Neuro Final Review

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johnpc
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Neuro Final Review
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2014-12-03 10:16:32
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Final Exam Review
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  1. hierarchy of nervous systemfunction
    Ions: Na+, K+, Cl-, Ca2+

    • Proteins: ion channels; receptors; other
    • functional proteins

    Cells: Neurons and Glia

    Synapses: Inhibitory, Excitatory, Neurotransmitters, IntegrationNetworks: stomatogastric ganglion; nigrostriatal pathway (PD)

    Systems: dopaminergic system

    Organisms

    Behaviors
  2. Two major classes of brain cells
    • • Neurons
    • • Glia
  3. Camillo Golgi
    Reticular Theory
  4. Ramon y Cajal
    Neuron Doctrine
  5. The Neuron Doctrine
    • 1. Neurons are Cells
    • 2. Neuron is an Anatomical Unit
    • 3. The Law of Dynamic Polarization
    • 4. The Neuron is an Embryological (Developmental)Unit
    • 5. The Neuron is a Metabolic (trophic) Unit (1872)
    • 6. The Neuron is a Basic Information ProcessingUnit (1943)
  6. Types of synapses
    • axodendritic
    • dendrodentritic
    • axosomatic
    • axoaxonic
  7. schwann cells
    • Peripheral Nervous System
    • myelinate
    • regeneration
  8. Oligodendrocyte
    • central nervous sytem
    • myelination
  9. astrocytes
    • most abundant cells in human brain
    • remove excess glutamte
    • buffering
    • supply glutamine
    • metabolic support
    • neuronal-glial signaling
  10. microglia
    • 10%
    • macrophages
  11. radial glial cells
    • progenitors to other glia and neurons
    • scaffold for migration neurons to cortex
  12. Human Brain
  13. Human Spinal Cord
  14. Spinal Cord laminae I-VI
    Dorsal horn (sensory)
  15. Spinal Cord laminae VII
    Lateral horn (spinocerebellar bathways & autonomic system)
  16. Spinal Cord laminae VIII-IX
    • Ventral Horn
    • VIII = interneurons for coordination
    • IX = to muscles
  17. Spinal Cord correlation to body parts
  18. Brain fluid compartments
    • blood supply (arteries and veins/capillaries)
    • Cerebral spinal fluid
    • extracellular matrix
  19. Blood Brain Barrier Scientist
    • Paul Eherlich
    • Edwin Goldmann
  20. Blood Brain Barrier
    • Due to tight junctions, separation of fluid compartments
    • limits what can enter the brain
  21. Substances that can pass Blood Brain Barrier
    • transporter
    • lipid or lipid soluble materials
    • brain cannulas
  22. Peripheral Nervous System parts(3)
    • Somatic
    • Autonomic
    • Enteric
  23. Nerve Net
    • Hydra, cindarians
    • No accumulation, diffuse through body
  24. Flatworm Nervous system
    ladder-like chord
  25. Crayfish Nervous sytem
    • ganglion and connectives
    • miniature brains
    • 2-head ganglion
    • can act independently
  26. Intracellular Unit Recording
    • Microelectrode placed within cell and record 
    • can measure post-synaptic potentials
  27. Micromanipulator types
    • manual
    • motorized
    • piezoelectric
  28. Single Unit Recording
    • Neuron activity outside cell
    • only record action potential
  29. Muti-unit recording
    • extracellular recording
    • numerous neurons in one area
    • multiple electrodes
    • 512 channels
  30. Neuroanatomical Tracing- Anterograde tracers
    • Soma -> terminals
    • viruses (Herpes simplex)
    • Proteins(PHA-L)
  31. Neuroanatomical Tracing - Retrograde tracers
    • Terminal -> soma
    • Horseradish peroxidase
    • fluorogold
  32. Functional neuroanatomy
    Lesion and Stimulation studies
  33. Optogenetics
    implant gene reacting to light to neurons
  34. Nernst Equation
  35. Reversal Potentials
    • Voltage of cell that determines whether ions move in or out 
    • At value, no movement
  36. resting potential
    • The neuron is in equilibrium
    • – No change in membrane potentia
    • l– THEREFORE
    • • No net movement of ions
  37. Resting membrane potential dependance
    • K+
    • Not always the case-other ions present, especially with lower concentration K+ range
    • K+ is most permeable ion
  38. K+ force direction
    • electrical in
    • chemical out

    favors moving out
  39. Na+ force direction
    • electrical in
    • chemical in

    favors moving in
  40. Cl- force direction
    • electrical out
    • chemical in

    favors moving in
  41. Ion movement (current) is dependent onthree factor
    • – Chemical gradients
    • – individual ion distribution

