LTP

LTP

1. SIGNALS COME INTO DENTATE GYRUS FROM ENTORHINAL CORTEX ALONG PERFORANT PATHWAY.

   • CA3 CELLS AXONS CALLED SHAFFERS COLLATERALS. CONNECT WITH CA1 CELLS. SIGNALS GO BACK OUT INTO ENTORHINAL CORTEX

2. CA1 cells have 2 types of receptor: AMPA and NMDA both permeable to sodium. NMDA also to calcium. But blocked by magnesium so no flow of ions through receptor.

   • low frequency action potential travels down shares collateral. This releases glutamate. Glutamate binds to AMPA and NMDA receptors.
     • AMPA receptors open. Glutamate flows into cell. Slight depolarisation event. Not enough to trigger LTP.

3. BUT: when a high frequency action potential travels down shares collaterals, more glutamate released. Results in more high frequency action potential.

   • Glutamate and sodium flow into cell. Bigger depolarisation event. Then BANG! Electrostatic repulsion blows the lid off the magnesium blockade in the NMDA receptor.
     • Now sodium and calcium enter through the NMDA receptor. Calcium acts as secondary messenger. Binds to proteins. Early phase LTP - few hours.
       • Next you get new AMPA receptors being made in the post synaptic cell at the CA1/CA3 synapse. They only insert into the membrane when there's a lot of calcium about.
         • More AMPA receptors now available for future depolarisation events.
           • Late phase: prolonged calcium influx ultimately results in new gene expressions. More synthesis of proteins. It also results in growth factors.
             • Growth factors result in formation of new synapse between CA1 and CA3 cellss. Basis of synaptic plasticity.
   • More glutamate: binds to receptors as usual. AMPA receptors open longer.