Learning & Memory 2

Amnesia

• Hippocampus consilidates memories for long term shortage
• cortex stores LTMs
• amnesia: deficits in learning and or memory caused by damage to hippocampus
  • loss of relational learning not. stimulus response, motor, or perceptual learning
  • retrograde and anterograde
• anterograde amnesia: difficulty learninf new information after brain damage occurs
  • causes: korsakoffs syndrome- mammillary body degradation, alzheimers disease, damage to the medial temporal lobes @ the hippocampus
  • HM’s case: bilateral damage of the medial temporal lobe, could not form new memories, could recall early childhood memories
  • demonstrates that the hipp is not the location of stored LTM, not needed for retrieval of LTM, not locarion of STM, is responsible for consolidating STM to LTM
• retrograde amnesia: difficulty rememberinf events that occurred before brain damage
  • accompanies anterograde amnesia (time beriod just before damage is lost)
  • demonstrates the hipp consolidates STM to LTM, if damaged before memories are transferred to the cortex then the memories are lost
• amnesia impairs declarative memory formation AKA relattional learining, episodic memory, spatial learning
• does notimpair non-declarative memory formation, motor learnin intact, perceptual learning intact, stimulus response learning intact

Long-Term Potentiation

• neurotransmitter: glutamate
• ionotropuc receptors on postsynaptic membrane, NMDA receptors, AMPA receptors, major role in establishing LTP

Overview of Long term potentiation

• synaptic plasticity: structural or biochemical changes made to synapses
• changes can occur in presynaptic, postsynaptic neurons, or both
• includes long term potentiation
• long term potentiation: synaptic strengthening
• increases the likelihood that prresynapticactivity→ postsynaptic EPSP, presynaptic and postsynaptic changes, changes to glutamate receptorrs, NMDA and AMPA receptors
• long lasrting-months
• occurs in the hippocampal formation and other brain regions
  • many axond frrrom enthorhinal cortex synapse on denate gyrus
• population EPSP: summed EPSP producedby recorded neuron population
• prior to LTP: single pulse stimulation small population epsp
• establishing LTP: 100 pulse of electrical stimulation within a few seconds, temporal summation→stimulation must be rapid

• LTP is long lasting: single pulse stimulation produces largerr population EPSPs hours to days later
• LTP can be generated via repeated electrode stimulation ot via learning
• molecular mechanism underlying simple learning like classical conditioning
• neurral circuitry: synapses are strengthened through LTP due to glutamate dependedt changes to the synapses
• Hebb rule: neurons that fire together wirre together

1. a neuron and postsynaptic neuron are simultaneously active
2. changes to synalse strengtthen and increase the likelihood of EPSP

Prior to LTP

1. somatosensory neurons send strong EPSPs to motor neurons→blink response
2. auditory neuron does not→ does not produce blink response

• 2 glutamate receptors:
  • NMDA receprors on post synaptic membranes: Ca2+ ion channel
  • AMPA receptors: most stores in nonsynaptic regions of the postsynaptic neuron (Na ion channel)
• NMDA receptors: ligand gated ion channel: glutamate binding opens calcium channel
• voltage gatted ion channel: calcuim channel blocked bt Mg2+
• synaptic transmission prior to LTP

1. AP at presynaptic neuron
2. Glu binds at AMPA and NMDA
3. NMDA blocked
4. AMPA allows in some Na
5. Weak EPSP produced

Introduction of LTP

• repeated pairing of 2 stimuli

1. stimualtion of motor neurons via somattosensory neuron
2. simultaneous release of Glu from auditory neuron
3. repeated

• glutamate alone in weak synapses cannot activatte NMDA receptors
• requires: glu binding + postsynaptic depolarization→ induction of LTP
• dendrritic spikes: action potential in dendrites
  • can occur in hippocampus CA1 neurons
  • occur when AP in axon o f the same neuron spreadsto dendrites
• induction of LTP

1. depolarization in postsynaptic neuron
2. dendritic spike. + glu binding
3. Ca2+ enters via NMDA
4. Ca2+. begins signaling cascade
5. activates CaMKII: calcium dependednt enzyme
6. triggeres AMPA receptors to move into postsynaptic membrane

After LTP Established

• NMDA receptors and more AMPA receptors
• Synaptic Transmission in potentiated synapse

1. AP in presynaptic neuron
2. Glu binds at AMPA and NMDA receptors
3. Many AMPA receptors open
4. Lots of Na2+ enters
5. Postsynaptic neuron depolarized
6. Mg2+ repelled from NMDA
7. Ca2+ enters
8. STRONG EPSP

• \   
  1. Auditory synapse is stronger
  2. Auditory neuron activation produces      strong EPSP in motor neuron
  3. Blink!