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Fig 2.9

WITHOUT SYNAPSES NEURONS COULD NOT ‘TALK’ TO ONE ANOTHER AND WE WOULD HAVE NO BEHAVIOR. Sensory neuron SYNAPSES on interneuron. Interneuron SYNAPSES on motor neuron. Receptor SYNAPSES on sensory neuron. Fig 2.9

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Fig 2.9

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  1. WITHOUT SYNAPSES NEURONS COULD NOT ‘TALK’ TO ONE ANOTHER AND WE WOULD HAVE NO BEHAVIOR Sensory neuron SYNAPSES on interneuron Interneuron SYNAPSES on motor neuron Receptor SYNAPSES on sensory neuron Fig 2.9 A simple sensory-motor (reflex) arc. A simple reflex is set in motion by a stimulus to the skin (or other part of the body). The nerve impulse travels to the spinal cord and then back out to a muscle, which contracts. Reflexes provide an “automatic” protective device for the body. Motor neuron SYNAPSES on muscle

  2. Figure 3.4  Temporal and spatial summation

  3. SYNAPSES 1. Structure of the synapse A. Presynaptic cell 1.Terminal button 2. Synaptic vesicles 3. Reuptake mechanisms B. Synaptic cleft C. Post-synaptic cell Postsynaptic membranes and receptors

  4. SYNAPTIC TRANSMISSION 2. Types of synapses A. axonal-dendritic (axon to dentrite) B. axonal-somatic (axon to soma) C. axonal-axonal (axon to axon –usually inhib) *****

  5. SYNAPTIC TRANSMISSION 3. Effects of presynaptic action potentials on polarization of post-synaptic cell A. excitatory post-synaptic potential (EPSP) B. inhibitory post-synaptic potential (IPSP) ******

  6. 02-30a PRIOR TO RELEASE OF NT POSTSYNAPTIC CELL IS IN RESTING STATE AND POLARIZED AT –70mV W. W. Norton

  7. 02-30b AFTER RELEASE OF NTs POSTSYNAPTIC CELL BECOMES DEPOLARIZED (LESS NEGATIVE) AND ONE CAN RECORD EXCITATORY POSTSYNAPTIC POTENTIALS. WHEN THESE ADD UP TO AT LEAST 10Mv AND ‘THRESHOLD’ IS REACHED THE POSTSYNAPTIC CELL WILL FIRE (ALL-OR-NONE) W. W. Norton

  8. 02-30b ? W. W. Norton

  9. 02-30b IF THE NT THAT IS RELEASED IS AN INHIBITORY NT IT PRODUCES GREATER POLARIZATION IN POSTSYNAPTIC CELLS AND ONE RECORDS IPSPs Inhibitory postsynaptic potential W. W. Norton

  10. SYNAPTIC TRANSMISSION 4. Summation of EPSPs and IPSPs on pos-synaptic cell by A. temporal summation B. spatial summation ******

  11. SYNAPTIC TRANSMISSION 5. Neurons synapse on one another and produce additive effects of EPSPs and IPSPs by A. convergence B. divergence ***********

  12. Figure 2.1b An example of a neuron, or nerve cell, showing several of its important features. The right foreground shows a nerve cell fiber in cross section, and the upper left inset gives a more realistic picture of the shape of neurons. The nerve impulse usually travels from the dendrites and soma to the branching ends of the axon. The neuron shown here is a motor neuron. Motor neurons originate in the brain or spinal cord and send their axons to the muscles or glands of the body.

