Question

Long term potentiation (LTP) is the strengthening of synapses in response to repetitive stimulation. Describe how baseline EPSPs are measured in response to stimulation. Describe the stimulation that causes induction of LTP. Describe the cellular response at the postsynaptic side that strengthens the synapse in the early phase. What is necessary to maintain LTP over long periods? How do you discriminate between early and late phase LTP?

 

Answer 1

Answer 2

The baseline EPSPs are measured in An excitatory postsynaptic potentials (EPSP) is a temporary depolarization of postsynaptic membrane caused by the flow of positively charged ions into the postsynaptic cell as a result of opening of ligand-sensitive channels. An EPSP is received when an excitatory presynaptic cell, connected to the dendrite, fires an action potential. The EPSP signal is propagated down the dendrite and is summed with other inputs at the axon hilllock. The EPSP increases the neurons membrane potential. When the membrane potential reaches threshold the cell will produce an action potential and send the information down the axon to communicate with postsynaptic cells. The strength of the EPSP depends on the distance from the soma. The signal degrades across the dendrite such that the more proximal connections have more of an influence

The induction of NMDA receptor-dependent long-term potentiation (LTP) in chemical synapses in the brain occurs via a fairly straightforward mechanism. A substantial and rapid rise in calcium ion concentration inside the postsynaptic cell (or more specifically, within the dendritic spine) is most possibly all that is required to induce LTP. But the mechanism of calcium delivery to the postsynaptic cell in inducing LTP is more complicated.

In a chemical synapse, the postsynaptic membrane is the membrane that receives a signal (binds neurotransmitter) from the presynaptic cell and responds via depolarisation or hyperpolarisation. The postsynaptic membrane is separated from the presynaptic membrane by the synaptic cleft.

Persistent increased activity of protein kinase M ζ (PKMζ) is thought essential for maintaining LTP. Additional spatial and temporal features that govern LTP and LTD induction are embodied in the synaptic tagging and capture (STC) and cross capture hypotheses.

The early and late phase LTP discriminate the Changes in synaptic efficacies need to be long-lasting in order to serve as a substrate for memory. Experimentally, synaptic plasticity exhibits phases covering the induction of long-term potentiation and depression (LTP/LTD) during the early phase of synaptic plasticity, the setting of synaptic tags, a trigger process for protein synthesis, and a slow transition leading to synaptic consolidation during the late phase of synaptic plasticity. We present a mathematical model that describes these different phases of synaptic plasticity. The model explains a large body of experimental data on synaptic tagging and capture, cross-tagging, and the late phases of LTP and LTD. Moreover, the model accounts for the dependence of LTP and LTD induction on voltage and presynaptic stimulation frequency. The stabilization of potentiated synapses during the transition from early to late LTP occurs by protein synthesis dynamics that are shared by groups of synapses. The functional consequence of this shared process is that previously stabilized patterns of strong or weak synapses onto the same postsynaptic neuron are well protected against later changes induced by LTP/LTD protocols at individual synapses.

Answer 3