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The Central Nervous System – Chp 9

The Central Nervous System – Chp 9. The Brain. PHYSIOLOGY – Human Physiology BRAIN FUNCTIONS (Advanced Human Physiology). OUTLINE- Brain Functions. Behavior Sleep and arousal Emotions Memory and Learning Language Personality Movement - Integration. Brain Functions. Behavior

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The Central Nervous System – Chp 9

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  1. The Central Nervous System – Chp 9

  2. The Brain • PHYSIOLOGY – Human Physiology • BRAIN FUNCTIONS (Advanced Human Physiology)

  3. OUTLINE- Brain Functions • Behavior • Sleep and arousal • Emotions • Memory and Learning • Language • Personality • Movement - Integration

  4. Brain Functions • Behavior • Sleep and arousal • Emotions • Memory and Learning • Language • Personality • Movement - Integration

  5. Brain Function Figure 9-14

  6. Behavioral State • Four different systems which appear to modulate sensory and cognitive processes and motor output • Neurons composing them form diffuse modulatory systems • These clumps of neurons form nuclei sending axons which travel toward various areas of the brain • The nuclei are located in reticular formation in brain stem • The 4 processes are: - the noradrenergic modulatory system - the serotonergic modulatory system - the dopaminergic modulatory system - the cholinergic modulatory system

  7. Brain Function: Behavioral State • Four modulatory systems

  8. Role: sleep-wake cycle, attention, arousal, anxiety, pain and mood Promotes brain responsiveness Part of the Reticular Activating System (RAS) Noradrenergic modulatory system

  9. Drugs that interfere with epinephrine / norepinephrine metabolism will affect this system. Amphetamine and cocaine block NE reuptake  remain in the synapse longer How to mess up the system?

  10. MAOI = Monoamine oxidase inhibitor: prescribed against depression – risky Tricyclic antidepressants: block NE reuptake Ritalin: mode of action not yet understood Clinical applications

  11. Role: - Pain, locomotion - mood and emotional behavior (aggression and depression) - Part of the RAS - modulates sleep Serotonergic modulatory system

  12. Amphetamines: block reuptake LSD: serotonin agonist – hallucinogen How to mess up this system?

  13. Anti-depressant: - SSRI – selective serotonin reuptake inhibitor (prozac, paxil, zoloft) - MAOI: decrease degradation of monoamine (parnate) - Tricyclic antidepressants: inhibit reuptake (elavil) Clinical applications

  14. Roles: - motor control - reward center (linked to additive behavior) Dopaminergic modulatory system

  15. Involved in motor control  helps with smoothness of movement, muscle tone Disease: Parkinson’s disease due to a deficit of dopamine secretion Dopamine/substantia nigra

  16. Reward pathway Rates offered choices, will take the drug even if it has deleterious effects on its health Dopamine/ Ventral tegmental area

  17. Many drugs affect this pathway: nicotine, cocaine, morphine, heroin This pathway is down-regulated  withdrawal symptoms develop if the person stops taking the drug. Physiological dependence: The drug overwhelms the receptors in the synapse  they are pulled out  more drug is needed for the same effect  if the drug is stop the person suffers withdrawal symptoms How to mess it up?

  18. Role: - Sleep-wake cycle, arousal - learning and memory - control sensory info. passing by the thalamus Cholinergic modulatory system

  19. Reticular activating system keeps “conscious brain” awake Some of the previous modulatory systems are part of the RAS States of Arousal – Sleep cycle Figure 9-20a

  20. Four stages with two major phases Slow-wave sleep Adjust body without conscious commands REM sleep Brain activity inhibits motor neurons to skeletal muscle, paralyzing them Dreaming takes place Sleep Electroencephalograms (EEGs) show brain waves throughout the day

  21. Somnanbulism: - occurs during stage 3 or 4 of sleep and not during REM sleep Narcolepsy - various symptoms and causes - person falls asleep - maybe due to insomnia during the night

  22. Clinical applications • Coma • “brain death” • Senility • “lock-in syndrome” • What are these 4 pathological states? • Which brain areas are affected?