  13. SYNAPTIC TRANSMISSION 5. Neurons synapse on one another and produce additive effects of EPSPs and IPSPs by A. convergence occurs when B. divergence occurs when *********** more than one axon terminates on a neuron different axon terminals from a single neuron terminates on different neurons

  14. NEUROTRANSMITTERS • Criteria for existence of neurotransmitter • a. must be mechanisms in presynaptic cell for its •       1. synthesis •       2. storage •       3. release • 4. Inactivation • *******

  15. Sequence of Events at a Synapse Figure 3.8  Some of the major events in transmission at a synapse Animation

  16. Sequence of Events at a Synapse 1 3 synthesis vesicles Figure 3.8  Some of the major events in transmission at a synapse 4 Presynaptic terminal 5 5 2 cleft vesicles ? 6 Postsynaptic cell Animation

  17. NEUROTRANSMITTERS • Criteria for existence of neurotransmitter • stimulation of the neuron must result in its release • must have specialized postsynaptic receptors • agonists will mimic and antagonists will block its effect

  18. NEUROTRANSMITTERS • Different Neurotransmitters (and quick associations) B. Amines Dopamine (Parkinsonism, Schizophrenia, Reward) Norepinephrine (Learning, fear) Acetylcholine (Motor, memory, Alzheimers) Serotonin (Depression (SSRIs), aggression)

  19. NEUROTRANSMITTERS • Different Neurotransmitters (and quick associations) • B. Neuropeptides • Opioids, endorphins (pain, addiction) • CCK (satiation, eating) • Oxytocin (milk-letdown, maternal behavior) • GABA, Glutamate (inhibition, learning) • **********

  20. DRUG EFFECTS ON NTS 3. Pharmacology • Agonists • Antagonists • inhibitors, false transmitters, inhibitors of inactivation, depleting agents,etc. • **********

  21. Synapses, Abused Drugs, and Behavior • How Drugs Affect Synapses • Agonist-a drug that mimics or increases the effects of a neurotransmitter • Antagonist-a drug that blocks or takes away from the effects of the neurotransmitter • Affinity-ability of a drug to bind a receptor • Efficacy-the degree to which the drug activates the receptor once bound

  22. Figure 3.15  Events at a dopamine synapse and how certain drugs affect the processDrugs can alter any stage of processing at a synapse, from synthesis of the neurotransmitter through release and reuptake. 1. 3 2. 4. 5

  23. Figure 3.15  Events at a dopamine synapse and how certain drugs affect the processDrugs can alter any stage of processing at a synapse, from synthesis of the neurotransmitter through release and reuptake. 1.AGO ANTAG 3 2. ANTAG 4. ANTAG 5 AGO

  24. Dopamine is a neurotransmitter that excites postsynaptic neurons. If a drug were injected into an animal that blocked dopamine from attaching to its receptors, what would happen to the postsynaptic neurons?

  25. Dopamine is a neurotransmitter that excites postsynaptic neurons. If a drug were injected into an animal that blocked dopamine from attaching to its receptors, what would happen to the postsynaptic neurons? They would be less likely to produce further action potentials.

  26. DISEASE CONDITIONS PRODUCED BY DISRUPTIONS IN NEUROTRANSMISSION Parkinson’s Disease Symptoms-rigidity, muscle tremors, slow movement, difficulty initiating movement Brain Changes-Selective loss of cells in substantia nigra and amygdala/decrease in dopamine Possible Causes genetics exposure to toxins (MPTP) smoking decreases risks/these data have been questioned

  27. BRAIN STRUCTURES THAT ARE DISRUPTED IN PARKINSON PATIENTS Figure 8.16  Connections from the substantia nigra: (a) normal and (b) in Parkinson’s diseaseExcitatory paths are shown in green; inhibitory are in red. The substantia nigra’s axons inhibit the putamen. Axon loss increases excitatory communication to the globus pallidus. The result is increased inhibition from the globus pallidus to the thalamus and decreased excitation from the thalamus to the cerebral cortex. People with Parkinson’s disease show decreased initiation of movement, slow and inaccurate movement, and psychological depression.

