1. Neurotransmitters Neuropeptides Amines Amino acids 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
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3. Distribution of VGLUTs
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4. Glutamate Synapse
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5. Glutamate Receptors AMPA receptors Kainate receptors NMDA receptors
GluA1-4
Kainate receptors
GluK1-5
NMDA receptors
GluN1
GluN2A-C
GluN3A-B
Metabotropic receptors
mGluR1-8
Glutamate Receptors
Iontotropic
Metabotropic
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AMPA Receptor

6. All ionotropic glutamate receptor channels conduct Na+ ions into the cell
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7. NMDA receptor properties
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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
Impoverished
Enriched

11. Quantifying Dendritic Arborization

12. Hippocampal Brain Slicing

13. Hippocampal Pathways
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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
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21. GABA Synapse
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22. GABA Receptors GABAA receptors GABAB receptors GABAC receptors
Iontotropic
Metabotropic
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GABAA Receptor

23. GABAA receptor properties
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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)
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26. Neurobiology of Anxiety
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27. Neurobiology of Anxiety
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28. Neurochemistry of Anxiety
Corticotropin-releasing factor (CRF)
Norepinephrine (NE)
Serotonin (5-HT)
Dopamine (DA)
GABA 28

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. 29

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

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. 31

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

33. Benzodiazepines
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34. BDZ binding and antianxiety effect
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35. Barbiturates
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36. Antidepressants
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