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06.10.2013
The amygdala detects whether a stimulus (person or event) is threatening and the hippocampus, the center of short-term memory, links the fear response to the context in which the threatening stimulus or event occurred. The young child has limited capacity to manage this overwhelming stress and experiences increased arousal — fear and anxiety (physical and emotional sensations). These quite concerning consequences of overwhelming stress must be considered in a larger developmental context — including aspects of the child and the availability of supportive adults. This website was made possible by grant number 90YD0268 from the Office of Head Start, Administration for Children, Youth and Families, U.S. Figure 1: Schematic depicting the amygdala, the brain site most critical for fear learning. Information regarding the conditioned stimulus (CS) and unconditioned stimulus (US) is transmitted to the amygdala by way of sensory areas in the thalamus and cortex. Department of Psychiatry and Behavioral Sciences, Yerkes National Primate Research Center, Emory University, Atlanta, Georgia, USA. BASED IN SOUTHERN CALIFORNIA, The BrightLife Center for The Rapid Relief of Post-Traumatic Stress specializes in rapid, permanent, 100% drug-free eradication of post-traumatic stress and related challenges.
Post-Traumatic Stress Disorder, or PTSD, is the name given for a particular constellation of anxiety-related symptoms that can occur following the experience or witnessing of life-threatening events such as military combat, natural disasters, terrorist incidents, serious accidents, or violent personal assaults like rape. At the time you experienced the original traumatic incident, the fear you experienced was completely reasonable and understandable. The initial mental record of a traumatic event is stored first in the hippocampus, the site of short-term memory.
Recall that when a person brings back to conscious awareness a traumatic memory, that memory temporarily returns to the hippocampus so that it can once again be experienced consciously. Our work is so effective, we have been featured on numerous local, national and even international print, radio and television, including our appearances in the Montreal Gazette, KNX 1070 NewsRadio in Los Angeles, Esquire Magazine, as well as the Discovery Health Channel's six-part television series, Things That Go Bump: Facing Our Fears. When we're done, the brain automatically sends the newly edited memory back to the cerebral cortex, forever freed of the traumatic components of the memory. If you experience flashbacks, nightmares, panic, anxiety or fight or flight symptoms as a result of what you know to be traumatic experiences of your past, let us help you! To request more information, or to sign up for our powerful and effective PTSD-relief services, please click here to contact us, or feel free to call our 24-hour voicemail messaging system toll-free at (866) LIFE-NOW. BrightLife Phobia and Anxiety Release Center has been awarded the prestigious "A+ Rating" for outstanding Service Quality and Customer Satisfaction by the Southland Better Business Bureau! BrightLife's Founder and Executive Director Robert Mantell is a member in good standing of the American Counseling Association (Membership #06162446). BrightLife's Founder and Executive Director Robert Mantell is a member of the American Academy of Experts in Traumatic Stress.
BrightLife's Founder and Executive Director Robert Mantell is a member of the National Center for Crisis Management.
BrightLife's Founder and Executive Director Robert Mantell is a member of the California Counseling Association. BrightLife's Founder and Executive Director Robert Mantell is a member of the International Association of Marriage and Family Counselors.
Fear - an innate emotion in the brain contributes to autism, post-traumatic stress disorder - PTSD.
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. In the laboratory, intense electrode stimulation of FEAR neurocircuitry prompts an animal to try to flee.
The concept of genetically determined, innate neurocircuitry for FEAR can be demonstrated with a loss-of-function experiment using knockout mice. Knockout mice contain the same, artificially introduced mutation in every cell, abolishing the activity of a preselected gene. 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.
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.
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 laboratory, fear responses can be learned when neutral stimuli are paired with electric shock.
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.
Porges points out that "when we're stressed or anxious, we use our facial muscles, which include the ears.
When circumstances change and one detects danger, Porges explains that our automatic defense system employs either "the sympathetic-adrenal system to mobilize for fight and flight behaviors," or, when circumstances are perceived to be so dire that fight or flight is useless, the ancient unmyelinated vagal system immobilizes us, just like an animal freezes when escape from a predator is impossible.
