Oxytocin, acting as an autotransmitter, gives rise to release of calcium from intracellular store(s) within magnocellular neurons in the supraoptic nucleus (SON). A possible target for a rise in intracellular calcium is the GABAA receptor, since it is known that the functioning of this receptor may depend (directly) on the intracellular free calcium concentration. Therefore the effect of oxytocin on the GABAergic synaptic input in the SON was analyzed. In situ patch clamp recordings from individual neurons of the SON were performed. Spontaneously occurring, bicuculline sensitive GABAergic inhibitory synaptic currents (IPSCs) were pharmacologically isolated from the excitatory glutamatergic synaptic input. This isolated GABAergic synaptic input was spontaneously and tonically active, arising from both somatic as well as from dendritic synaptic contacts and operated a chloride conductance. Application of oxytocin during such recordings, strongly reduced the amplitude of the IPSCs in 73% of the recordings. This reduction was (i) completely reversed by washing, (ii) blocked by a specific oxytocin receptor antagonist, and (iii) observed in slices from both female and from male animals. Thus autotransmission involving disinhibition of magnocellular neurons may explain why oxytocin facilitates it own release.
|Journal||Advances in experimental medicine and biology|
|Publication status||Published - 1996|