  23. OUTLINE- Brain Functions • Behavior • Sleep and arousal • Emotions - Moods • Memory and Learning • Language • Personality • Movement - Integration

  24. Emotion and Motivation The link between emotions and physiological functions. The limbic system controls many emotions. • The amygdala is an important center of fear, anxiety. • Emotions can influence somatic, autonomic, endocrine and immune responses. Figure 9-21

  25. Emotions: Role of the Amygdala Removal of amygdala (in monkeys) induces: • tameness & lack of fear • indiscriminate eating patterns • greatly increased & inappropriate sexual behavior Electrical stimulation of the amygdala in animals induces: • fear • autonomic arousal

  26. Moods • Similar to emotions but longer-lasting • Mood disorders • Fourth leading cause of illness worldwide today • Depression • Sleep and appetite disturbances • Alteration of mood and libido • Antidepressant drugs alter synaptic transmission

  27. Influenced by adrenergic and serotonergic, cholinergic circuits. Medications affecting these pathways will affect mood Blocking reuptake and/or blocking turn-over in synapse will induce lifting in mood  anti-depressant Adrenergic pathway: tricyclic antidepressants block norepinephrine reuptake Selective serotonin reuptake inhibitors (SSRI) block serotonin reuptake Mood

  28. Review • What is the difference between drug addiction and physical dependence?

  29. Drug addiction: the person or animal is driven by the pleasure sensation (compulsion). The dopamine pathway is involved, especially the nucleus accumbens (reward experiment with rats) • Physical dependence withdrawal symptoms present if the drug is discontinued. Due to changes in synapses

  30. OUTLINE- Brain Functions • Behavior • Sleep and arousal • Emotions • Memory and Learning • Language • Personality • Movement - Integration

  31. Memory has several types Short-term and long-term Reflexive and declarative Memory

  32. Memory Processing  memory traces Figure 9-22

  33. Memory Alzheimer’s disease is a progressive disease of cognitive impairment characterized by memory loss

  34. Explicit or implicit memory?

  35. Do you remember an event that occurred during a special trip, years ago? Do you remember what you ate yesterday? 3 weeks ago? Short term – Long term and working memory

  36. Short-term memory: few seconds to few hours- easily lost Working memory: short time memory limited to a few number For long term memory, repetition is needed  consolidation – protein synthesis is needed for long term memory

  37. Temporal lobe: hippocampus is a gateway for memory storage Diencephalon is also involved in memory formation Brain areas involved in memory

  38. So where are stored long term memories?

  39. Amnesia • Often due to trauma • Anterograde or retrograde

  40. Learning has two broad types Associative (2 stimuli are associated  Pavlov’s dog) Nonassociative Habituation (decreased response to irrelevant signals but response to significant stimuli) Sensitization (opposite of habituation: strong response to a repeating stimuli –first exposure was distasteful or scary) Learning

  41. The sensory neuron, receiving constant stimulation, slows down its response  less neurotransmitter released at the synapse. Ex: blanking out excess sounds Habituation

  42. Stimulating the sensory neuron results in an increased response (release of neurotransmitter) Ex: Strong fear response to an insect if we have been stung once Sensitization

  43. Associative learning • Ex: Pavlov’s dog • Learning through long term memory of events • At neuron level: Long Term Potentiation  synapses are reinforced • And memory consolidation through protein synthesis

  44. Presynaptic axon Glutamate 6 1 Glutamate is released. 1 2 Net Na+ entry depolarizes the postsynaptic cell. Ca2+ Na+ Mg2+ Depolarization ejects Mg2+ and opens channel. 3 3 Ca2+ enters cytoplasm. 4 AMPA receptor 2 4 NMDA receptor 5 Cell becomes more sensitive to glutamate. Na+ Ca2+ Paracrine release Paracrine from postsynaptic cell enhances glutamate release. 6 5 Postsynaptic cell Ca2+ entry activates second messenger pathways. Long term potentiation Figure 8-30

  45. Brain Functions • Behavior • Sleep and arousal • Emotions • Memory and Learning • Language • Personality • Movement - Integration

  46. Language Cerebral processing of spoken and visual language Damage to Wernicke’s causes receptive aphasia (word salad) Damage to Broca’s area causes expressive aphasia Figure 9-23a

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