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  1. What is a motor unit?
    Motor neuron + muscle fibers innervated
  2. What are the types of muscle fibers innervated by motor neurons?
    • S=SLOW - weak, small, for sustained contractions, red
    • FR= FATIGUE RESISTANT - fast, intermediate size, pink
    • FF= FAST FATIGUE - brief, powerful contractions, white
  3. During a muscle contraction, which motor neurons are activated 1st?
  4. Which types of muscle fibers are activated 1st?
    S type (slow twitch)
  5. What is the difference between alpha and gamma motor neurons?
    • Alpha= large diameter, innervate contractile (extrafusal) fibers (S, FR, and FF)
    • Gamma= small, innervate muscles of stretch receptors (intrafusal), called 'fusimotor'
  6. Which motor neurons conduct faster?
  7. Identify the three different types of muscle/tendon receptors:
    • 1a primary = senses stretch and muscle length (involved in tap reflex)
    • Group 2= muscle length
    • Golgi tendon organs= muscle tension
  8. Which muscle receptor system serves the tendon tap reflexes?
    1a primary (monosynaptic reflex arc in the spinal cord)
  9. Which muscle receptor organ causes disynaptic inhibition to the ipsilateral motor neurons?
    Golgi Tendon Organ
  10. What is one of the major diseases that affects motor neurons?
    Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig's Disease, 10% genetic mutation, 90% spontaneous mutation
  11. What is the main organization pricipal of lower motoneurons?
    Organized by movements (direction and force)
  12. What is the main organization principal of upper motoneurons?
    Organized on the basis of muscles (innervation destiny and function)
  13. What is one of the major cortical locations of upper motoneurons?
    Precentral Gyrus
  14. Are motoneurons in the precentral gyrus the only source of corticospinal neurons?
    No! only 1/3 from precentral gyrus
  15. Where are Betz cells located?
    Primary motor cortex (precentral gyrus) - cross in midline of medulla to innervate anterior horn neurons
  16. The motor cortex is organized into columns of cells with similar actions. What are those actions?
    Evoke movement in the same direction
  17. What is the major cause of upper motoneuron lesions?
    Cerebrovascular Accident (CVA) involving motor and premotor cortex or internal capsule
  18. What is the cause of hyperreflexia following upper motoneuron lesions?
    Return and pathological increase of muscle tone and reflexes after CVA
  19. What accounts for the fact that an upper motoneuron lesion involving the facial nerve leaves the individual with a defect in their ability to smile symmetrically while they are still able to bilaterally move their forehead?
    Lower facial muscles innervated by contralateral cortex ONLY; upper face muscles are bilaterally innervated
  20. Name two cortical regions besides the precentral gyrus that contribute axons to the corticospinal tract
    • Parietal lobe
    • Frontal motor cortex
  21. What is the role of the basal ganglia in controlling movement?
    Facilitate ongoing movements
  22. Why is dopamine important in movement control?
    Essential for normal movements and regulatory control through basal ganglia
  23. Identify the basal ganglia nucleus that contains dopamine containing neurons
    Substantia nigra
  24. Name the major nuclei that comprise the basal ganglia:
    • Striatum
    • Globus pallidus
    • Subthalamic nucleus
    • Subtantia nigra
  25. What is the return pathway for basal ganglia activity to affect cortically-induced movements?
  26. Name the brain site and the primary lesion in Parkinson's disease
    Disinhibition/excitation of the substantia nigra
  27. What role does disinhibition play in mediating actions of the basal ganglia?
    Disinhibiton is a reduction of inhibition (GABA) on thalamus that results in excitation of the cerebral cortex
  28. What are the characteristics of Huntingdon's Disease and what region of the brain is involved?
    • Degeneration in striatum
    • Hyperkinesia (spontaneous movements)
    • Dementia and personality disorders
    • Chorea (continuous movements of face, tongue, or limbs - appear coordinated)
    • Athetosis (slow, writing movements of hands/fingers)
    • Hemiballismus (wild, flailing movements of one arm and leg)
  29. How does the cerebellum get information from the motor cortex?
    Cerebral cortex --> pons (crossover) --> cerebellar cortex
  30. Describe the 2 loops through the cerebellum that relate to motor control
    • Loop 1: Planning and Execution - wide regions of cerebral cortex make connections through pons to lateral cerebellar hemispheres. (Dentate nucleus --> thalamus --> motor cortex --> activate movement) Dentate neurons fire before onset of movement.
