This video segment explains the neurobiological underpinnings of stress responses, focusing on the amygdala's role. It highlights that excessive amygdala activation, which mediates allostatic load and is part of the salience network, leads to the over-release of noradrenaline and dopamine. This surge of catecholamines impairs prefrontal cortex function by stimulating alpha-1 receptors, causing cognitive inflexibility and cerebral hypoperfusion due to vasoconstriction. Consequently, a vicious cycle is established: stress-induced catecholamines reinforce fear conditioning in the amygdala while simultaneously weakening the prefrontal cortex's ability to regulate cognition and exert top-down control over the amygdala, thereby reducing the fear and threat response.

Dr. Rege

Excessive amygdala activation. You see, the amygdala mediates all allostatic load. The amygdala forms an important component of the salience network. The salience network mediates arousal, reward, and the modulation of stress, essentially trying to get the organism back to operate along the homeostatic paradigm.

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So, therefore, if the amygdala, which mediates all allostatic load, is excessively stimulated, then this results in the release of excessive levels of noradrenaline and dopamine. Now, excessive noradrenaline and dopamine impairs the prefrontal cortex because it stimulates alpha-1 receptors. And alpha-1 receptors are associated with cognitive inflexibility, but also vasoconstriction and thereby resulting in cerebral hypoperfusion.

[music]

So, this sets up a vicious cycle where the stress-induced catecholamine surge strengthens fear conditioning in the amygdala, whilst diminishing the prefrontal cortex's capacity for improved cognition, but also top-down control over the amygdala, i.e., reducing the fear response or reducing the threat response.

How Excessive Amygdala Activation ‘Rewires’ Fear

excessive amygdala activation. You see,
amygdala mediates all allostatic load.
Amygdala forms an important component of
the salience network. The salience
network mediates arousal, reward, and
the modulation of stress, essentially
trying to get the organism back to
operate along the homeostatic paradigm.
[music] So, therefore, if the amygdala,
which mediates all allostatic load, is
excessively stimulated, then this
results in the release of excessive
levels of noradrenaline dopamine. Now,
excessive noradrenaline and dopamine
impairs prefrontal cortex because it
stimulates alpha-1 receptors. And
alpha-1 receptors is associated with
cognitive inflexibility, but also
vasoconstriction and thereby resulting
in cerebral hypoperfusion. [music]
So, this sets up a vicious cycle where
the stress-induced catecholamine surge
strengthens fear conditioning in the
amygdala, whilst diminishing the
prefrontal cortex capacity for improved
cognition, but also top-down control
over the amygdala, i.e. reducing
the fear response or reducing the threat
response.

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How Excessive Amygdala Activation ‘Rewires’ Fear

Transcription