    – Electrical gradients – distribution of all charged particles

    – Permeability
  42. Calculate resting membrane Potential
    • Goldmann, Hodgkin, Katz equation
  43. Ion Channel Types
    • Leak channels
    • • Voltage-gated channels
    • • Ligand-gated channels
  44. Action Potential
  45. Action potential amplitude
    determined by Na+concentration ratio
  46. Conducting conductances
    ix = gx(Vm - Ex)

    • Vm is set by voltage clamp
    • i is measured
    • Ex is known
  47. Tetrodotoxin(TTX)
    • Saxitoxin
    • blocks sodium channels
    • voltage gated channels
  48. Tetraethylammonium (TEA)
    Blocks voltage gated potassium channels
  49. Late current
    • Produced by K+
    • blocked by TEA
  50. Early Current
    • Produced by Na+
    • Blocked by TTX
  51. IV Curve
    • Can tell what membrane potential channels start opening
    • reversal potential
  52. Na+ Inactivation
    Ball and chain mechanism
  53. Absolute Refractory Period
    • Rate limiting step
    • Impossible to create an AP

    • Na inactivation
    • Ligand-Gated Na+ channels
    • High conductance of K+ in hyperpolarization
  54. Relative Refractory Period
    Must need higher voltage to reach threshold
  55. Spike frequency adaptation
    • Amplitude decreases
    • Time between APs increases
    • slowing down and cessation of AP
  56. Fast Afterhyperpolarization
    delayed rectifier K+ voltage-gated channels
  57. Slow Afterhyperpolarization
    Ca2+ activated K+ channels
  58. BAPTA
    • Neural adaptation
    • Habituation
    • absorbs Ca2+
    • prolonged response in fast beat rate
  59. λ = space/length constant
    λ = (rm/ri)^1/2

    • ^ rm ^λ
    • ^ ri   vλ

    Distance where current falls to 37% of max (V0)
  60. Electrical Transmission
    Direct flow of ions through gapjunctions– Instantaneous– Primarily in PNS
  61. Chemical Transmission
    Release of neurotransmitterfrom a vesicle into the synapticcleft– NT then binds receptors– Slow
  62. Synapsin
    • regulates how many vesicles can be released.
    • • Holds the vesicle to the cellcytoskeleton until phosphorylated by Ca2+-Calmodulin Kinase II
  63. Exocytosis and SNARE Hypothesis
  64. Parts of Human brain with electrical synapses
    • Hippocampus
    • cortex
    • Retina and olfactory bulbs
  65. Membrane resistance
    Rm (leak channels) More LC = ↓Rm ; Less LC = ↑R
  66. Membrane capacitance
    = Cm (neuron size) Larger = ↑Cm; Smaller = ↓Cm
  67. Time constant
    • time to reach 37% of maximum amplitude
    • τ = RmCm
    • τ is one measure of a neuronal property called input resistance
  68. increase action potentialconduction velocity
    • Increase the diameter of the axon– Decreases Ri relative to Rm

    • Myelin– Increases Rm and decreases Cm

    • • Concentrate Na+ & K+ channels in gaps– (Nodes of Ranvier)
    • • Regenerates at nodes– Saltatory conduction
  69. Multiple Sclerosis
    demyelinating auto-immune disease
  70. Why dendrites have voltage-gated channels
    amplification
  71. AP backpropagation
    • Signal back to dendrites indicating level of neuronal output.
    • 1) Some forms of synaptic plasticity
    • 2) Ca2+ signaling (Ca2+-activated K+ channels; intracellular signal/reactions)
    • 3) Neurotransmitter release from dendrites (dendrodendritric synapses)
  72. Post-synaptic potential properties
    • Graded
    • Conduct Passively
    • Can vary in duration
  73. Excitatory post-synaptic potential (EPSP)
    Depolarization Mostly involve Na+
  74. Direction of PSP determined by:
    • • The ionic identity
    • • The equilibrium or reversal potential
  75. Inhibitory post-synaptic potential (IPSP)
    Hyperpolarization Mostly involve K+ or Cl
  76. effects from activatingG-protein coupled receptors
    • 1. Directly activate ion channel
    • 2. Feedback Inhibition or Autoinhibition
    • 3. Activate 2nd messenger systems
  77. Neurotransmitter Removal
    • Enzymatic degradation
    • – Acetylcholine by acetylcholinesterase

