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Updated: Jun 16, 2026

Whole-cell Patch-clamp Recordings from Morphologically- and Neurochemically-identified Hippocampal Interneurons
Published on: September 30, 2014
Synchronized bursts of miniature inhibitory postsynaptic currents
Ion R Popescu1, Linda A Morton, Alier Franco
1Department of Cell and Molecular Biology, Tulane University, New Orleans, LA, USA.
Spike-independent miniature postsynaptic currents are generally stochastic and are therefore not thought to mediate information relay in neuronal circuits. However, we recorded endogenous bursts of IPSCs in hypothalamic magnocellular neurones in the presence of TTX, which implicated a coordinated mechanism of spike-independent GABA release. IPSC bursts were identical in the absence of TTX, although the burst incidence increased 5-fold, indicating that IPSC bursts were composed of miniature IPSCs (mIPSCs), and that the probability of burst generation increased with action potential activity. IPSC bursts required extracellular calcium, although they were not dependent on calcium influx through voltage-gated calcium channels or on calcium mobilization from intracellular stores. Current injections simulating IPSC bursts were capable of triggering and terminating action potential trains. In 25% of dual recordings, a subset of IPSC bursts were highly synchronized in onset in pairs of magnocellular neurones. Synchronized IPSC bursts displayed properties that were consistent with simultaneous release at GABA synapses shared between pairs of postsynaptic magnocellular neurones. Synchronized bursts of inhibitory synaptic inputs represent a novel mechanism that may contribute to the action potential burst generation, termination and synchronization responsible for pulsatile hormone release from neuroendocrine cells.
Spike-independent miniature postsynaptic currents are generally stochastic and are therefore not thought to mediate information relay in neuronal circuits. However, we recorded endogenous bursts of IPSCs in hypothalamic magnocellular neurones in the presence of TTX, which implicated a coordinated mechanism of spike-independent GABA release. IPSC bursts were identical in the absence of TTX, although the burst incidence increased 5-fold, indicating that IPSC bursts were composed of miniature IPSCs (mIPSCs), and that the probability of burst generation increased with action potential activity. IPSC bursts required extracellular calcium, although they were not dependent on calcium influx through voltage-gated calcium channels or on calcium mobilization from intracellular stores. Current injections simulating IPSC bursts were capable of triggering and terminating action potential trains. In 25% of dual recordings, a subset of IPSC bursts were highly synchronized in onset in pairs of magnocellular neurones. Synchronized IPSC bursts displayed properties that were consistent with simultaneous release at GABA synapses shared between pairs of postsynaptic magnocellular neurones. Synchronized bursts of inhibitory synaptic inputs represent a novel mechanism that may contribute to the action potential burst generation, termination and synchronization responsible for pulsatile hormone release from neuroendocrine cells.
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