Physiology of emotion

1. Physiology of Emotion

2. History Aristotle : People are THINKING ANIMAL.What makes peoplr special is they can overcome their brutish emotions . Rousseau : Emotiuons are what makes people special and gives us reason for living. Hippocrates : Brain is the site of emotion

3. Introduction The word emotion is derived from the latin word emovere which means to stir up to get agitated Complex feeling state with psychic, somatic, autonomic and behavioral components.

4. Emotion has two components: Mental Physical Mental component: Cognition- Awareness of sensation and it’s cause. Affect- The feeling itself. Conation- urge to take action.

5. Oh it’s a roar. The roar seems to be that of lion (Cognition) I feel frightened (Affect) Must run to safety (conation) Roaring of lion (stimulus)

6. Physical components: Changes in viscera and skeletal muscle Coordinated activity of autonomic and somatic nervous system Example: tachycardia, tachypnoea , cutaneous vasoconstriction etc in fear

7. Theories of emotion James-Lang theory Cannon-Bard theory Schachter -Singer theory. Current Theory

8. James lange theory Developed independently by Williams James and Carl Lange in 1884 According to the theory an emotional event causes response in ANS. This response is detected by CNS to produce an emotional experience. Different emotional stimuli produces different bodily response and lead to different emotions

9. James-Lange theory

10. Cannon-Bard Theory Walter Cannon and Phillip Bard – 1927 T he physiological reaction and the emotion are assumed to occur at the same time. Emotional stimuli simultaneously produce a response in the ANS and in the cerebral cortex. The emotional experience is the combination of these two system.

11. Cannon-Bard Theory The influence of the cerebral cortex in controlling emotion is show in the phenomenon of Sham rage. When animals have their cortex removed they go in extreme rages at the slightest provocation. The response is often unrelated to provocation and is short lived

12. Cannon-Bard Theory

13. Schachter -Singer theory Also called cognitive arousal theory. A two-stage theory stating that for an emotion to occur, there must be (1) physiological arousal and (2) an explanation for the arousal. Emotions are produced when autonomic arousal is noticed by the person. He/She tries to come up with an explanation for the arousal and depending on the explanation, label their emotion.

14. Schachter -Singer theory

15. Current Theory No single neural system produces emotions Different emotions may depend on different neural circuits, but many of these circuits converge in the same parts of the brain The limbic system may be involved in some emotional experiences, but it is not the sole neural system underlying emotion Feelings (emotion) result from the interplay between: The amygdala, hypothalamus, brain stem & autonomic nervous system.

16. Limbic system Limbus means a ring Limbic system part of cortical and subcortical structure forming a ring around brainstem. The French physician Paul Broca first called this part of the brain "le grand lobe limbique " in 1878. Formerly called rhinencephalon . The components of the limbic system located in the cerebral cortex have fewer layers than the classical 6-layered neocortex , and are classified as allocortex or archicortex .

17. Limbic system Consist of limbic lobe and related subcortical nuclei. Limbic lobe includes Cingulate gyrus Isthmus Hippocampal gyrus Uncus Subcortical nuclei i nclude Amygdala Septal nuclei Hypothalamus Anterior thalamic nuclei

18. Limbic system From Arthur C Gyuton Physiology

19. Limbic system

20. Connections of limbic system

21. Papez circuit Described by James Papez in 1937. Papez Proposed that there is an emotion system that links the cortex to the hypothalamus. D iscovered the circuit after injecting rabies virus into a cat's hippocampus and monitoring its progression through the brain. O ne of the major pathways of the limbic system and is chiefly involved in the cortical control of emotion.

22. Papez circuit The original circuit proposed by Papez is shown by thick lines and more recent connections as proposed by Paul D. MacLean are shown by thin line

23. Amygdala Buried within the anterior-inferior temporal lobe. Essential in the control of love, friendliness, affection, fear, rage, aggression

24. Amygdala Connections

25. Amygdala connections

26. Amygdala nuclei

27. Amygdala nuclei Medial nucleus: Sensory input, especially odour, relayed to forebrain and hypothalamus Central nucleus: Sensory input via cortex and thalamus, relayed to hypothalamus and brainstem nuclei Basal nucleus: Sensory input relayed to rest of amygdala and to PAG

28. Central nucleus Plays the major role in emotional response patterns Affects hypothalamus and both branches of ANS: Increased HR and BP; ulcers, urination, and defecation Affects brainstem nuclei to increase arousal (VTA), vigilance (LC), cortex activation (DLTN and nucleus basalis ) and startle (pons) Destruction of central nucleus limits emotional response patterns. Electrical stimulation of central nucleus triggers fear, agitation, stress illness