    • • Reuptake and recycle
    • – Classical neurotransmitters (via ion-dependent transporters)
    • – Glial interactions
    • • glutamate -> glutamine precursor and released

    • Diffusion

    • • Hydrolysis
    • - ATP
    • • Degraded in cleft (no recycling) - neuropeptides
  78. Chemical signaling consists of
    • • A molecular signal
    • • neurotransmitter

    • • A receptor molecule
    • • transduces information provided by the signal

    • • A target molecule
    • • i.e. an ion channel that is altered to cause an electrical response inthe postsynaptic cell
  79. Criteria defining a neurotransmitter
    • SUBSTANCE MUST
    • ……be synthesized in neuron (1)
    • …be present in vesicles in thepresynaptic terminal (2)
    • …be released in response to presynaptic depolarization (3)
    • …bind to receptors on the postsynaptic cell (4)
    • …have a mechanism of signal termination (5)
  80. SMALL MOLECULE NEUROTRANSMITTERS
    • • Biogenic Amines
    • • Acetylcholine (ACh)
    • • Adenosine triphosphate (ATP)
  81. AMINO ACID NEUROTRANSMITTERS
    • • γ-aminobutyric acid (GABA)
    • • Glutamate
    • • Glycine
  82. • Biogenic Amines
    • – Norepinephrine (NE) aka Noradrenaline
    • – Epinephrine (E) aka Adrenaline
    • – Dopamine (DA)
    • – 5-hydroxytryptamine (5-HT or serotonin
    • – Histamine
  83. Catecholamines
    • – Norepinephrine (NE) aka Noradrenaline
    • – Epinephrine (E) aka Adrenaline
    • – Dopamine (DA)
  84. SOLUBLE GASES Neurotransmitters
    • – Nitric oxide
    • – Carbon monoxide
  85. Activation of ion channels
    • voltage/stretch
    • ligand extracellular/intracellular
  86. Techniques for identifying Neurotransmitter in CNS
    • Presynaptic
    • in situ hybridiation for enzymes, transporter mRNA
    • antibodies to transmitters

    • Postsynaptic
    • antibodies to receptors
    • in situ hybridization for transmitter receptor mRNA
  87. ACh antagonists
    IBO & 18MC
  88. GABA Synthesis
  89. GABAA Receptor
    • Major inhibitory transmitter
    • Cl- ions
    • Cerebral cortex, hippocampus, &cerebellum

    Multiple Binding Sites
  90. GABAPositive modulators/Agonists:
    Benzodiazepines :Diazepam (Valium),Chlordiazepoxide (Librium)

    Barbiturates: phenobarbital

    Agonist: muscimol
  91. GABAAntagonists
    • Picrotoxin
    • Bicuculline
    • (Convulsants)
  92. GABA presynaptic receptor purpose
    Inhibit voltage-gated calcium channels
  93. GABA postsynaptic receptor purpose
    • 1) Inhibit adenylyl cyclase
    • 2) Hyperpolarization and delayed postsynaptic inhibition (synapse periphery)
  94. Glycine
    • Major inhibitory neurotransmitter in spinalcord and brainstem
    • • Permeable Cl-
    • • Strychnine is antagonist– Leads to over-excitation, leading to seizures
  95. Glutamate
    Major excitatory neurotransmitter• Precursor for GABA

    • • Roles in:
    • – Learning and memory (synaptic plasticity)
    • – Cognitive function (cortex and hippocampus)
    • – Motor and cerebellar function
    • – Excitotoxicity
    • • brain trauma and neurodegenerative diseases
    • – Pathogenesis of schizophrenia
    • • Negative symptoms and cognitive dysfunction
  96. Glutamate Synthesis
  97. NMDA
    – Permeable to Na+, K+, LOTS of Ca2+

