2.3.9: Postsynaptic Potential

Postsynaptic potentials (PSPs) are graded fluctuations in the dendritic regions of neurons, which serve as recipients of synaptic inputs from neighboring cells. These inputs can exert either depolarizing or hyperpolarizing influences on the neuron.

When a postsynaptic potential leads to depolarization, it gains the nomenclature of an excitatory postsynaptic potential (EPSP). This terminology is apt as it signifies its role in prodding the neuron's membrane potential closer to the pivotal threshold value. EPSPs emerge from the opening of ion channels that selectively permit the passage of sodium ions. On the contrary, hyperpolarization in a postsynaptic potential instigates an inhibitory postsynaptic potential (IPSP). This distinction is rooted in its propensity to impel the neuron's membrane potential further away from the threshold. IPSPs trace their genesis to the strategic opening of chloride ion channels, thus facilitating the influx of chloride ions into the cellular milieu. Alternatively, they can be evoked through the augmentation of potassium ion permeability, which orchestrates the outward diffusion of potassium ions from the cellular interior. In this sophisticated discourse, the interplay of EPSPs and IPSPs takes center stage, intricately modulating the exquisite balance required for neuronal signaling precision.²⁸

Summation

The amalgamation of these minute electrical changes at the cell membrane of a neuron can propel a neuron toward its threshold level, a phenomenon termed summation (Figure 23). Consider a scenario where the cumulative voltage shift across the membrane amounts to a +15 mV. This change signifies a transition from a resting potential of -70 mV to a threshold-proximate level of -55 mV. The graded potentials merge, driving the membrane to the critical threshold. Notably, these summative effects manifest in an initial segment.

Summation can manifest in two distinct forms: spatial and temporal. Spatial summation entails the confluence of graded potentials originating from diverse loci on the neuron. On the other hand, temporal summation revolves around the sequential occurrence of multiple action potentials within a single neuron, thereby a notable shift in membrane potential (Figure 23). Furthermore, the realms of spatial and temporal summation can intertwine synergistically. Consider a scenario where both excitatory and inhibitory inputs are concurrently triggered. In such instances, the concurrent emergence of EPSPs and IPSPs tends to offset each other to a certain degree (Figure 23).

Figure 23 | Temporal and Spatial Summation | Spatial summation involves the simultaneous activation of numerous synapses, while temporal summation results from the sequential activation of a single synapse over time.

Figure 24 | Postsynaptic Summation | ²⁹ The postsynaptic neuron integrates incoming signals from multiple presynaptic neurons, either through spatial or temporal summation. The combined effects determine whether the postsynaptic neuron will reach the threshold for action potential generation, highlighting the dynamic nature of synaptic integration in neural networks.

The synaptic dynamics and their role in shaping neuronal signaling involves a neurotransmitter that instigates the transient opening of membrane channels, spanning approximately one msec. Remarkably, the resultant postsynaptic potential, which manifests as a consequence of this event, endures for around 15 msec. This phenomenon sets the stage for summation. When these same membrane channels are consecutively reactivated, EPSPs accumulate, amplifying their impact. This rapid sequence of summative activations can culminate in reaching the critical threshold necessary to initiate an action potential in the postsynaptic cell. However, converting an action potential from the presynaptic neuron into an action potential within the postsynaptic neuron at the chemical synapse level is not instantaneous, unlike in an electric synapse. It unfolds over a finite interval termed the synaptic delay, which spans roughly 0.5 to 1 msec. This time gap can elongate depending on the complexity of the neuronal pathway, contingent upon the number of synapses involved.

Synaptic effectiveness is not static; it can be subject to modulation. The phenomenon of presynaptic inhibition serves as an example of attenuation. Here, the neurotransmitter released by the presynaptic neuron, specifically at axoaxonic synapses, reduces the quantity of neurotransmitter discharged by the postsynaptic axon terminal in response to an arriving action potential.³⁰ Conversely, presynaptic facilitation presents an enhancement mechanism. In this scenario, an axoaxonic synapse triggers the release of a greater quantity of neurotransmitters upon an action potential that arrives at the postsynaptic axon terminal. Consequently, a larger EPSP ensues, accentuating the synaptic response (Figure 25). Typically, when an action potential occurs, a fixed number of synaptic vesicles, known as a "quantum," are released, releasing a consistent amount of neurotransmitters. Neuromodulators or diffusible gasses released by neighboring neurons can increase the activity of calcium ion channels in the presynaptic neuron. The increase in presynaptic calcium concentration leads to a phenomenon where a larger quantum of synaptic vesicles is released upon the arrival of an action potential at the axon terminus. In other words, more neurotransmitter-containing vesicles are released in response to each action potential due to the heightened presynaptic calcium levels.³¹ Additionally, disfacilitation refers to a decrease in synaptic excitation, leading to hyperpolarization and disinhibition involves a temporary reduction in synaptic inhibition within a projection neuron. This phenomenon occurs when a separate group of interneurons inhibits the activity of other interneurons.³²

Figure 25 | Modulation of Neuronal Activity | This illustration depicts key synaptic processes: Facilitation, Inhibition, Disfacilitation, and Disinhibition. Facilitation represents an increase in synaptic excitation, while Inhibition involves a reduction in synaptic transmission, leading to hyperpolarization. Disfacilitation signifies a decrease in synaptic excitation, resulting in hyperpolarization. Conversely, disinhibition is characterized by a temporary decrease in synaptic inhibition, potentially enhancing excitatory synaptic transmission.