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Neurotransmitters

Neurotransmitters. Neuropeptides Opioid peptides Enkephalins (ENK) Endorphins (END) Peptide Hormones Oxytocin (Oxy) Substance P Cholecystokinin (CCK) Vasopressin (ADH) Neuropeptide Y (NPY) Brain-derived Neurotrophic factor Hypothalamic Releasing Hormones GnRH TRH CRH Lipids

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Neurotransmitters

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  1. Neurotransmitters • Neuropeptides • Opioid peptides • Enkephalins (ENK) • Endorphins (END) • Peptide Hormones • Oxytocin (Oxy) • Substance P • Cholecystokinin (CCK) • Vasopressin (ADH) • Neuropeptide Y (NPY) • Brain-derived Neurotrophic factor • Hypothalamic Releasing Hormones • GnRH • TRH • CRH • Lipids • Anandamide • Gases • Nitric Oxide (NO) • Amines • Quaternary amines • Acetylcholine (ACh) • Monoamines • Catecholamines • Epinephrine (EPI) • Norepinephrine (NE) • Dopamine (DA) • Indoleamines • Serotonin (5-HT) • Melatonin • Amino acids • Gamma-aminobutyric acid (GABA) • Glutamate (GLU) • Glycine • Histamine (HIST)

  2. Glutamate Synthesis • Glutamine • Glutaminase • Glutamic Acid • Glutamate • Aspartic Acid • Aspartate

  3. Distribution of VGLUTs

  4. Glutamate Synapse

  5. Glutamate Receptors • AMPA receptors • GluA1-4 • Kainate receptors • GluK1-5 • NMDA receptors • GluN1 • GluN2A-C • GluN3A-B • Metabotropic receptors • mGluR1-8 Iontotropic Metabotropic AMPA Receptor

  6. All ionotropic glutamate receptor channels conduct Na+ ions into the cell

  7. NMDA receptor properties

  8. Types of Memory (iconic memory) (7 bits for 30seconds)

  9. Cellular Mechanism for Learning Hebbian Synapse: Frequent stimulation can change the efficacy of a synapse

  10. Enrichment Protocol Enriched Impoverished

  11. Quantifying Dendritic Arborization

  12. Hippocampal Brain Slicing

  13. Hippocampal Pathways

  14. Long-Term Potentiation (LTP) each triangle represents a single action potential Slope of the EPSP (one characteristic measure of an action potential) baseline response potentiated response Hippocampus has a three synaptic pathway Stimulate one area (mossy fibers) and record the action potentials in another (CA1) Stimulate multiple times to get a baseline response Once a stable baseline is established give a brief high frequency stimulating pulse Use the same stimulating pulse as in baseline but now see a potentiated response This potentiated response can last hours, days, or even weeks (LTP)

  15. Normal Synaptic Transmission Glutamate Channels: NMDA Mg2+ block no ion flow AMPA Na+ flows in depolarizes cell

  16. LTP Induction With repeated activation the depolarization drives the Mg2+ plug out of the NMDA channels Ca2+ then rushes in through the NMDA channels Ca2+ stimulates a retrograde messenger to maintain LTP Ca2+ also stimulates CREB to activate plasticity genes

  17. LTP-induced Neural Changes

  18. Neurobiological Changes via Learning Dendritic changes: • Increased dendritic arborization • Increased dendritic bulbs Synaptic changes: • More neurotransmitter release • More sensitive postsynaptic area • Larger presynaptic areas • Larger postsynaptic areas • Increased interneuron modulation • More synapses formed • Increased shifts in synaptic input Physiological changes: • Long-Term Potentiation • Long-Term Depression

  19. Learning Requires Protein Synthesis! Anisomycin: (protein synthesis inhibitor) blocks long term memory

  20. GABA Synthesis • Glutamate • Glutamic Acid Decarboxylase (GAD) • GABA

  21. GABA Synapse

  22. GABAReceptors • GABAA receptors • GABAB receptors • GABAC receptors Iontotropic Metabotropic GABAA Receptor

  23. GABAA receptor properties

  24. Anxiety Disorders • feelings of concern or worry • increased muscle tension • restlessness • impaired concentration • sleep disturbances • irritability • increased heart rate • Increased sweating • other signs of “fight-or-flight” response

  25. Three-Component Model of Anxiety • General Anxiety Disorder (GAD) • Panic Attacks • Panic Disorder • Phobias • Social Anxiety Disorder (SAD) • Posttraumatic Stress Disorder (PTSD) • Obsessive Compulsive Disorder (OCD)

  26. Neurobiology of Anxiety

  27. Neurobiology of Anxiety

  28. Neurochemistry of Anxiety Corticotropin-releasing factor (CRF) Norepinephrine (NE) Serotonin (5-HT) Dopamine (DA) GABA

  29. GABA and Anxiety • Benzodiazepines (BDZ) and barbiturates cause sedation and reduced anxiety by binding to modulatory sites on the GABA receptor complex • BDZ binding sites are widely distributed in the brain. • They are in high concentration in the amygdala and frontal lobe.

  30. GABA and Anxiety Inverse agonists bind to BDZ sites and produce actions opposite of BDZ drugs—increased anxiety, arousal, and seizures. Theβ-carbolinefamily produces extreme anxiety and panic. They are presumed to uncouple the GABA receptors from the Cl– channels so that GABA is less effective.

  31. GABA and Anxiety Animal studies have found that natural differences in anxiety levels are correlated with the number of BDZ binding sites in several brain areas. PET scans of patients with panic disorder show less benzodiazepine binding in the CNS, particularly in the frontal lobe.

  32. Drugs for Treating Anxiety Anxiolytics Sedative–hypnotics Benzodiazepines Barbiturates Antidepressants

  33. Benzodiazepines

  34. BDZ binding and antianxiety effect

  35. Barbiturates

  36. Antidepressants

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