  28. DRUG TREATMENTS FOR PARKINSON PATIENTS Parkinson’s Disease L-Dopa Treatment IS ONE treatment * precursor for dopamine demonstrates individual effectiveness does not stop progression of the disease numerous side effects (nausea, restlessness, sleep problems, low blood pressure, hallucinations, and delusions) WHY the side effects? *Therapies Other Than L-Dopa antioxidants, dopamine receptor stimulants, glutamate blockers, neurotrophins, drugs that decrease apoptosis, pallidotomy, cell transplants

  29. BECAUSE DOPAMINE IS RELEASED AT MANY SYNAPSES ALL OVER THE BRAIN AND PRODUCES EFFECTS SPECIFIC TO THESE SITES. ONE NOTABLE SIDE EFFECT OF L-DOPA (DA AGONIST) IS PSYCHOSIS NOTE: SCHIZOPHRENICS WHO EXPERIENCE PSYCHOSIS ARE GIVEN NEUROLEPTICS WHICH ARE DOPAMINE ANTAGONISTS ONE OF THE SIDE EFFECTS OF NEUROLEPTICS IS MOTOR DISORDERS-TARDIVE DYSKINESIA

  30. Drugs ‘of abuse’ have effects by acting on receptors in the brain Nicotine Attaches to nicotinic receptors Increases dopamine release in the nucleus accumbens Opiates Derived from opium poppy Attach to opioid receptors in the brain Result in increased dopamine release PCP Inhibits some glutamate receptors Results in reinforcement in the nucleus accumbens Marijuana/Cannabinoids Bind to specific receptors in the brain Leads to euphoria

  31. Other drugs of recreation Hallucinogenic and stimulant Drugs (amphetamine, cocaine,etc.) Distort Perception Many resemble activities of neurotransmitters Caffeine Constricts blood vessels in the brain Interferes with the effects of the neurotransmitter adenosine (ANTAG) Alcohol-multiple effects on brain NTs Inhibits flow of sodium across the membrane Expands the surface of membranes Decreases serotonin activity (ANTAG) Facilitates GABA responses (AGO) Blocks glutamate receptors (ANTAG) Increases dopamine activity (AGO) Video

  32. HORMONES AND BEHAVIOR Hormones are chemicals secreted by endocrine organs in the body into the circulatory system Hormones act at a distance from where they are released NTs act close to release point Hormones act on receptors in other organs and in the brain Hormones act on general metabolism, arousal, and growth Hormones act in the brain to regulate behavior

  33. WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ?

  34. WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ? 1 2 3

  35. WHAT ARE THE ENDOCRINE (HORMONE-PRODUCING) ORGANS ? pituitary adrenals ovaries

  36. Hormonal Changes Associated with the Menstrual Cycle in Women LH and FSH from pituitary Estrogen Progesterone Ovarian changes follicular ovulationluteal

  37. Age of onset of menarche in different cultures- Effect of diet? 1840 1970

  38. HORMONES also affect BEHAVIOR Behaviors activated by hormones include Sexual behavior Maternal behavior Aggression Arousal Eating Drinking Learning Etc.

  39. RAT SEXUAL BEHAVIOR-differences between males and females Female Hop-darts Ear-wiggles Lordosis reflex Male Mounts Intromits ejaculates Rat SEX Male sexual behavior activated by androgens Method: baseline-castration-test-testosterone-test Result: behavior intact-reduced-reinstated Female sexual behavior activated by estrogen & progesterone Method: baseline-ovariectomy-test-E&P-retest Result:behavior intact-eliminated-reinstated

  40. IN HUMANS, ANDROGENS INFLUENCE MALE SEXUAL DESIRE IN BOTH MALES AND FEMALES WOMEN TREATED WITH ANDROGENS INTACT YOUNGER WOMEN, UNTREATED WOMEN TREATED WITH ESTROGENS WOMEN GIVEN PLACEBO

  41. SEX DIFFERENCES IN ADULT BEHAVIOR ARE DUE TO • Differences in genes (XX,XY) • Differences in prenatal hormone exposure • Differences in upbringing • Differences in cultural norms • All of which produce • Differences in brains • Differences in hormones • Differences in gender identity • HENCE-differences in feelings,attitudes, and behavior

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