# The Effect of Intracellular Calcium Buffer Bapta on Epileptiform Activity of Hippocampal Neurons

## TL;DR

This paper investigates how the calcium buffer BAPTA affects epileptiform activity in hippocampal neurons, showing that it alters the rhythm and may have neuroprotective effects.

## Contribution

The study reveals distinct responses of GABAergic and glutamatergic neurons to BAPTA, highlighting the role of calcium-binding proteins in neuroprotection.

## Key findings

- BAPTA accumulation reduces the amplitude of PDS clusters in GABAergic neurons, shifting activity to a classical burst mode.
- In glutamatergic neurons, BAPTA shortens PDS cluster duration but has minimal effect on amplitude.
- Endogenous calcium-binding proteins help switch epileptiform rhythms to recovery rhythms and protect neurons.

## Abstract

The rhythm of epileptiform activity occurs in various brain injuries (ischemia, stroke, concussion, mechanical damage, AD, PD). The epileptiform rhythm is accompanied by periodic Ca2+ pulses, which are necessary for the neurotransmitter release, the repair of damaged connections between neurons, and the growth of new projections. The duration and amplitude of these pulses depend on intracellular calcium-binding proteins. The effect of the synthetic fast calcium buffer BAPTA on the epileptiform activity of neurons induced by the GABA(A)-receptor inhibitor, bicuculline, was investigated in a 14-DIV rat hippocampal culture. In the epileptiform activity mode, neurons periodically synchronously generate action potential (AP) bursts in the form of paroxysmal depolarization shift (PDS) clusters and their corresponding high-amplitude Ca2+ pulses. Changes in the paroxysmal activity and Ca2+ pulses were recorded continuously for 10–11 min as BAPTA accumulated. It was shown that during BAPTA accumulation, transformation of neuronal patch activity occurs. Moreover, GABAergic and glutamatergic neurons respond differently to the presence of calcium buffer. Experiments were performed on two populations of neurons: a population of GABAergic neurons that responded selectively to ATPA, a calcium-permeable GluK1 kainate receptor agonist, and a population of glutamatergic neurons with a large amplitude of cluster depolarization (greater than −20 mV). These neurons made up the majority of neurons. In the population of GABAergic neurons, during BAPTA accumulation, the amplitude of PDS clusters decreases, which leads to a switch from the PDS mode to the classical burst mode with an increase in the electrical activity of the neuron. In glutamatergic neurons, the duration of PDS clusters decreased during BAPTA accumulation. However, the amplitude changed little. The data obtained showed that endogenous calcium-binding proteins play a significant role in switching the epileptiform rhythm to the recovery rhythm and perform a neuroprotective function by reducing the duration of impulses in excitatory neurons and the amplitude of impulses in inhibitory neurons.