asked if there was a difference in the fEPSP between the same pathways with or without PTX. We examined whether inhibiting GABAA transmission altered the reduction of the cortical or subcortical pathways in the presence of NE (Figure 4A); and if inhibiting GABAA transmission altered the potentiation of the cortical or subcortical pathways in the presence of ISO (Figure 4B).


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)

Comparison across experiments confirms the dependence on GABAA receptors for the differential actions of NE and the β agonist isoproterenol (ISO) in the subcortical and cortical pathways. Additional comparison of subcortical and cortical pathways across different experiments supports the finding that the cortical pathway is differently regulated by NE and ISO. The GABAA antagonist (PTX) reduces the reduction on the amplitude of fEPSPs in both the cortical and subcortical pathways in response to NE (A). Second, there was more reduction in the cortical pathway than the subcortical (A). In the presence of PTX the potentiation of the cortical pathway by ISO was reduced (B). Together these data suggest that inhibiting GABAA transmission contributes to a significant change in the cortical fEPSPs response to NE and ISO but not to the subcortical fEPSP.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: Comparison across experiments confirms the dependence on GABAA receptors for the differential actions of NE and the β agonist isoproterenol (ISO) in the subcortical and cortical pathways. Additional comparison of subcortical and cortical pathways across different experiments supports the finding that the cortical pathway is differently regulated by NE and ISO. The GABAA antagonist (PTX) reduces the reduction on the amplitude of fEPSPs in both the cortical and subcortical pathways in response to NE (A). Second, there was more reduction in the cortical pathway than the subcortical (A). In the presence of PTX the potentiation of the cortical pathway by ISO was reduced (B). Together these data suggest that inhibiting GABAA transmission contributes to a significant change in the cortical fEPSPs response to NE and ISO but not to the subcortical fEPSP.
Mentions: We directly compared the fEPSP responses across experimental groups in order to obtain a comparison of how GABAA affected NE and ISO responses in the cortical and subcortical pathways. To do this we compared the experiments with and without GABAA inhibition (blocked with PTX) as a single experiment and first asked if there was a main effect as a result of PTX being present. Second, we again compared across experiments and asked if there was a difference in the fEPSP between the same pathways with or without PTX. We examined whether inhibiting GABAA transmission altered the reduction of the cortical or subcortical pathways in the presence of NE (Figure 4A); and if inhibiting GABAA transmission altered the potentiation of the cortical or subcortical pathways in the presence of ISO (Figure 4B).

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