Question

what happens to STDP(spike timing dependent plasticity) if all biological neuron in brain just generate inhibitory postsynaptic potential(IPSP) not generate EPSP?why?

Answer 1

Spike-timing dependent plasticity in inhibitory circuits. Inhibitory circuits in the brain rely on GABA-releasing interneurons. For long, inhibitory circuits were considered weakly plastic in the face of patterns of neuronal activity that trigger long-term changes in the synapses between excitatory principal cells.

Spike-timing-dependent plasticity (STDP) refers to a form of associative synaptic plasticity in which the temporal order of the presynaptic and postsynaptic action potentials determines the direction of plasticity, that is, whether synaptic depression or potentiation is induced. In the most common form of STDP, long-term potentiation is induced if the presynaptic spike precedes the postsynaptic spike (pre→post), whereas long-term depression is induced if the postsynaptic spike precedes the presynaptic spike (post→pre). In addition to the order of the pre- and postsynaptic spike, STDP is sensitive to the interspike interval, the time elapsed between the two spikes. In general, short intervals produce maximal plasticity, while longer intervals produce little or no change in synaptic strength.

An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential.The opposite of an inhibitory postsynaptic potential is an excitatory postsynaptic potential (EPSP), which is a synaptic potential that makes a postsynaptic neuron more likely to generate an action potential. IPSPs can take place at all chemical synapses, which use the secretion of neurotransmitters to create cell to cell signalling. Inhibitory presynaptic neurons release neurotransmitters that then bind to the postsynaptic receptors; this induces a change in the permeability of the postsynaptic neuronal membrane to particular ions. An electric current that changes the postsynaptic membrane potential to create a more negative postsynaptic potential is generated, i.e. the postsynaptic membrane potential becomes more negative than the resting membrane potential, and this is called hyperpolarisation. To generate an action potential, the postsynaptic membrane must depolarize—the membrane potential must reach a voltage threshold more positive than the resting membrane potential. Therefore, hyperpolarisation of the postsynaptic membrane makes it less likely for depolarisation to sufficiently occur to generate an action potential in the postsynaptic neurone.

Depolarization can also occur due to an IPSP if the reverse potential is between the resting threshold and the action potential threshold. Another way to look at inhibitory postsynaptic potentials is that they are also a chloride conductance change in the neuronal cell because it decreases the driving force.This is because, if the neurotransmitter released into the synaptic cleft causes an increase in the permeability of the postsynaptic membrane to chloride ions by binding to ligand-gated chloride ion channels and causing them to open, then chloride ions, which are in greater concentration in the synaptic cleft, diffuse into the postsynaptic neuron. As these are negatively charged ions, hyperpolarisation results, making it less likely for an action potential to be generated in the postsynaptic neuron. Microelectrodes can be used to measure postsynaptic potentials at either excitatory or inhibitory synapses.