Role of amygdala in the experience of fear

Role of amygdala in the experience of dismayThe amygdalae (from the Greek for almond) are two groups of almond-shaped nuclei locate deep wi cut down the medial temporal lobes of the brain in complex vertebrates, including tender-hearteds, (see common fig tree 1 below). Research has shown that the amygdalae perform a primary purpose in the bear upon and memory of turned on(p) actions, and are considered to be recrudesce of the limbic trunk. pic Fig 1 Location of Amygdala. (Image from imemat.blogspot.com) The regions descri tail end as amygdalae are a junto of several nuclei with distinct functions. Among these nuclei are the baso side(prenominal) complex, the cortical substance and the centromedial nitty-gritty, (see Fig 2 below). The basolateral complex pot be further subdivided into the lateral, the chief(a) and the auxiliary revolutionary nuclei. Anatomically, the amygdala and more pauseicularly, its centromedial nucleus, may be considered as a incite of the bas al ganglia. The amygdala sends impulses to various parts of the brain, for example, to the hypothalamus to initiate the sympathetic ill at ease(p) system to the thalamic reticular nucleus to increase reflex movement and to the laterodorsal tegmental nucleus for the activation of various neurotransmitters such(prenominal) as dopamine, norepinephrine and epinephrine. The cortical nucleus is involved in the aesthesis of smell and pheromone- processing. It receives input from the olfactory electric light and olfactory cerebral cerebral cortex. The lateral amygdalae, which send impulses to the rest of the basolateral complexes and to the centromedial nuclei, receive input from the sensorial systems. The centromedial nuclei are the main outputs for the basolateral complexes, and are involved in emotional arousal in rats and cats. pic Fig 2 Nuclei of the rat amygdaloid complex. (ABmc = accessory basal magnocellular leg ABpc = accessory basal parvicellular component Bpc = basal nucleus magnocellular subdivision e.c. = external capsule Ladl = lateral amygdala medial subdivision range = lateral amygdala medial subdivision Lavl = lateral amygdala ventrolateral subdivision Mcd = medial amygdala dorsal subdivision Mcv = medial amygdala adaxial subdivision Mr = medial amygdala rostral subdivision Pir = piriform cortex s.t. = stria terminalis). (Image from Physiol rpm 83 805) The amygdala filters sensory information and acts as a dissever of interpretation seam. The basolateral amygdala receives sensory information from the thalamus and cortex and then in front a signal to the appropriate target areas (see Figure 3 below). It is in like manner known as the amygdala proper, and the several areas of the brain that it targets are part of a broader network that serves much more vary functions. Because the basolateral amygdala is full of life for emotion, a better understanding of the chemicals within these brain circuits should lead to alter pharmacological treatments for emotional dysfunction in psychiatric disorders. pic Fig 3 The basolateral amygdala. (Image from Current Biology, Vol.10, (4)) Within most of these disorders is a common symptom in that the patient often says I didnt think, I just reacted. Straker, D. (2006) believes they may be exactly right. All sensory data, with the exception of the sense of smell, is sent by the body first to the thalamus which then forwards it to both the relevant part of the cortex and to the amygdala. The information is sent out over two reduplicate nerve pathways the thalamo- amygdala pathway (the short street) and the thalamo-cortico-amygdala pathway (the long route). The short route transmits a expeditious estimated representation of the situation, in which no cognition is involved. This pathway activates the amygdala which, through its central nucleus, elementrates emotional receipts before the mind can form a complete representation of the stimulus. The amygdala does a quick threat as sessment by comparing the sensory data real with already stored fear solutions. If any of these are triggered, then the amygdala floods the cortex with chemicals to stop it taking over. The result is action without conscious theme. (See Fig 4 below). Subsequently, the information that has travelled via the long route and been processed in the cortex reaches the amygdala and tells it whether or non the stimulus represents a real threat. Should a real threat be presented the amygdala will then activate the efferent structures responsible for physical manifestations of fear, such as increase cheek rate and blood pressure, sweaty hands, dry mouth, and tense muscles. The parallel operation of our stated (hippocampal) and implicit (amygdalic) memory systems explains why we do not remember traumas experienced rattling early in our lives. At that age, the hippocampus is still immature, patch the amygdala is already able to record unconscious memories. Early puerility traumas can dis turb the mental and behavioral functions of adults by mechanisms that they cannot access consciously. In complex vertebrates, including humans, the amygdalae perform primary roles in the formation and storage of memories associated with emotional events. Amunts et al (2005) indicate that, during fear instruct, sensory stimuli reach the basolateral complexes of the amygdalae, particularly the lateral nuclei, where