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Acta Physiologica Congress

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Acta Physiologica 2012; Volume 206, Supplement 692
The 63rd National Congress of the Italian Physiological Society
9/21/2012-9/23/2012
Verona, Italy


OXYTOCIN MODULATES A CLASS OF HIPPOCAMPAL GABAERGIC INTERNEURONS IN MICE
Abstract number: P1.50

TALPO1 F, SPAIARDI2 P, BIELLA1 G, CHINI3 B, TOSELLI1 M

1Dept Biology and Biotechnology, Pavia Univ., Pavia, Italy
2Dept Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy
3CNR, Institute of Neuroscience, Milano, Italy

Oxytocin (OT) is a pituitary hormone traditionally known for the functions it performs peripherally. However oxytocin is also a neuropeptide and in the central nervous system it regulates several neuroendocrine and cognitive functions. OT deficiency seems to be involved in autistic disorders and brings to impairment of cognitive flexibility and social behaviours, associable with limbic system and hippocampus. This prompted us to study the modulation performed by OT at hippocampal level.

All the experiments were performed using the whole-cell patch-clamp technique on transversal brain slices. During application of the selective OT receptor agonist [Thr4,Gly7]-oxytocin (TGOT), we observed a significant increase of both frequency and amplitude of spontaneous inhibitory postsynaptic currents (GABAA receptor-mediated) recorded from CA1 pyramidal neurons. Furthermore, we analyzed the effect of TGOT application on the membrane potential of CA1 neurons. Drug application induced a depolarizing effect on GABAergic interneurons located in stratum pyramidale, that, in some cases, exceeded the threshold for the generation of action potentials. In contrast no effect was observed on the membrane potential of pyarmidal neurons and GABAergic interneurons located in stratum oriens and radiatum. These data suggest that OT increases the excitability of a class of hippocampal inhibitory interneurons and this, in turn, may indirectly depress the activity of CA1 pyramidal neurons.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 692 :P1.50

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