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  1. Fatal Familial Insomnia
    genetic condition. Causes failure to enter deep sleep. Can lead to death
  2. Parasomnias
    sleep related disorder that can occur during arousals from sleep
  3. Amphetamines
    promotes awake state by increasing monoamine transmission (serotonin - raphe nuclei and NE - locus of coerulus to the thalamus)
  4. Modafanil
    promotes awake state by increasing monoamine transmission (serotonin - raphe nuclei and NE - locus of coerulus to the thalamus). Also Histamine and Orexin mechanism
  5. Caffeine
    promotes awake state via adenosine receptor antagonist
  6. Benzodiazepine
    promotes sleep state by increasing GABA output from VLPO (hypothalamus) to inhibit cholinergic (pons-midbrain junction), histamine (TMN) and monoamines (raphe nuclei and locus of coerulus).
  7. Antihistimine
    promotes sleep by blocking histamine transmission (TMN)
  8. Kluver Bucy Syndrome
    Bilateral medial temporal lesion (amygdala). decreased anxiety towards fear, hypersexuality, visual agnosia, hyperorality
  9. Urbach-Wiethe Disease
    Calcification of the anterior-medial temporal lobe. Loss of ability to percieve fear, recognize fear, or a deficit in experiencing fear.
  10. Korsakoff's Syndrome
    Amnesia observed in chronic alcoholics. Vit B1 deficiency and degeneration in mammillary bodies and medial thalamus
  11. Alzheimer's Disease
    progressive and exaagerated neurodegeneration of limbic system effecting the elderly. Beta amyloid plaques and tau tangles are present in histo stains. Specifically Entorhinal Cortex (medial temporal lobe) or basal forebrain and cerebral cortex
  12. Trisynaptic Circuit
    Hippocampal formation important for learning and memory formation; Associate Cortex <---> Entorhinal Cortex --perforant pathway--> Dentate Gyrus --mossy fiber--> CA3 --schaffer collateral--> CA1 ----> Subiculum ----> Entorhinal COrtex (back)
  13. Morris Water Maze
    Tests learning in Hippocampus. Hippocampal lesion results in rodent unable to find hidden platform even after numerous days of practice.
  14. Prefrontal Cortex Lesions
    Phineas Gage personality change after lesion here. Left lesion causes depression. Right lesion causes mania.
  15. Basal Ganglia Loop Review (Know what is excitatory and inhibitory)
    Voluntary Motor or Autonomic emotional feedback (Amygdala). Cortex ++++> Striatum ----> Pallidum ----> Thalamus ++++> Cortex (feedback)
  16. Familial vs Sporadic Alzheimers Disease
    Familial version is rare and due to an inherited mutation in PS1, PS2, or APP genes. Highly penetrant so for sure will get Alzheimers. Sporadic version is more common and due to a Single Nucleotide Mutation (point mutation) in ApoE (apoE4 mut causes Cys---> Arg 112). This is of low penetrance so at a higher risk for Alzheimers but not neccessarily doom to get the disease if you have apoE4 mutation.
  17. Aricept
    Treatment for Alzheimers disease. Acetylcholinesterase inhibitor (increases levels of AcH at synaptic junction).
  18. Memantine
    Treats Alzheimers via glutamatergic modulator on NMDA receptor. Remember AD is primarily a degeneration of glutamatergic synapses and LTP mechanisms.
  19. Positive vs. Negative Schizophrenia
    In general a malfunction of dopamine pathway. Positive symptoms (VTA-mesolimbic projections) are the presence of abnormal behavior, delusions, and hallucinationsc caused by hyperdopamine transmission to D2 receptors mostly. Treat with antipsychotic drugs (APD) which are D2 receptor antagonists. Negative symptoms (VTA-mesocortical projection) are absence of normal social behavior such as apathy, avolition, anhedonia, alogia, and inappropriate affect caused by low dopamine activity. These chronic symptoms do not respond to APD and are difficult to treat.
  20. Parkinsonian Syndrome
    An extrapyramidal (nigrostriatal) side affect of APD treatment of schizophrenia. Resting tremor, rigidity, difficulty initiating movement. Treat with anticholinergic drugs.
  21. Tardive dyskinesia
    An extrapyramidal (nigrostriatal) side affect of APD treatment of schizophrenia and L-DOPA treatment of Parkinson's disease. Characterized by uncontrollable movement of the face, mouth and tongue. No effective treatment for Tardive.
  22. Clozapine
    Atypical APD to treat Schizophrenia. Binds non-dopaminergic receptors (5HT2A, H1, A1). Works for positive and negative symptoms. Less side affects than typical APD
  23. Chlorpromazine (phenothiazines) and Haloperidol (butyrophenones)
    Typical APD to treat only postitive symptoms of Schizophrenia. Binds D2 dopamine receptors only. Has side affects like Tardive dyskinesia and parkinsonian syndrome.
Card Set
Neuro Diseases and Drugs Lab 10
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