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HMB200 2014 Lecture 25.pdf

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Human Biology
John Yeomans

  Lecture  25:  Plasticity  and  Learning   Neurons  and  Learning   - Pavlov  thought  memories  were  made  in  the  cortex   à  later  discovered  hippocampus  was  important   - In  the  brains  of  mammals,  the  hippocampus  is  actually  bouncing  around  as  the  blood  vessels  come  in   àblood   vessels  make  the  brain  move  à  hard  to  record  neurons   - Need  a  monosynaptic  connection  to  show  how  presynaptic  neuron  and  post  synaptic  neuron  are  changing  during   learning   - Simple  circuit  approach—Aplysia  (sea  slug)   - A  single  monosynaptic  connection  can  cause  either  habituation  or  sensitization   - Studied  the  circuits   - These  synapses  can  change   - Aplysia  breathes  by  pushing  water  through  gills   - breathe  by  pushing  water  through  their  gill   - If  tides  are  too  strong,  tides  can  damage  gills  (so  its   protected  by  mantle)   - Gill  withdrawal  reflex  –  gills  withdraws  and  retracts  into   the  body  if  you  touch  it   - Gill  withdrawal  reflex  is  due  to  a  monosynaptic  circuit   - Gill  withdraws  with  a  strong  stimulus  (ex.  when  you   poke  the  animal)  but  withdraws  less  and  less  with   repeated  touches  à  habituation   - Habituation  was  monosyna ptic  circuit,  in  which  these   huge  motor  neurons  (10x  larger  than  motor  neurons  in   mammals)  are  easier  to  record  from   - Monosynaptic  Gill  Withdrawal  reflex.   - Giant  motor  neurons  are   easy  to  record  from   - Associated  with  less  synaptic  strength   - Monosynaptic  connec tion  is  changing  à  habituation   - Habituation  due  to  monosynaptic  connection   - 7  giant  Motoneurons  identified  that  produced  the  response   - 30  sensory  neurons  identified  that  can  activate  this  response   - Connection  between  sensory  motor  neurons  and  motor  neurons  are  becoming  weaker   - Suggests  the  monosynaptic  gill  withdrawal  reflex  habituates  due  to  a  weaker  synaptic  strength  in   this  monosynaptic  connection   - Synapse  must  be  critical  for  the  learning   - Short  term  habituation  due  to  a  monosynaptic  change  in  this  presynapt ic  response  (less  calcium  entry  results   in  less  transmitter  released)  à  presynaptic  depression  decreases  postsynaptic  motor  response   - Monosynaptic  cause  of  the  gill  withdrawal  reflex!   - Habituation,  sensitization,  conditioning.   - Facilitation  of  the  response:  poking  the  animal  in  the   head  à  if  strong  enough  it  will  scare  the  animal   • Changes  the  animal  in  such  a  way  that  now   it  responds  more   • Gill  withdrawal  reflex  becomes  bigger  after   a  single  intense  stimulus  à   potentiating/sensitizing  stimulus  is  poking   the  head   • After  poking  of  the  head  =  activation  of   some  inner  neurons  =  facilitating  inner   neurons   - Facilitating  inner  neurons  increase  transmitter   release  and  increase  presynaptic  release   - Sensitization  in  gill  withdrawal  reflex:  inner  neurons  produce  more  transmitter  release   - Due  to  a  change  in  presynaptic  terminal  by  inner  neurons   - Only  3  inner  neurons  activate  presynaptic  terminal  =  more  cAMP  =  more  calcium  entry  =  greater  response   - Release  of  serotonin  activates  cAMP  in  the  terminal   à  cAMP  activates  kinase  =  more  calcium  entry       - Sensitization  in  the  animal,  increase  in  gill  withdrawal  reflex  (due  to  sensitizing  stimulus)   à  due  to   serotonins  increased  release  in  presynaptic  terminals  =  more  calcium,  greater  postsynaptic  response,   EPSP  goes  up  =  stronger  gill  withdrawal   - Short  term  and  long-­‐term  changes   - Short  term  habituation  due  to  monosynaptic  change   - Long  term  memories  à  in  humans,  long  term  memory  by  spacing  training     - Spacing  training  also  works  in  aplysa   àlong  term  habituation  with  repeated  training   - Can  also  get  long  term  sensitization   by  spacing  sensitizing  trails   à  will  remember  for  weeks   - Both  short  term  and  long  term  changes  are  due  to  monosynaptic  changes   à  in  each  case  there  is  a   transmitter  (results  in  the  activation  of  kinases   à  results  in  proteins  and  genes)   - Synaptic  changes,  proteins  and  genes.   - Less  calcium  entry,  and  less  transmitter  release  from  presynaptic  terminal   - Presynaptic  depression  causes  this  decrease  in  post  synaptic  response   - Learning  and  memory  due  to  monosynaptic  c hanges  in  transmitter  proteins  and  genes     Facilitation  of  response:   • Poke  the  head   • Strong  enough  stimulation  will  scare  the  animal   • Sensitizing  stimulus   • Activation  of  facilitating  inner  neurons   • Sensitization  of  gill  withdrawal  reflex  is  due  to     • More  of  a  short  term  change       Mechanisms  of  Plasticity   -  Habituation  leads  to  smaller  EPSP  (due  to  changes  in  presynaptic  terminal   à  less  glutamate  release  due  to  less   calcium  entry);  Sensitization  leads  to  larger  EPSP  in  postsynaptic  motor  neuron  (more  glutamate  rel ease  =  more   calcium  entry)   - Changes  in  presynaptic  terminal  lead  to  more  or  less  glutamate  release  (via  changes  in  Ca++  entry).   - Sensitization  involves  more  cAMP,  protein  kinase  A,  and  K+  channel  changes   à  more  Ca  2+   - Sensitization  is  facilitated  by  serotonin  (a  monoamine  that  stimulates  the  2  messenger  cAMP  à  activates   PKA  à  channel  changes  resulting  in  more  calcium  and  bigger  EPSP)   - Long  term  changes  require  gene  transcription,  protein  synthesis  via  CREB.   - Is  this  the  same  as  mammals?   - Monosynaptic  change  and  a  cascade  of  chemical  changes     Memory  in  Aplysia   • Spaced  trials  à  long  term  habituation  and  sensitization   – Over  days:  adds  new  complexity   à  need  to  store  memory  for  a  longer  time  =  more  synaptic  change   • Long  term  memory  requires  gene  transcription,  protein   synthesis  and  synaptic  growth   • Kinases  activate  gene  transcription  factor  CREB  in  Aplysia  and  flies  to  cause  long  term  memory   • Is  this  the  same  as  mammals?  Mammals  have  NMDA  to  get  calcium,  using  different  kinases  and  NMDA  receptors,   but  the  same  principle  e xists  in  terms  of  gene  transcription  and  synaptic  growth     Hippocampus   - Hippocampus  is  needed  for  new  long -­‐term  declarative  memories  in  humans.   - In  rodents:  long  term  spatial  memories  and  (long  term  trace  memories  for  conditioning)  conditioning  requires   hippocampus   - Time  and  space  relationships  are  put  together  by  hippocampal  circuits   à  couldn’t  bee  seen  in  the  awake   brain   - Hippocampus  can  be  easily  cut  out  (separate  from  most  of  the  brain  areas)   à  Slices  allow  intracellular  study  of   neurons  and  synapses.   - Anyway  you  cut  the  hippocampus,  you  can  see  the  dentate  gyrus  and  pyramidal  cells   - Studying  pre  and  post  synaptic  neurons   - Showed  there  is  a  long  term  form   of  potentiation   - LTP  plasticity  has  many  properties  of  memory.     - Short  term  and  long  term,  associative  and  non  associative   - Problem:  Circuits  into  and  out  of  hippocampus  aren’t  known,  so  the  functions  of  neurons  aren’t  known.                   Hippocampal  splice:   • Can  pull  hippocampus  out  –  separate  from  other  brain  areas   • In  anyway  you  cut  it,  you  see  the  2  seeds  (dentate  gyrus  and   pyramidal  cells)   • Most  plastic  in  the  brain   – These  hippocampal  neurons  can  produce  memories  that   can  last  for  hours  with  one  single  potentiation  or   sensitizing  stimulus   – Long  term  potentiation  (last  for  days)   – Looks  like  long  term  memory   – Measuring  EPSP  re sponse     • There  is  a  long  term  form  of  potentiation  =  a  monosynaptic  change   in  connections  related  to  glutamate  activation   – This  long  term  plasticity/potentiation  has  many  properties   of  memory  (Short  term,  long  term,  associative,  non -­‐ associative)     • Stimulate  hippocampus  repeatedly  with  no  change   –  steady   synaptic  EPSP   • Doesn’t  change  if  stimulus  is  same  every  time   • Present  ONE  intense  stimulus  (high  frequency  tetanus)  =  next  time  you  test  =  2x  res ponse  in  hippocampus   • Test  100x  more  =  always  bigger   • Same  response,  getting  bigger  response  after  =  LTP     Long-­‐Term  Potentiation   • All  LTP’s  use  glutamate,  all  use  synaptic  plasticity,  all  look  like  learning  and  memory   • Three  glutamate  synapses  in  series,  dentate  gyrus,  CA3,  CA1.   • All  show  LTP  with  high-­‐frequency  stimulation  (100  Hz  “tetanus”).   • LTP  lasts  for  hours  (early  phase),  days  or  weeks  (late  phase).   • Input  specific,  and  associative.   • Study  different  inputs  and  show  how  they  are   associated   • All  LTP  use  glutamate,  all  use  synaptic  plasticity   • All  look  like  memory   • Like  learning  and  memory?   • Input  of  hippocampus  is  largely  come  from  entorhinal  cortex   (where  grid  cells  are
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