To put Porges's polyvagal theory in more academic terms, I consulted a chapter that Porges authored in The Integrative Neurobiology of Affiliation, edited by Carol Sue Carter, I.
In dealing with stress, Porges recommends to everyone to remember what it is to be a human.
A March 2009 report from the Society for Neuroscience, "Post Traumatic Stress Disorder," aligns with Amy F.T.
There is interesting evidence of a mechanism within the human brain that helps suppress troubling memories and thoughts in a way that is healing.
If language helps humans suppress fear, it is easier to understand why animals do not possess the same ability to suppress fear as people do.
The procedure consists simply of applying a burst of brain stimulation through indwelling electrodes for a period of one second, once a day, for a week or two. Giving animals seizure-inducing drugs every several days or even exposing them to very loud auditory stimulation also induces kindling, sometimes provoking fits in certain sensitive strains of animals.
Panksepp observes that "the emotional personality of these animals seems to change as they become kindled. As you may know, Temple Grandin is autistic and has made a career working with animals, especially in improving conditions for farm animals raised for food.
In Animals in Translation, Grandin and Johnson write: "It seems likely that animals and autistic people both have hyper-fear systems in large part because their frontal lobes are less powerful compared to the frontal lobes in typical folks. Regarding the frontal lobes, Grandin and Johnson write: "The frontal lobes fight fear in two ways. Grandin and Johnson point to a core difference between animals and autistic people on the one hand, and normal people on the other.
Prolonged and severe stress leads to cognitive deficits, but facilitates emotional behaviour. Male Wistar rats, 60–65 days old, were used for the chronic immobilization stress protocol. Whole-cell patch-clamp recordings, from excitatory principal neurons in the dorsal part of the LA (figure 1b), were obtained under IR-DIC visualization (BX50WI, Olympus, USA) with an EPC-9 amplifier (HEKA Elektronik, Lambrecht, Germany). The biological mechanisms that control mood, anxiety, stress, fear, and other emotional behavior have been focused almost exclusively on the role of certain neurotransmitters called monoamines.
More recently, research has begun to highlight other neurochemical systems, including cytokines, peptides, and bioactive lipids.
The ECS has been described in our previous article as a complex physiologic network within the human body comprised of cannabinoid receptors (CB1 and CB2).


Not surprisingly, cannabinoid receptors and the biochemical machinery necessary to synthesize and generate cannabinoids are present within areas of the brain known to control emotional behavior, mood, stress, and fear. Preclinical studies in mice have clearly shown that activation of cannabinoid receptors within the PAG via direct injection of anandamide reduces panic and anxiety behavior, or the “fight or flight” phenomenon.
However, before we jump the gun and feel like we have fear, anxiety, and stress responses all figured out, it’s not as simple as activating receptors through cannabinoid administration. This bidirectional or paradoxical response appears to be dose-dependent, where lower doses seem to reduce stress, anxiety, and panic, while higher doses may promote increased feelings of stress, panic, and fear. To illustrate what neuroscientists currently feel is happening, think of being in a car with the brake pedal and accelerator.
On the other hand, when dosing is too high, or there is an imbalance in the endocannabinoid system, whereby CB1 receptors are being over-activated in lieu of CB2, that’s like taking the foot off the brake pedal, thereby removing inhibition that was normally in place and allowing the engine to rev higher—increased fear, anxiety, and stress from activation of other circuits in the brain that are normally applying the brake. More recently, other preclinical research has demonstrated the important role of maintaining a healthy endocannabinoid system “tone” for improved stress resilience and reducing the residual post-traumatic anxiety, fear, and panic behaviors in mice that were chronically exposed to stress. One theory is that anadamide and 2-AG are acting as “gatekeepers” to keep the stress response and high emotional loads at bay and improving recovery to pre-stress levels once the stress burden is reduced to baseline. There is an emerging role in the interplay between the immune system and the neuro-endocrine system, such that the field of psychoneuroimmunology has exploded with new basic and preclinical research over the past 5 years. In this context, it’s interesting to note that a balanced ECS appears to be pivotal to a healthy stress response and mitigating fear, anxiety, and panic that tend to accumulate with dysfunctional responses to stress. A randomized, double-blind, placebo controlled trial in 15 humans demonstrated that up to 600 mg of CBD (cannabidiol) reduced measured anxiety compared to increased levels with a 10 mg dose of ?9-THC.