    • Loop 2: Refine ongoing movement - activation --> intermediate zone (cerebellar cortex) --> interposed nucleus --> red nucleus (spinal cord) --> motor cortex. Primary motor cortex is origin of this component
  31. In which phase of a movement control does the dentate nucelus participate?
    Planning and execution
  32. What are the two connections into the Purkinje cells of the cerebellar cortex?
    • Mossy fibers
    • Climbing fibers
  33. What is the main pathway through which cerebellar information gets back to regions of the motor cortex?
  34. Name a single pathological condition of the cerebellum and describe a few of the symptoms
    • Chronic Alcoholism (midline lesion): postural instability, ataxia (broad gait)
    • Neocerebellar syndrome (lateral hemisphere lesion): lack of movement coordination, decreased muscle tone and reflexes, ispilateral symptoms
  35. Neuroanatomy - NE
    Pons - locus ceruleus
  36. Neuroanatomy - Serotonin (5HT)
    Raphe nuclei - in pons, midbrain, and medulla
  37. Neuroanatomy - DA
    • Ventral Tegmental Area - midbrain (where it is made)
    • Neurons go to nucleus accumbens, medial prefrontal cortex, septal nuclei, and amygdala
    • Mesolimbic system
  38. Circuitry of limbic system
    Hippocampus --> Mammilary bodies (part of hypothalamus)--> Anterior nucleus of the thalamus (mammilo-thalamic tract)
  39. Neuroanatomy - ACh
    Cell bodies - Septal nuclei and nucleus basalis
  40. Urbach Wieth Syndrome
    • No fear conditioning and hard time recognizing fear in facial expressions
    • Can experience fear but not recognize it in others
  41. Anterograde Amnesia
    No new memories
  42. Temporally graded retrograde amnesia
    Loss of old memories within 2 years before surgery
  43. "Place cells"
    • pyramidal cells activated in response to sensory cues in the environment denoting "spatial location"
    • Spatial memory
  44. Haloperidol
    • Blocks dopamine D2 receptors
    • Side effect is motor dysfunction like Parkinsons
    • Tx for Schizophrenia
  45. Clozapine
    • Atypical = decreased side effects
    • Reduced effect blocking D2 receptors
    • Block 5HT receptors
  46. Schizophrenia neurochemicals
    • DA and maybe some 5HT?
    • Increased DA receptor activity
  47. Depression neurochemicals
    • NE and 5HT
    • Decreased activity
  48. Monoamine Oxidase
    Breaks down NE and 5HT
  49. Tricylics
    • Blocks NE and 5HT reuptake
    • Tx for depression
  50. SSRIs
    • Fluoxetine/Prozac
    • Depression tx
    • Only blocks 5HT reuptake (increased serotonin left in synapse)
  51. Korsakoff's syndrome
    • No new memories
    • Disorientation in space and time
    • Confabulation
    • Due to alcoholism (decrease of thiamine in diet - leads to destruction of mammilary bodies and/or mammilothalamic tract)
  52. Prefrontal Lobe Syndrome
    • Phineas Gage
    • Impairment in goal oriented behavior
    • Altered moral reasoning and social behavior
    • Increased impulsivity
    • Due to lesions of prefrontal cortex
  53. PTSD
    • Flashbacks
    • Avoidance
    • Hyperarousal -- increased anxiety
    • Decreased medial prefrontal cortex activity -- increases amygdala activity
  54. Kluver Bucy Syndrome
    • Oral tendencies - put things in mouth
    • Changes in emotions - neutral affect - loss of emotions (loss of amygdala)
    • Hypersexuality - loss of pathways from hypothalamus
    • Visual agnosia - inability to discriminate visual stimuli (loss of pathways from occipital lobe)
    • Due to damage of temporal lobe and amygdala (encephalitis, stroke)
  55. Alzheimer's disease
    • Progressive deterioration
    • Loss of memory
    • Mood disorder - anxiety depression
    • Motor dysfunction
    • Complete loss of cognitive function
    • Due to neurodegeneration that includes limbic structures
    • Tx: Aricept - blocks AChase activity - increased ACh
  56. CCK Actions
    • Gall bladder contraction
    • Increased pyloric constriction (holds nutrients in stomach)
    • Decreased gastric contractions
  57. Ghrelin
    • Made by stomach
    • Orexigenic
    • Increased by fasting
  58. Prader Willi Syndrome
    • Deletion on chromosome 15
    • 1:25,000
    • Decreased muscle tone
    • Mental retardation
    • Small gonads
    • Obsesity
    • Hyperphagia
    • Increased ghrelin secretion
  59. Leptin
    • From OB gene
    • Released by adipocytes
    • Decreases food intake
    • Site of action is hypothalamus
  60. Hypothalmic nuclei involved in control of food intake
    • Lateral hypothalamic area (LHA): activation increases food intake
    • Paraventricular nucleus (PVN): send axons to brainstem to decrease food intake
    • Arcuate nucleus (ARC): NPY projects to PVN and LHA and increases food intake (inhibited by leptin); Melanocortin project to PVN and LHA, decreases food intake, stimulated by leptin -- overall leptin effect is to decrease food intake
  61. Diabetes insipidus
    Loss of vasopressin (ADH) secretion due to head trauma, autoimmune disorder, or idiopathic
  62. Galactorrhea, ameorrhea, hyperprolactinemia
    • Inappropriate lactation; cessation of menstruation
    • Due to increased prolactin secretion
    • Causes decrease in FSH/LH
    • Usually from micro-adenoma
    • Remove tumor or tx with DA receptor agonist --> decreased prolactin secretion
  63. Hypothalamic releasing factors
    • For anterior pituitary
    • Synthesized in parvocellular neurons
    • Transported via axons to median eminence
    • Released - travel in portal vein
  64. Posterior pituitary hormones
    • Synthesized in magnocellular neurons
    • Transported via axons to posterior pituitary
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