LTP and LTD

Question 1

Early phase LTP

Answer 1

1. NDMA receptor activated by glutamate + depolarisation. Mg2+ block removed.
2. Ca2+ enters post-synaptic neuron
3. Ca2+-calmodulin binds + activates CaMKII
4. conformational change resulting in regulatory and catalytic subunits further away from each other
5. CaMKII autophosphorylation stabilises conformation
6. CaMKII phosphorylates other proteins
7. AMPAfication

Question 2

late phase LTP

Answer 2

1. cAMP activates PKA
2. PKA activates CREB proteins = TFs
   - CRE bound to CREB-2? - no transcription
   - CREB-2 replaced with CREB-1 + CREB-1 phosphorylated? - transcription of target genes

Question 3

what are nootopics?

Answer 3

drugs enhancing memory which also enhance LTP

Question 4

what are the types of LTDs?

Answer 4

• depotentiation - removal of a previous LTD

* `LTD de novo - triggering an LTD where there was no previous potentiation

Question 5

cerebellum LTD

Answer 5

1. granule cell parallel fibre synapses on purkinje cell (output cell)
   climbing fibre (carries error message) synapses on purkinje cell
2. parallel fibre and climbing fibre activated
3. climbing releases glutamate which binds to AMPA receptors on purkinje cell
   - voltage gated ca2+ channels open
   - increase in intracellular ca2+
   parallel fibre releases glutamate which binds to metabotropic glutamate receptors on purkinje cell
   - alpha subunit of g protein activates phospholipase C
   - DAG produced –> activates PKC
4. PKC activated by Ca2+ so pathways converge
5. PKC phosphorylates AMPA GluR2 subunit
6. membrane internalisation of AMPA receptors

Question 6

hippocampal LTD

Answer 6

1. low frequency stimulation depolarises CA1 neuron enough for a small amount of NMDA receptor activation
2. increase in intracellular Ca2+
3. triggers phosphatase action –> reduces LTD