The totality of the best available scientific evidence points to the importance of balancing the tone of the endocannabinoid system for supporting a healthy stress response. Within the amygdala, the critical plasticity underlying the acquisition of fear conditioning is thought to occur in the lateral amygdala and the lateral portion of the central nucleus (CEl). On average, just 1 to 4 three-hour Accelerated Personal Breakthrough Coaching sessions over the course of about a week as part of our 90-Day Accelerated Personal Breakthrough Coaching program are required to help you achieve substantial or complete relief from your challenges with post-traumatic stress.
People who suffer from PTSD often relive the experience through nightmares and flashbacks, have difficulty sleeping, and feel detached or estranged, and these symptoms can be severe enough and last long enough to significantly impair the person's daily life. It has subsequently been observed in all veteran populations that have been studied, including World War II, Korean conflict, and Persian Gulf populations, and in United Nations peacekeeping forces deployed to other war zones around the world. Although there are unique cultural- and gender-based aspects of the problem, it occurs in men and women, adults and children, Western and non-Western cultural groups, and all socioeconomic strata.
Although it has a limited set of tools to manage that, one of its most effective tools is fear. A chemical reaction then essentially burns the sensory information associated with the event (the sights, sounds or other sensory information present at the time) deeply into the cerebral cortex, where it effectively cements that information into long-term memory storage. 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. Humans stimulated in these same brain areas report being engulfed by intense anxiety." Panksepp provides examples of such human reactions. In the amygdala, FEAR circuitry and RAGE circuitry "are fairly clearly segregated, with FEAR being more lateral and RAGE more medial," explains Panksepp. Later in this narrative, we will talk about another drug, carbamazepine, that also facilitates GABA activity and reduces fear. 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. Arnsten's ideas about how stress can produce impairments in the prefrontal cortex (see Stress, attention, learning, memory, and ADHD).
Grandin, who has made a career working with animals, asserts: "I do know that once an animal has become traumatized it's impossible to un-traumatize him.
After the first brief ESB [electrical stimulation to the brain], nothing special happens, unless one observes the EEG, where one will note a momentary seizure immediately after the brain stimulation.
The induction of these epileptic states reflects a functional reorganization of the nervous system, since no structural changes have been found to result from kindling procedures.
The prefrontal cortex gives humans some freedom of action in life, including some freedom from fear. John Mitchell who propose that "all the different autistic savant abilities come from the fact that autistic people don't process what they see and hear into unified wholes, or concepts, rapidly the way normal people do." Grandin and Johnson explain that a normal person doesn't become conscious of what he's looking at until after his brain has composed the sensory bits and pieces into wholes. Interestingly, some of the key symptoms of stress disorders display contrasting behavioural manifestations. All animals were housed in groups of two or three with ad libitum access to food and water, unless specified otherwise in the stress protocols.
To this end, we selected neurons possessing large somata, which are typical of spiny excitatory principal neurons in the LA [19,20].
Chronic stress enhances long-term potentiation (LTP) at thalamic inputs to projection neurons in the lateral amygdala (LA). This stimulation configuration has been shown to activate auditory thalamic afferents to the LA [19]. After obtaining a stable baseline, LTP was induced by applying a 30 Hz tetanus protocol (100 stimuli at 30 Hz, given twice with a 20 s interval) that has been established in previous studies [11]. While monoamines like dopamine, serotonin, and norepinephrine play an important role in controlling mood and anxiety, the vast majority of drug-based therapies that target those “monoaminergic” systems are limited in their efficacy. By diving deeper into the science of bioactive lipids, we begin to unearth the potential role of the endocannabinoid system (ECS) in stress and fear responses. There are endogenous cannabinoid compounds such as anandamide and 2-AG, and their respective enzymes responsible for maintaining balance in the system by regulating the synthesis and breakdown of the active endocannabinoid compounds.
