Optical information is received by the retina in the eye, within the retina are the nerve cells responsible for vision. Impulse form these nerve cells then travel along the optic nerve to the visual thalamus. Like the eye auditory information is also important in collecting information about the surrounding environment. Sound waves reaching the ear are directed along the auditory canal into the tympanic membrane causing it to vibrate. Vibration of the membrane causes the malleus to move back and forth. This movement is passed on to the incus and stapes, the oval window is pushed in and out by movement of the stapes. This in turn causes waves of movement in the perilymph which distort the membranes and bring about movement in the hair cells of the organ of Corti which cause nerve impulses to be transmitted to the thalamus.
Except for smell all information about the physical world is transmitted like above from stimuli in the physical environment to specific centers in the thalamus. Information from the thalamus is then projected to the cortex as well as the amygdala.
The Amygdala named for its resemblance to an almond lies in the medial wall of the temporal lobes. It forms the key component of the limbic system in the brain. Studies in primates (Amoral et al 1992) have revealed the amygdala contains four prominent intrinsic fiber bundles which are involved in bringing information into the amygdala as well as outputting information to other parts of the brain. These fiber bundles separate the four main nuclei of the amygdala.
The lateral nucleus is the most laterally situated of the amygdaloid nuclei. It can receive input from the cortex and thalamus and is generally regard as the sensory interface of the amygdala. Primate experiments by Amoral et. al. demonstrate that the lateral nucleus projects to all subdivisions of the basal nucleus and the accessory basal nucleus.
The basal nucleus projects to the accessory basal nucleus as well as the central nucleus. The accessory basal nucleus sends a dense projection to the central nucleus. The central nucleus is the pivotal component of fear conditioning circuitry it provides various connections to brain stem areas that control a range of responses. Kapp’s conclusion of the central nucleus explains that it is a crucial part of a system where autonomic conditioned responses are expressed.
The central nucleus of the amygdala has direct projections to hypothalamic and brain stem areas that are involved in many of the symptoms of fear. Projections from the central nucleus of the amygdala to the hypothalamus appear to be involved in the activation of the sympathetic autonomic nervous system responsible for Paleness, pupil dilation and blood pressure elevation during fear. Projections from the central nucleus to the dorsal motor nucleus of the vagus nerve can cause parasympathetic activation resulting in ulcers, urination and defecation. Direct projections to the parabrachial nucleus cause increased respiration, for example panting and respiratory distress.
The activation of dopamine, norepinephrine and acetylcholine during fear causes behavioral and EEG arousal as well as increased vigilance and may be attributed to projections from the amygdala to the ventral tegemental area. Other projections to areas such as facial motor neuron causing facial expressions of fear and central grey leads to freezing, cessation of behavior.
Projections of the amygdala to the nucleus reticularis pontis caudalis are involved in fear potentiation of the startle reflex (Davis, 1992).
For a formerly neutral stimulus to produce a spectrum of behavioral effects used to define a state of fear of anxiety, it is only necessary to activate the amygdala, which in turn produce the complex pattern of behavioral changes by way of the innate connections to different brain target sites. Plasticity during fear conditioning probably results from a change in synaptic inputs in the amygdala rather than from a change in its efferent target areas. The ability to produce long term potentiation in the amygdala and the finding the local infusion of NMDA antagonists into the amygdala blocks the acquisition and extinction of fear conditioning is consistent with this hypothesis (Davis, 1992).
Fear conditioning and lesion studies associated with fear conditioning have brought to light most of the understanding about the amygdala and the flow of information during fear experience. From the information above we would expect that lesions to the amygdala would prevent a conditioned stimulus from producing fear. In fact several studies have shown that a neutral stimulus paired with aversive stimulation will alter neural firing in the amygdala and that lesions of the amygdala block the effects of a conditioned stimulus in a variety of behavioral test situations. Lesions of the amygdala eliminate freezing normally seen to a stimulus (light, tone) paired with shock (LeDoux et. al. 1992).In both adult and infant mammals, lesions of the central nucleus block conditioned changes in heart rate(Kapp et al 1979).
Lesions of the amygdala are also known to block several measures of innate fear in different species. Lesions of the central nucleus in wild rats have been shown to reduce emotionality in terms of fight or flight behavior with regard to reaction to a sedated cat. Some of the lesioned animals crawl over the cat and even nibble its ear a behavior not shown by normal rats.
Electrical stimulation of the amygdala has also been shown to produce the pattern of behaviors resembling a state of fear. Stimulation of the amygdala can alter heart rate, blood pressure and also respiration, prominent symptoms of fear. Electrical stimulation can also simulate other symptoms of fear including cessation of behavior (freezing) startle reflex. In humans electrical stimulation of the amygdala elicits feelings of fear and anxiety as well as autonomic reactions associated with fear.
A great deal of evidence from many laboratories using a variety of experimental techniques indicates that the amygdala plays a crucial role in conditioned fear. Many of the amygdaloid areas are involved in specific signs that are used to measure fear. Electrical stimulation of the amygdala produces a pattern of behaviors that mimic natural or conditioned states of fear. Lesions of the amygdala block innate or conditioned fear. Finally the amygdala appears to be a critical node in the pathway of fear where plasticity that mediates both the acquisition and extinction of conditioned fear. “A better understanding of the chemical composition and transmission properties of the amygdala may eventually lead to more effective pharmacological treatments for fear and anxiety disorders” (Davis 1992).
Aggelton, J The Amygdala: Neurobiological Aspects of Emotion, Memory and Mental Dysfunction, Wiley-Liss, 1992
Davis, M The role of the Amygdala in Fear and Anxiety Annual Review of Neuroscience, Vol. 15, 1992
LeDoux, J Emotion, Memory and the Brain Scientific American. June1994