they form associations with memories of that particular stimuli. These associations amid stimuli and the aversion may be talk terms by long-term potentiation, a lingering potential for touch on synapses to react more readily. Memories of emotional experiences that become imprinted in the reactions of synapses in the lateral nuclei do fear behaviour through their connections with both the amygdalaes central nucleus and the bed nuclei of stria terminalis (BNST). These central nuclei are involved in the production of umteen typical fear replys, including freezing (immo bility), tachycardia (speedy heartbeat), increased respiration, and stress-hormone release. Damage to the amygdalae impairs both the attainment and the expression of Pavlovian fear conditioning, which is a form of classical conditioning of emotional receipts. picFig 4 The Amygdala Bypass System. (Image from www.changingminds.org) Advances in neuroimaging technology such as fMRI, have allowed neuroscientists to show just how much of a role the amygdala plays in many psychological disorders. Donegan et al. (2003) studied patients with Borderline genius disorder who showed significantly greater leave amygdala body process than the ruler control airfields. Some of these borderline patients even had difficulties classifying neutral faces or classed them as being threatening. In support of these findings, in 2006, researchers at Monash University, Australia, detect increased levels of activity in the amygdala when patients with tender phobia were shown images of threatening faces or when they were confronted with frightening situations. These activity levels in the amygdala were in direct correlation with the severity levels of the social phobia. Similarly, depressed patients showed more activity in the left amygdala when interpreting emotions for all faces, and especially for portentous faces, although this hyperactivity was normalized when patients were prescribed antidepressants. cultural studies such as Williams et al (2006) showed that normal subjects exposed to images of frightened faces or faces of people from another race will show increased activity of the amygdala, even if that exposure is subliminal. However, according to Tsuchiya et al (2009), the amygdala is not essential for the processing of fear-related stimuli, since people with bilateral damage show rapid reactions to fearful faces. Early research on primates has also provided explanations for the functions of the amygdala in relation to emotional disorders. An early field by Brown Sh afer (1888) observed rhesus monkeys with a lesioned temporal cortex (including the amygdala) and erect that they suffered from significant social and emotional deficits. Kluver Bucy (1939) later expanded upon this observation by showing that large(p) lesions to the anterior temporal lobe produced not only fearlessness, only if also crude(a) emotional disturbances including increased sexual behaviour and a propensity to shopping mall objects in their mouths. Some monkeys also displayed an in superpower to recognize familiar objects and would fire both animate and inanimate objects indiscriminately, while also exhibiting fearlessness towards the researchers. This behavioural disorder was later named Klver-Bucy syndrome. However, their study can be criticised in that these lesions were so large and crude when compared to todays techniques, that researchers werent exactly sure of the structures responsible for these significant changes in behaviour. Improved techniques, such as u sing the neurotoxin ibotenic acid to work up more precise lesions are partly responsible for the more handsome understanding of the amygdale today. pic Fig 5 Sensory data routes, the fear response and the amygdala. (Image from http//thebrain.mcgill.ca/flash/index_a.html) Previous studies have examined activation of the amygdala in response to emotional facial stimuli, but these have been carried out in e really the U.S. or Western Europe, although none of these explored cross-cultural differences. Although agriculture shapes several aspects of human emotional and social experience, including how fear is perceived and expressed to others, very picayune is known about how culture influences neural responses to fear stimuli. In response to this gap in the research, a study by Chiao et al (2008) found that the bilateral amygdalas response to fear faces is, in fact, modulated by culture. using fMRI, they measured the amygdalas response to fear and non-fear faces in two distinc t cultures, inborn Japanese in Japan and Caucasians in the United States. Both culture groups showed greater activation in the amygdala to fear expressed by members of their own culture, (their in-group), than in any of the other emotional measures such as anger, happiness or neutrality. (See Fig 6 below). pic Fig 6 The amygdalas response to fearful facial expressions is culture- specific. (Image from Chiao et al 2008). As mentioned earlier, sensory data, apart from the sense of smell, is sent by the body to the thalamus and then forwarded to both the cortex and the amygdala. In relation to this sense of smell, when faced with a threatening situation, many organisms, including insects, weight and mammals, release volatile pheromones, signalling the danger to other members of the same species. Nearly 70 years ago, Karl von Frisch (1941), described