The researchers from Tulane University found that the stress neurotransmitter norepinephrine, commonly known as noradrenaline, increases fear processing in the brain by stimulating a specific population of inhibitory neurons in the amygdala to generate a recurrent bursting pattern of electrical discharges.1
Biology of fear
Fear is a primal, natural, and powerful human emotion. Fear and anxiety are the most common distinctions. Fear is typically thought of as an adaptive but phasic (transient) state generated by interaction with threatening stimuli, whereas anxiety is a more tonic state linked to prediction and preparedness— a distinction comparable to that between emotions and moods.
Fear and anxiety trigger a variety of adaptive and defensive behaviors aimed at getting away from the source of danger or motivational conflict. The setting and repertoire of the species influence these behaviors. When escaping a threat is possible, active coping methods are adopted, and the autonomic changes associated with these active strategies are mediated primarily by sympathetic activity (hypertension, tachycardia). Cannon first identified this as the fight-or-flight response.2
The fear response begins in the brain and travels throughout the body, causing the body to adjust for the best defense or flight response. The amygdala, a part of the brain, is where the fear reaction begins. The emotional salience of stimuli is detected by this almond-shaped cluster of nuclei in the temporal lobe of the brain. When we view a human face with emotion, for example, the amygdala is activated. With rage and terror, this reaction is more pronounced. A threat signal, such as seeing a predator, prompts the amygdala’s fear response, which activates areas involved in motor function preparation for fight or flight. It also activates the sympathetic nervous system and causes the release of stress hormones. This causes physical changes that equip us to be more effective in the face of danger: Pupils dilate, bronchi dilate, and breathing speeds up when the brain becomes hyper alert. Blood pressure and heart rate both increase. The amount of blood and glucose flowing to the skeletal muscles increases. Organs that are not necessary for living, including the gastrointestinal system, slow down. The hippocampus, a component of the brain, is closely linked to the amygdala. The prefrontal cortex and hippocampus assist the brain in interpreting the perceived threat. They are involved in a higher-level context processing that allows a person to determine whether a perceived threat is real. For example, seeing a lion in the wild can elicit a strong fear response, yet seeing the same lion in a zoo can elicit curiosity and the impression that the lion is cute. This is due to the fact that the hippocampus and frontal cortex process contextual information, and inhibitory circuits decrease the amygdala’s fear response and its consequences. Essentially, our brain’s “thinking” circuitry reassures our “emotional” sections that we are fine.3
A new study looks into why fear memories are so ingrained in our minds
Neuroscientists believe they have discovered a mechanism for the creation of terror memories in the amygdala, the brain’s emotional center.
A terrifying occurrence is likely to stay with us for the rest of our life. But why does it stick with us, whereas other types of events become increasingly harder to recollect as time goes on?1
Fear expression requires patterned synchronization of network activity in the basolateral amygdala (BLA). Neuromodulatory systems play a critical role in regulating changes in behavioral states, but the mechanisms underlying this neuromodulatory control of brain-behavioral transitions were mostly unknown.
Tulane University researchers have discovered that chemogenetic Gq activation and 1 adrenoreceptor activation in mouse BLA parvalbumin (PV) interneurons cause previously undescribed stereotyped phasic bursting in PV neurons, as well as time-locked synchronized bursts of inhibitory postsynaptic currents and phasic firing in BLA principal neurons. In an in vivo and in an ex vivo slice model, this Gq-coupled receptor activation in PV neurons suppresses gamma oscillations and enhances fear memory recall, which is similar to BLA gamma suppression during conditioned fear expression.
In response to Gq activation mediated by the 1A and hM3D receptors, they observed recurrent bursts of action potentials in PV interneurons. Because it was not suppressed by blocking ionotropic glutamate and GABA receptors and was not induced by sustained photostimulation of BLA PV neurons, the PV neuron phasic bursting was determined to be mediated by a postsynaptic intrinsic Gq signaling mechanism rather than local circuits or depolarization-induced activation. This indicated that Gq neuromodulation plays a key role in switching the operational mode of PV interneurons from tonic activation to alternating cycles of activation and inhibition via an internal mechanism that is independent of depolarization and fast chemical synaptic transmission.4
If an individual is held at gunpoint, the brain of that individual secretes a lot of norepinephrine, which is similar to an adrenaline rush. This alters the electrical discharge pattern in specific circuits of the emotional brain, concentrated in the amygdala, triggering a state of heightened arousal in the brain, which aids memory formation, particularly fear memory.
Researchers believe that this is the same process that goes awry in PTSD, causing one to be unable to forget distressing events.1