Brain Mechanisms of Emotion 1 of 6 I. WHAT IS AN EMOTION? A. Three components (Oately & Jenkins, 1996) 1. caused by conscious or unconscious evaluation of an event as relevant to a goal that is important a) positive when goal is advanced b) negative when goal is impeded 2. results in or produces action readiness a) interrupt b) compete c) replace action the organisms is currently involved in 3. experienced as a distinctive mental state that is sometimes accompanied by bodily changes, expressions or actions B. Theories of Emotion 1. James-Lange a) Physiological changes first b) Interpretation produces the emotion 2. Cannon-Bard a) Emotional experience is separate from emotional expression b) Simultaneous processing leads to (1) Physiological changes (2) Emotion c) Criticized James theory (1) because severing the spinal cord did not stop emotion (2) no correlation between physiological state and emotion d) thought that thalamus determined the emotional character of an event 3. Evidence a) Support for James (1) There are some physiological differences between some of the emotions (2) Spinal cord damage does produce some diminution of emotional experience (3) Forcing an emotional expression does produce some feeling in that direction II. THE LIMBIC CONCEPT A. Broca outline the limbic area but did not discuss function B. The Papez Circuit 1. Papez built on his work and called the limbic system an emotion system 2. discuss the figure 3. compatible with both the James-Lange and the Cannon- Bard theories 4. evidence comes from a) rabies that destroy the hippocampus b) anterior hypothalamus damage can result in spontaneous laughing and crying 5. MacLean claimed that the limbic system liberates animals from the ritualistic behavior of the brain stem C. Difficulties with the single emotion system concept 1. hippocampus no longer thought to be part of the emotion system 2. we have a diversity of emotions and should probably expect a diversity of brain areas to be involved
Brain Mechanisms of Emotion 2 of 6 a) we have no solid evidence that makes a 1-to-1 link between a brain area and an emotion III. FEAR AND ANXIETY A. Crucial question: how does incoming sensory information lead to behavioral and physiological responses associated with fear and anxiety? Probably through the amygdala B. The Kluver-Bucy Syndrome 1. bilateral temporal lobectomy results in a) psychic blindness b) oral tendencies c) hypermetamorphosis: compulsion to examine everything d) altered sexual behavior e) emotional changes (1) dramatic decrease in fear (2) normal experience of emotion seemed to be decreased (3) normal expression of emotion seemed to be decreased C. The Amygdala 1. associated with symptoms of Kluver-Bucy Syndrome a) removal of other subcortical areas probably responsible for some like psychic blindness 2. anatomy of the amygdala a) divided into three nuclei (1) basolateral nuclei (2) corticomedial nuclei (3) central nucleus b) Receives sensory feeds from all sensory systems c) each sensory system projects with different patterns and interconnections allow all the sensory information to be integrated d) two major pathways connect the amygdala with the hypothalamus (1) ventral amygdalofugal pathway (2) stria terminalis e) review my picture of the amygdala as the primary appraiser
Brain Mechanisms of Emotion 3 of 6 3. The effects of amygdala destruction and stimulation a) amygdala damage is associated with decreased emotionality and the inability to recognize fear in humans b) stimulation of the amygdala leads to fear and anxiety in humans 4. A neural circuit for learned fear a) It appears to give emotional coloring to memories (1) No response by amygdala neurons prior to fear conditioning (2) After training, neurons in the central nucleus show a response (3) Amygdala lesions stop the ANS response to fear b) Animal findings extend to humans (1) fmri shows increased brain activity there (2) also elicits cingulated and insular cortex responses, which is probably related to emotional experience IV. ANGER AND AGGRESSION A. Different types of aggression may be regulated differently by the nervous system 1. multifaceted behavior that is not the product of a single isolated system 2. androgen levels affect aggression B. Two types of aggression 1. predatory aggression a) attacks against a different species b) few vocalizations c) bites at head and neck d) low levels of sympathetic activity 2. affective aggression a) showy b) many vocalizations c) posturing
Brain Mechanisms of Emotion 4 of 6 d) high levels of sympathetic activity C. The hypothalamus and aggression 1. Sham Rage a) If anterior hypothalamus and diencephalons are destroyed b) Disappears if the posterior hypothalamus is destroyed c) Thought that posterior hypothalamus is necessary and that diencephalons inhibits 2. Electrical stimulation of the hypothalamus a) Stimulation of the hypothalamus leads to many behaviors (1) Sniffing (2) Panting (3) Eating (4) Expressions of fear and anger b) Two primary functions of the hypothalamus (1) Homeostasis (2) Organization of coordinated (a) Visceral response (b) Somatic motor response (3) Probably part of the system normally involved in the expression of emotions c) Stimulation of the medial hypothalamus results in affective aggression d) Stimulation of the lateral hypothalamus leads to predatory aggression D. The midbrain and aggression 1. medial forebrain bundle connects the lateral hypothalamus and the ventral tegmentum a) leads to predatory aggression 2. dorsal longitudinal fasciculus connects the medial hypothalamus and the periaqueductal gray matter a) leads to affective aggression E. The amygdala and aggression 1. amygdala destruction has an effect on social interaction a) dominant male loses position 2. electrical stimulation of basolateral nuclei produces affective aggression through the ventral amygadalofugal pathway 3. lesions of the basolateral nuclei reduce affective aggression 4. lesions in corticomedial nuclei or the stria terminalis reduce predatory aggression a) corticomedial nucleus probably has an inhibitory role 5. psychosurgery has been used to reduce human aggression through destroying the amygdala
Brain Mechanisms of Emotion 5 of 6 F. Serotonin and aggression 1. 5-HT neurons project from the raphe nuclei into the medial forebrain bundle and from there into the hypothalamus and various limbic structures 2. lower serotonin turnover rate in isolated mice that became more aggressive 3. drugs that block the production or release of 5- HT increase aggressive behavior 4. dominance hierarchy can be manipulated by adjusting 5-HT levels a) lower 5-HT produces increased aggression b) aggression not completely related to dominance; some suggestion of elevated confidence 5. specifically the 5-HT 1A and 5-HT 1B receptors have been implicated a) antagonists for these receptors increase aggressiveness b) agonists for these receptors decrease anxiety and aggressiveness in mice c) distribution of these receptors (1) raphe nuclei (2) amygdala (3) periaqueductal gray (4) basal ganglia V. REINFORCEMENT AND REWARD A. Olds & Milner located self-stimulation centers B. Called pleasure centers but this might not be accurate 1. we don t know that pleasure was experienced by the animals; it may have been a compulsion 2. even if it was pleasure it might not be due to a center but to a diffuse scattering of sites C. self-stimulation sites found in limbic areas 1. septal area 2. lateral hypothalamus 3. medial forebrain bundle 4. ventral tegmental area 5. dorsal pons D. displeasure centers 1. medial hypothalamus 2. lateral midbrain tegmental areas E. brain stimulation in humans 1. report pleasure in many of these locations 2. stimulate some areas because there is an anticipated award that they never quite achieve F. dopamine and reinforcement 1. dopamine agonists increase self-stimulation 2. dopamine antagonists decrease self-stimulation 3. drugs of addiction are all associated with the mesocorticolimbic dopamine system 4. problems a) cutting the medial forebrain bundle does not have a devastating effect on selfstimulation as would be predicted
Brain Mechanisms of Emotion 6 of 6 b) self-stimulation sites are not identical to the brain sites that receive DA input from the midbrain