FEAR neurocircuitry in the brain generates emotions that are "characterized by generalized apprehensive tension, with a tendency toward various autonomic symptoms such as tachycardia (rapid heartbeat often with palpitations), sweating, gastrointestinal symptoms, and increased muscle tension," writes Jaak Panksepp in Affective Neuroscience: The Foundations of Human and Animal Emotions (1998).
The electrocardiogram (ECG) image above right (links to source) is from the Merck Manual Online Medical Library's entry for "Ventricular Tachycardia." The top strip's series of repeating wide uncoordinated spikes indicates a rapid heartbeat. Fear can generate this kind of heart rhythm. A normal ECG strip, with very coordinated spikes, is shown at the bottom for comparison.
The brain's FEAR neurocircuitry:
In Affective Neuroscience, Panksepp points to the work of Walter Hess during the 1930s in determining that electrical stimulation to certain brain areas can produce rage behavior in animals. Hess won the Nobel Prize in 1949. Panksepp writes: "It has long been known that one can enrage both animals and humans by stimulating very specific parts of the brain, which parallel the trajectory of the FEAR system." He adds: "Brain tumors that irritate the circuit can cause pathological rage, while damage to the system can promote serenity."
Like other emotive circuits we discuss in Part 2 of CorticalBrain.com, the neurocircuitry for fear is genetically encoded in the mammalian brain. Panksepp writes: "The emotional experience of fear appears to arise from a conjunction of neural processes that prompt animals to hide (freeze) if danger is distant or inescapable, or to flee when danger is close but can be avoided."
In the laboratory, intense electrode stimulation of FEAR neurocircuitry prompts an animal to try to flee. Panksepp explains that such stimulation "leads animals to run away as if they are extremely scared." He writes: "If given the opportunity, animals will avoid environments where they have received such stimulation in the past, and if no avenue of escape is provided, they will freeze as if in the presence of a predator."
The concept of genetically determined, innate neurocircuitry for FEAR can be demonstrated with a loss-of-function experiment using knockout mice. Such mice are engineered to lack the activity of one or more genes. Although it has since been removed from the internet, Richard Twyman created the following useful definition of knockout mice in a website about the human genome.
Knockout mice contain the same, artificially introduced mutation in every cell, abolishing the activity of a preselected gene. The resulting mutant phenotype (appearance, biochemical characteristics, behaviour etc.) may provide some indication of the gene's normal role in the mouse, and by extrapolation, in human beings. Knockout mouse models are widely used to study human diseases caused by the loss of gene function.
Researchers Chong Chen et. al knocked out just one copy of a particular gene and created a knock-out mouse with unusual characteristics related to fear. In Animals in Translation: Using the Mysteries of Autism to Decode Animal Behavior (2005), Temple Grandin and Catherine Johnson recount how researchers "discovered that they hadn't just knocked out some aspect of learning; they'd also knocked out fear. A normal mouse, with a normal amount of fear, does not fight to the death. He fights until he's beaten, or sees he's going to lose, and then he yields. Fear keeps him alive. The knockout mice were almost fearless, and they fought to the death." Grandin and Johnson write: "The researchers would come to the lab first thing in the morning and find dead mice in the cages. Their backs were broken and there was blood everywhere."
In normal animals, Panksepp notes in Affective Neuroscience that with "very weak stimulation, animals exhibit … a freezing response, common when animals are placed in circumstances where they have previously been hurt or frightened. Humans stimulated in these same brain areas report being engulfed by intense anxiety." Panksepp provides examples of such human reactions. One patient reports: "Somebody is now chasing me, I am trying to escape from him." Another had "an abrupt feeling of uncertainty just like entering into a long, dark tunnel." Another sensed being near the sea with "surf coming from all directions."
In terms of general trajectory, FEAR circuitry runs parallel to and most certainly interacts with RAGE neurocircuitry, contributing to, as Panksepp puts it "the balance between fight and flight reactions." It is in lower, more primal, regions of the brain, specifically the periaqueductal gray (PAG) that the FEAR neurocircuitry is most easily aroused. Panksepp explains that fear is aroused with electrical stimulation of "lateral and central zones of the amygdala, the anterior and medial hypothalamus, and, most clearly (and at the lowest current levels), within specific PAG areas of the midbrain."
FEAR neurocircuitry projects even farther "down to specific autonomic and behavioral output components of the lower brain stem and spinal cord," which Panksepp explains control physiological processes including increased heart rate, increased blood pressure, the startle response, elimination, and perspiration. In the amygdala, FEAR circuitry and RAGE circuitry "are fairly clearly segregated, with FEAR being more lateral and RAGE more medial," explains Panksepp.
Panksepp points out that benzodiazepines (e.g., diazepam, trade name Valium) couple with receptors along the FEAR circuit that "are closely coupled to gamma-aminobutyric acid (GABA) function in the brain." He writes: "Just as glutamate is the brain's most prolific excitatory transmitter, its metabolic product GABA, via one decarboxylation step, is the most pervasive inhibitory transmitter and is capable of suppressing fear as well as many other emotional and motivational processes." In other words, benzodiazepines facilitate GABA activity and thereby reduce fear. Later in this narrative, we will talk about another drug, carbamazepine, that also facilitates GABA activity and reduces fear.
It is interesting, as Panksepp points out, that "animals and humans do not focus on their bodily injuries when they are scared …." Fear-induced analgesia emerges in part, "from arousal of pain-inhibition pathways such as serotonin and endogenous opioids, near the PAG… ."
Many animals have innate fears. Panksepp writes: "External stimuli that have consistently threatened the survival of a species during evolutionary history often develop the ability to unconditionally arouse brain fear systems." For example, laboratory rats that have never before encountered a cat or ferret exhibit "increased freezing and inhibition of other motivated behaviors" when the odor of a cat or ferret is introduced into their environment. Panksepp notes that the fear response is species-specific. For example, rats prefer to enter dark holes but show reduced social activity when exposed to bright lights. Benzodiazepines counter the anxiety rats display when exposed to bright lights.
In the laboratory, fear responses can be learned when neutral stimuli are paired with electric shock. This kind of fear arousal is called a "conditioned response." In humans for example, when pain or other threatening stimuli occurs in the context of other specific external events, thereafter the external events, although nonthreatening in and of themselves, can trigger arousal in FEAR neurocircuitry. Regarding post-traumatic stress disorder (PTSD), Panksepp concludes that "deep subcortical networks" can "become sensitized and can operate independently of your higher cognitive faculties."
Panksepp explains that when the central nucleus of the amygdala "is lesioned on both sides of the brain, animals no longer exhibit increased heart rates to stimuli they had learned to fear. It is now becoming clear that the central nucleus is one major brain area where conditional synaptic control of fear is created." As Panksepp points out, "damage to the amygdala can reduce fear conditioning in humans just as it does in animals… ." In addition to reduced fear, Panksepp reports that "such brain-damaged individuals are no longer able to recognize the facial expressions of emotions."Next-> The polyvagal theory, autism, and PTSD
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