Activity-Dependent Potentiation of an Asynchronous Component of GABA-ergic Synaptic Currents in Cultured Hippocampal Neurons

• Published in: Neurophysiology (New York) 2014-02, Vol.46 (1), p.10-15
• Main Authors: Borisyuk, A. L., Stepanyuk, A. R., Dovgan’, A. V., Belan, P. V.
• Format: Article
• Language: English
• Subjects: Acids; Anatomy & physiology; Asynchronous; Biomedical and Life Sciences; Biomedicine; GABA; Neurons; Neurosciences
• ISSN: 0090-2977; 1573-9007
• DOI: 10.1007/s11062-014-9400-2

After stimulation of GABA-ergic synaptic connections in a culture of hippocampal neurons by a series of depolarizing current pulses (5-45 sec -1 , 5-20 stimuli), an inhibitory postsynaptic current (IPSC) consisting of a phasic component and an asynchronous component develops in the postsynaptic neuron. In experiments with simultaneous recording from two synapticaly connected neurons, we found that 2-min-long depolarization of the presynaptic cell to +40 mV also led to the development of the asynchronous IPSC component (аIPSC) induced by a single action potential (AP) in the presynaptic neuron. In this case, the decay time of IPSC was, on average, three times greater than in the first case. Analogous potentiation of аIPSC was observed in a part of the synaptic connections after their longlasting (15 min) stimulation by series of depolarizing current pulses (45 sec -1 , 20 stimuli, betweenseries intervals 23 sec). Such potentiation of аIPSC was preserved for a long time (from 3 to 17 min). Simultaneously with potentiation of аIPSC, we observed potentiation of plateau-like inward current through the membrane of the presynaptic neuron in some synaptic connections. The charge transferred by this current through the membrane of the presynaptic cell correlated significantly with the decay time of evoked IPSC in the postsynaptic neuron (mean correlation coefficient 0.83±0.10). This fact can be considered an indication that the above-mentioned inward current mediates potentiation of the above IPSC. The obtained data allow us to hypothesize that the above-described form of plasticity can regulate the efficacy of GABA-ergic synaptic transmission in the hippocampus in the physiological modes of synaptic activity.