These structures include the prefrontal cortex, amygdala, hippocampus, and periaqueductal gray (PAG) of the midbrain. Other studies using a similar model in animals have shown decreased fear-avoidant and conditioned responses to pain or punishment. Other animal studies utilizing systemic injections of ?9-THC (not directly into the PAG of the midbrain) have demonstrated mixed responses, eliciting either anxiogenic (promoting increased levels of anxiety) or anxiolytic (decreasing levels of anxiety).
These opposing effects are likely a result of the involvement of other neurotransmitter circuits within the brain that, when inhibited, actually create a hyper-excitable response of stress, anxiety, and fear. When the cannabinoid system is functioning to decrease fear, stress, and panic, the foot is being taken off of the accelerator in the areas of PAG-midbrain centers.
Interestingly, the greater the exposure to stress, the greater the magnitude of the response to treatment (by improving the ECS and cannabinoid signaling). Moreover, there is evidence from preliminary human studies that disrupting endocannabinoid signaling and regulation has important impacts on the HPA (hypothalamic-pituitary-adrenal) axis by increasing signs of anxiety and depression.
The crosstalk between the immune system, cytokine signaling, and the nervous system influencing behavior, anxiety, and mood has been proposed by numerous preclinical studies. This preclinical and emerging human clinical data support the use of a CBD-rich or CBD-overweighted extract of cannabis for modulating fear, anxiety, and a healthy stress response.
Our goal is to spread awareness of and education about hemp-derived CBD products, so send us your questions and we’ll address them in future installments! Cannabidiol blocks long-lasting behavioral consequences of predator threat stress: possible involvement of 5HT1A receptors. Evidence for a potential role for TRPV1 receptors in the dorsolateral periaqueductal gray in the attenuation of the anxiolytic effects of cannabinoids. Distinct effects of {delta}9-tetrahydrocannabinol and cannabidiol on neural activation during emotional processing.
Translational evidence for the involvement of the endocannabinoid system in stress-related psychiatric illnesses.


Pharmacological exploitation of the endocannabinoid system: new perspectives for the treatment of depression and anxiety disorders. The medial division of the central nucleus of the amygdala (CEm) projects to various brain areas that produce fear and panic symptoms seen in people with fear-related disorders. This problem is also associated with impairment of the person's ability to function in social or family life, including occupational instability, marital problems and divorces, family discord, and difficulties in parenting. A national study of American civilians conducted in 1995 estimated that the lifetime prevalence of PTSD was 5% in men and 10% in women. Collectively, these techniques assist clients to separate the memory of past events from the emotional trauma associated with those events.
Robert Mantell assisted a client to eliminate an intense twenty-year phobia in just 15 minutes! 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 mouse models are widely used to study human diseases caused by the loss of gene function. The middle ear muscles are regulated by the facial nerve, a nerve that also regulates eyelid lifting. The Society for Neuroscience reports: "Patients with PTSD have heightened levels of norepinephrine, a chemical involved in arousal and stress. Those who suffered from PTSD remembered their trauma visually, more like a flashback, while those without PTSD remembered their trauma as a verbal narrative. Animals never unlearn a bad fear." Grandin and Johnson point out that animals are aware of tiny details in their environments and can become afraid of these tiny details. This induced epileptic fit gets larger and larger as the days pass, and after a few days, the ESB begins to provoke brief periods of outright convulsive activity. Here, we report that in rats subjected to chronic immobilization stress, long-term potentiation (LTP) and NMDA receptor (NMDAR)-mediated synaptic responses are enhanced in principal neurons of the lateral amygdala, a brain area involved in fear memory formation. This difference is strikingly evident in the effects of stress on the output of two brain areas critically involved in learning and memory—the hippocampus and amygdala.
Control animals, which were age matched with the stress-treated animals, were housed in separate cages.