    • – Role in cellular model of learning and memory
    • • Long term potentiation (LTP) and depression (LTD)

    • – Role in neuropathology
    • • Excitoxicity
  98. Non-NMDA
    • Kainate (Kainic acid)
    • • Permeable to Na+, K+(some cases small amount of Ca2+)

    • – AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)
    • • Very fast
    • • Permeable to Na+, K+(some cases small amount of Ca2+)
    • • “Normal” fast transmission involving glutamate
    • • Very mobile
  99. Metabotropic Glutamate Receptors
    • G-protein coupled receptors (mGluR1-8)
    • – Postsynaptic – One of two actions
    • • Excitatory - Phospholipase C (increase intracellular Ca2+)
    • • Inhibitory - Activate K+ channels

    • – Presynaptic – reduce glutamate release
    • • Block Ca2+ channels
    • • Autoreceptors
  100. Dopaminergic pathways
    • – Tuberinfundibular tract:
    • • Arcuate n.  hypothalamus  pituitary gland
    • • Prolactin (peptide hormone) release

    • – Nigrostriatal system:
    • • Substantia nigra  dorsal striatum (caudate and putamenpartof basal ganglia)
    • • role in the control of movement
    • • affected in Parkinson’s Disease

    • – Mesolimbic system:
    • • VTA  nucleus accumbens (ventral striatum)
    • • “reward pathway”
    • • reinforcing effects of drugs that are commonly abused

    • – Mesocortical system:
    • • VTA  cortex
    • • Cognitive function including short-term memories,planning, and problem solving
    • • Affected in Schizophrenia
  101. Dopamine Inactivation
  102. Types of synaptic plasticity
    • Short Term
    • - Paired Pulse Ratio

    • Long Term
    • - Long-term Potentiation (LTP
    • )- Long-term Depression (LTD)
    • - Spike Timing Dependent Plasticity (STDP)
  103. Paired Pulse Facilitation
    Paired activations of a synapse onto a Layer 2/3 cortical neuron.“Residual Ca2+” in terminal for 10 to 100 msecs after first stimulusincreases probability of release.
  104. Hippocampal Long-Term Potentiation
    • Potentiation of PSPs following highfrequency stimulation
    • Two General Types:
    • • Associative – NMDA dependent
    • • Non-associative – NMDA independent Presynaptic component

    • Two phases:
    • • Early phase
    • • Late phase
  105. LTP Associativity
    • •Presynaptic firing must be paired (associated) withpost-synaptic depolarization to generate LTP
    • •If post-synaptic neuron is held at an hyperpolarizedVm, no LTP occurs
    • •If pre-synaptic firing is weak, no LTP

    The NMDA Receptor provides the keyelement underlying associative LTP
  106. Early LTP
    AMPA receptorinsertion
  107. Late Phase LTP
    • •Long-term maintenance of LTPrequires new protein synthesis andmay be associated with the growthof new synapses (structuralplasticity)
    • •This late phase of LTP involves thecAMP/PKA/MAPK/CREB pathwayand may be required for long termmemory
  108. Impaired Expression of NMDA Receptors
    Disrupts Spatial Learningand Fear Conditioning Memory
  109. NMDA mediated Long-TermDepression
    • • Brought about by small, slow rises in Ca2+concentration
    • • Low Ca2+ stimulates Calcineurin preferentiallyover CaMKII, so phosphatase activitydominates kinase activity
  110. Spike Timing Dependent Plasticity
    • Pre- fires 5-30 ms before post → LTP
    • Pre- fires 5-30 ms after post → LTD
  111. Parkinson’s Disease Symptoms
    • Bradykinesia
    • Muscle Rigidity
    • Resting Tremor
    • Postural Instability
    • Akinesia
  112. Parkinson's Cause
    • Dimished substantia niagra(nigrostriatal pathway)
    • >80% DA cell loss
  113. Parkinson’s Disease Treatment
    • Replacement of lost DA with L-DOPA or DA agonists. Efficacy typically decreasesover time