29. Effect of amygdala

30. Amygdala lesion Reduced ability to identify motivational and emotional significance of events Electrical stimulation of amygdala can lead to emotional attacks (rage) Kluver-Bucy Syndrome: Results from bilateral removal of the amygdala and inferior temporal cortex. Includes: loss of fear Indiscriminate dietary behaviour Greatly increased autoerotic sexual activity Tendency to attend to every visual stimulus Tendency to examine all objects by mouth Visual agnosia (cannot recognize objects visually) Inability to recognize facial expression

31. Effect of emotion Autonomic nervous system In threatening situation sympathetic nervous system releases norepinephrine that causes Palm sweating Increased heart rate Focused attention Greater skin conductance Immune system Depressive disorders are associated with decreased lymphocyte production

32. Effects of emotion Endocrine disturbances HPA activity: elevated in stress increased in depression Thyroid axis activity: In depression both hypothyroidism (5-10%) & hyperthyroidism (20-30%) found. Growth hormone: NE and dopamine stimulates growth hormone secretion whereas somatostatin inhibits it . Decreased csf somatostatins are found in depression, increased level is seen in mania

33. Physiology of special emotion Fear Site: The hypothalamus and amygdaloid nuclei Effects of lesion : After destruction of amygdala the fear reaction and its autonomic and endocrine manifestation are absent.eg monkeys are normally terrified of snakes but after bilateral lobectomy they approach snake pick them n eat them In humans amygdala damage causes deficient fear response to visual and auditory stimulus

34. The classical and curious case of Phineus Gage. Phineas P. Gage (July 9, 1823 – May 21, 1860) was an American railroad construction foreman now remembered for his improbable survival of an accident in which a large iron rod was driven completely through his head, destroying much of his brain's left frontal lobe. T he damage to Gage’s frontal cortex had resulted in a complete loss of social inhibitions, which often led to inappropriate behaviour. In effect, the tamping iron had performed a frontal lobotomy on Gage, but the exact nature of the damage incurred to his brain has been a subject of debate ever since the accident occurred.

35. Physiology of special emotion Anxiety: It is normal emotion in appropriate situation but excessive anxiety & anxiety in inappropriate situation is disabling. Site: associated with bilateral increase in blood flow in discreet portion of anterior end of each temporal lobe. Facts : Anxiety is relieved by benzodiazepine which binds to GABA receptors and increase conductance of these ion channels.

36. Physiology of special emotion Rage and placidity: Rage- extreme form of anger Placidity - Calm and peaceful Site: Neocortex , ventromedial hypothalamic nuclei Facts: Human maintains a balance between rage and placidity. Major irritation make normal individual loose temper but minor stimuli are ignored.

37. Motivation Motivation literally means that which moves the will. It is a factor in most of the behaviour . Factors that are responsible for goal direction of a behaviour are the motivation for that behaviour .

38. Reward and punishment Rewards: Things that an individual work for They make the behaviours leading to them more often to occur. Punishments: Opposite of rewards Associated with avoidance leading to behaviour where an individual tries to escape a painful situation.

39. Reward and punishment Neural mechanism involved: The neural mechanism of motivation has ben obtained by studying the effect of brain self stimulation. An unanaesthetised animal (rat) regulates the rate at which electrical stimuli are delivered through electrode implanted in defined area of limbic system.

40. Reward and punishment The brain area where stimulation leads to repeated bar pressing are located in: The medial fore brain bundle Midbrain tegmentum Nucleus accumbens Dorsal brain stem Ventral tegmental area Stimulation of these sites produce pleasurable sensation like relief of tension, relaxed feelings

41. Reward and punishment The brain area where stimulation is avoided are: Lateral portion of posterior hypothalamus Dorsal midbrain Entrorhinal cortex Stimulation of these sites produces sensation ranging from vague fear to terror

42. Neurotransmitter involved in reward system The catecholamines (dopamine and norepinephrine), morphine, enkephalin are involved in the pathways mediating reward system. Drugs that increase the self stimulation are: Amphetamine- cause increase release of dopamine Cocaine- binds and inhibit dopamine transporter-dopamine uptake is reduced-extracellular dopamine level is increased.

43. Neurotransmitter involved in reward system Drugs that block postsynaptic D3 dopaminergic receptors such as chlorpromazine hydrochloride lower activity in catecholamine pathways and decrease self stimulation.

44. Self stimulation reward pathway dopamine

45. Physiology of addiction A kind of dependence which manifests as: compulsive non-medical use of a substance loss of control over its use despite negative consequences Despite many differences, virtually all substances with the potential for addiction affect dopamine levels in the pleasure / reward pathway of the brain.

46. Physiology of addiction

47. Physiology of addiction

48. A presentation by Dr Anwar H Siddiqui