For each cell, the stimulation intensity for LTP induction was the same as that used to elicit the pre-tetanus baseline. A number of recent studies have demonstrated a role of CB2 receptors classically associated with the immune system in anxiety and depression-related behavior in animal models and human clinical studies. For example, Australian Vietnam veterans experience many of the same symptoms that American Vietnam veterans experience. For example, rats prefer to enter dark holes but show reduced social activity when exposed to bright lights. When you are interested in what someone is saying, you lift your eyelids and simultaneously your middle ear muscles tense. In contrast to reptiles, mammals have a great demand for oxygen and are vulnerable to any depletion in oxygen resources. Similar to most mammals, we come into the world with great dependence on our caregivers, and that need to connect and be connected to others remains throughout our lives." He emphasizes the need to create safe environments for ourselves in which we can socially engage. After a week or so, the brief stimulation produces a full-blown motor fit, unambiguous both behaviorally and in the poststimulation EEG. This is accompanied by electrophysiological and morphological changes consistent with the formation of ‘silent synapses’, containing only NMDARs.
There is considerable evidence showing how repeated stress impairs hippocampal function at multiple levels of neural organization [1–4]. On the 11th day, animals either underwent fear conditioning, or were sacrificed for Golgi staining or for slice electrophysiology.
To evaluate the magnitude of LTP achieved in any given neuron, the average initial slope of the EPSP recorded during the last 5 min of the recording session (35–40 min post-tetanus) was compared with the pre-tetanus average baseline. The metabolic demand for mammals is approximately five times greater than that for reptiles of equivalent body weight. Thereafter, the animal will always have a seizure when it receives this burst of brain stimulation. At the cellular level, various animal models of stress cause dendritic atrophy and suppress hippocampal long-term synaptic potentiation (LTP) mediated by the NMDA (N-methyl-d-aspartate) subtype of glutamate receptors (NMDARs) [1,5,6].
All procedures related to maintenance and experimentation were approved by the Institutional Animal Ethics Committee, National Centre for Biological Sciences (NCBS), Bangalore, India. Comparison of the percentages of LTP between groups (control versus stress) was tested with a two-tailed, independent Student's t-test. Gradually even other stimuli become capable of triggering seizures, especially loud sounds and flashing lights. Together, these synaptic changes would enable amygdalar neurons to undergo further experience-dependent modifications, leading to stronger fear memories. Impaired NMDAR-dependent LTP and dendritic atrophy, in turn, are believed to be key factors contributing to chronic stress-induced deficits in hippocampal learning and memory [3,7–9]. Rats in the experimental group were subjected to chronic immobilization stress for 10 consecutive days as described earlier [17,18]. Only cells with membrane potentials more negative than ?60 mV and action potentials that exceeded 0 mV were included in this study. Strikingly, NMDAR-dependent LTP in the lateral amygdala (LA) also plays a pivotal role in forms of emotional memory such as classical fear conditioning [10,11].
This stress paradigm consisted of complete immobilization (2 h per day, 10.00–noon) in rodent immobilization bags without access to either food or water. Further, series resistance (Rs) was tested and recordings were not used if they changed by more than 10% from beginning to end or if the Rs exceeded 20 M?. Just trees, trees, and more trees." The authors point out that animals will react fearfully to any stimulus that resembles, in terms of sensory perception, an initial fearful experience. Hence, stress may leave its mark in the amygdala by generating new synapses with greater capacity for plasticity, thereby creating an ideal neuronal substrate for affective disorders. Why then does repeated stress facilitate amygdala-dependent fear learning [12–16], when previous studies report stress-induced suppression of NMDAR-dependent LTP in the hippocampus [1,5,6]? Summary graphs depict the time course of LTP induced by 30 Hz tetanus (100 pulses per train at 30 Hz, two trains delivered 10 s apart). They describe a dog's encounter with a red hot-air balloon which severely frightened the animal.
These findings also highlight the unique features of stress-induced plasticity in the amygdala that are strikingly different from the stress-induced impairment of structure and function in the hippocampus.
The goal of this study is to investigate the synaptic basis for this contrast in the amygdala. Subsequently, the dog reacted fearfully to any red, circular object, even the read aerial markers that draw attention to power lines.



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