the consternation response in a species of small freshwater fish called the European minnow (Phoxinus phoxinus). Frisch, who was one o f the founders of the scientific study of tool behaviour, demonstrated that when a minnow was eaten by a predator, a chemical released from its damaged skin would be reacted to by other minnows that were reason out by. They would at first dart about randomly, form a smutty school and then retreat from the source of the chemical. Frisch called this substance schreckstoff, meaning shuddery stuff, and we now know that analogous chemicals are used throughout the animal and plant kingdoms. A team of researchers from the University of Lausanne in Switzerland (Brechbuhl et al, 2008) have shown that mice detect alarm pheromones by means of a recently identified sensory system in the nose by examining a structure called the Grueneberg ganglion (GG), which in mammals is located on both sides in the tip of the nose, close to the openings of the nostrils. When the GG was first detect by Hans Grueneberg in 1973, its anatomy was not known in such detail and so it was thought to be a non-sen sory structure. It is only very recently that the olfactory system has come to be viewed as containing 3 distinct channels, each with a unique structure and function. The main channel is involved in detecting aromatic molecules the second channel is called the vomeronasal system, and is an accessory olfactory system which is now known to be involved in the detection of pheromones the GG constitutes a third component of the olfactory pathway, one that was thought to be involved in mother-pup recognition and suckling behaviour, because it is present at the time of birth. The researchers sought to investigate the role of the GG in behaviour. Because of its location, the GG is easily accessible, so they were able to cut the axons of GG neurons in live mice (axotomy), thus preventing any signals from stretchiness the brain. But after numerous tests for nipple finding and other realizable functions, the team actually found that the ganglion played a role in danger communication. pic Fig 7 Scanning electron microscope images of the mouse Grueneberg ganglion. left(a) a cluster of neurons (GC) in a meshwork of fibroblasts (Fb) Right and a higher magnification of a single GG neuron (green), with its axon (red) and thin ciliary process (blue). Scale bars 20 microns (L) and 5 microns (R). (Image from Brechbuhl et al, (2008)). 30 days after the axotomy, the researchers then compared how mice with and without their Grueneberg ganglia responded to alarm pheromones. According to Broillet, the contrast was very striking. Normal mice with the ganglia showed fear immediately by freezing while mice without the ganglia seemed to be un bear upon and they carried on as before, apparently unaware of the danger signals that affected the normal mice. Although their sense of smell did not seem to be affected as they were able to sniff out cookies hidden in their cages as well as the normal mice. This study clearly shows that in mice the GG is involved in detecting alarm pheromones, r ather than in mother-pup interactions, as was previously thought. It is able to perform this primitive function thanks to a specialized yet very basic structure as the GG consists simply of a small group of cells separated from the external environment by a water-permeable sheet of epithelial cells. Its location, far away from the main olfactory system, enables rapid detection of alarm pheromones. Such a mechanism is crucial an organisms excerpt rate, and the GG is found in every mammalian species examined so far, including humans. However, whether or not alarm pheromones affect, or even exist in humans, has been a subject for debate in the scientific community. Since pheromones are not detectable by the human sense of smell, scientists believe that pheromones are sensed by the vomeronasal organ (VNO), part of the olfactory system and located inside the mouth or nose. For many years, the existence of the VNO produced much speculation because it had only been found now and then in adult humans, and when it was found, it was believed to be vestigial. However, Johnston et al, (1985) conducted a study in which the noses of light speed human adults were examined post-mortem and the VNO was found in the septums of 70% of those examined. Since then, much evidence has been poised to support these findings of a presence of the VNO in most adult humans, but many scientists still believe it to be a functionless organ that was transmittable from some ancestor of humans. However, recent genetic research has shown the possibility of a receptor in the nose that could sense pheromones. When searching the human genome for genes that had similar sequences to those of rodent pheromone receptors, a team of researchers from The Rockefeller University in New York and the Yale University School of music identified for the first time a candidate pheromone receptor gene in humans. The findings, reported in Nature Genetics, may shed brisk light on the molecular basis of social c ommunication between humans, including the fear response. In conclusion, despite the saying, have no fear, to live without the ability to experience and recognise fear is to be deprived of a rattling neural mechanism that enables appropriate social behaviour, and possibly even survival.