EPSC neuroscience is concerned with the mechanism by which neurons’ synaptic inputs and outputs communicate. The process of postsynaptic integration and synthesis determines the period during which spikes are generated. It also defines the amount of information transfer that a neuron can receive before firing. In a previous study, the authors demonstrated that the EPSC decay time constant duration was a reliable predictor of the AP generation time.
Studies in the field have shown that the kinetics of the EPSC is governed by GC morphology and their temporal summation windows. The AMPAR-EPSC ion channel kinetics determines the speed of EPSC decay in the GC. This determines the length of the EPSP and its time window. Their density and shape characterize the GCs in the NEURON, and their morphology is essential in determining their EPSP properties.
What is the hippocampus?
The hippocampus is the brain’s central memory region, receiving synaptic inputs from neurons in the same area. These neurons share common electrotonic locations. Their properties are determined by the number of receptors and their size. The underlying quantal events select the rate of EPSC decay and its duration. The hippocampus is a good candidate for studying synaptic plasticity. A study published in the journal Neuron showed that the speeding of the neuron governs cellular membrane conductance.
Invertebrates, the most important excitatory neurotransmitter is glutamate, associated with the EPSP. In invertebrates, this neurotransmitter is known as acetylcholine. In invertebrates, GABA is the primary transmitter. The more proximal the cell is, the more it influences EPSPs. The more proximal the connections, the stronger the inhibition of the postsynaptic cell.
Features determine by EPSC in the auditory system.
Several features determine the duration of EPSC in the auditory system. The late postnatal stages of development are the most important for assessing synaptic plasticity. The pre-hearing gerbils were examined in the auditory brainstem to identify the structural features of the auditory system. In the adult Mongolian gerbils, the structures of the ear and the medial trapezoid body change. During this period, asynchronous activation of the inputs and rapid postsynaptic integration of information is required for the proper function of the mature auditory neurons.
The early phase of AMPAR-EPSC kinetics may relate to the de-potentiation of extrasynaptic NMDARs and its effect on the latency of the EPSP-spike coupling. It may be necessary to reduce the latency of the EPSP-spiked response to preserve the temporal precision of the spikes. Acute and chronic gsyn8-induced bursts of glutamate are the critical factors in defining the early phase of AMPAR-EPSC.
Properties of EPSCs
Several studies have shown that the intrinsic properties of EPSCs during different developmental stages influence the EPSP of neurons. During the development of the GC, the amplitude of the EPSP doubles. The doubling of the EPSP represents synaptic facilitation. Therefore, this phenomenon can be interpreted in twin-pulse facilitation, homosynaptic plasticity, and epilepsy.
AMPAR-quantal EPSC kinetics, which involves triggering a spike, is the best predictor of future seizures. The AMPAR-quantal EPSC waveform determines its amplitude. The amplitude of an EPSP depends on the intrinsic membrane properties of the cell. The half-width and rise time of an EPSP vary among cells of different ages.
In contrast, the EPSC latency of P14-15 rats is similar to that of P8-10 rats. These results indicate that the changes in the GCs’ intrinsic properties may contribute to the fidelity of the afferent information processing. However, the latency of EPSCs is influenced by a synaptic gym and afferent sensitivity. These changes, along with the differences between the two GCs, also affect the amplitude of the EPSPs.
Moreover, EPSP-spike coupling is graded, and the larger an EPSP, the more likely the postsynaptic cell will be able to fire. The NMDA-mediated EPSCs are more complex than their counterparts, which means that a single NMDA-mediated EPSP can have a much more significant impact on a postsynaptic cell.