    • • Administer DA breakdown inhibitors
    • • Inhibit MAO and COMT

    • • Administer Deprenyl
    • • Blocks MPTP metabolism  MPP+

    • Deep brain stimulation of thalamus and basal ganglia

    • • Stem cell replacement
    • • Replace lost dopamine neurons in the substantia nigra
  114. Schizophrenia Symptoms
    • • Positive symptoms (those related with psychoses)
    • – Hallucinations (typically auditory)
    • – Delusions (abnormalities in inferential thinking)
    • – Disorganized speech and behavior

    • • Negative symptoms (absence of some normal human quality)
    • – Flattened affect (blunt emotions)
    • – Cognitive dysfunction (impoverished speech, planning, and workingmemory)
    • – Loss of motivation and interest (avolition)
    • – Loss of ability to experience pleasure (anhedonia) and socialwithdrawal
  115. Cause of Schizophrenia
    Misconnection syndrome

    Overactive dopaminergic system

    genetics and environment
  116. Treatments for Schizophrenia
    • First Generation Antipsychotics (FGAs)
    • – DA receptor antagonist (primarily D2)
    • – Chlorpromazine (Thorazine) and Haloperidol
    • problems: abnormal motor function, involuntary movements, Parkinsonian symptoms

    • • Second Generation Antipsychotics (SGAs)
    • – Less affinity for D2receptor; also 5-HT2A receptor antagonist
    • – LSD hallucinations (5-HT2A agonist)
    • – Clozapine (Clorazil) and Aripiprazole (Abilify)
  117. Noradrenergic system
    • Locus coeruleus
    • Sympathetic NS
  118. Norepinephrine Metabolism/Reuptake
    • Catechol-O-methyltransferase (COMT)

    • Monoamine oxidase (MAO)

    • • Norepinephrine transporter (NET)
    • – Reuptake is the main mechanism of NE inactivation
    • – Amphetamine also blocks NET
  119. Norepinephrine receptors
    • • Alpha-1 (G-protein)– Excitation
    • • Alpha-2 (G-protein)– Autoreceptors (presynaptic)– Inhibition
    • • Beta 1 and 2 (G-protein)– excitation
  120. Neurobiology of ADHD
    • alterations in dopaminergic activity in the prefrontal cortex (PFC)
    • – Not enough dopamine (DA)
  121. Treatments for ADHD
    • • Amphetamines (affect both DA and NE)
    • – Benzedrine (1937)

    • – Methylphenidate (Ritalin) -1955 (1961 in children)
    • • ADHD diagnosis and stimulant use has increased markedly

    – Adderall (today)
  122. Catecholamine Synthesis
    Tyrosine > DOPA > Dopamine > Norepinephrine > Epinephrine
  123. Serotonin (5-HT) Termination
    • • 5-HT Elimination-
    • – primarily by presynaptic reuptake
    • – Selective serotonin reuptake transporter(SERT)

    • • 5-HT Metabolism-
    • – Monoamine oxidase (MAO)
  124. Serotonergic System
    • Raphe nuclei
    • Pons > spinal cord
  125. serotonergic functions
    • • Regulation of sleep and wakefulness
    • – Melatonin

    • Anxiety

    • • Aggression
    • – Low 5-HT linked to increased aggression

    • Mood
  126. Treatment for MDD
    • • Tricyclic antidepressants (1st generation)
    • – Block presynaptic reuptake transporters for 5-HT and/or norepinephrine
    • – Example: Imipramine

    • • Monoamine oxidase (MAO) inhibitors (1st generation)
    • – Block metabolism of serotonin and monoamines
    • – More neurotransmitter available for release (counters neurotransmitter depletion)

    • • Selective serotonin reuptake inhibitors (SRRIs) (2nd generation)
    • – Fluoxetine (Prozac)
  127. Brain areas involved in depression
    Prefrontal cortex and hippocampus
  128. Major cholinergic pathway
    Septal nuclei, Nucleus basalis -> cortex & Hippocampus
  129. Alzheimer’s disease
    – ACh neuron loss in Basal Forebrain
  130. Myasthenia Gravis
    – Autoimmune disorder, antibodiesagainst ACh receptors, muscleweakness
  131. • Lambert-Eaton syndrome
    – Autoimmune disorder, antibodiesagainst voltage gated calciumchannels, muscle weakness

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