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2017 | 77 | Suppl.1 |
Tytuł artykułu

Prenatal stress induces changes in excitatory and inhibitory synaptic transmission in the dorsal raphe nucleus of adolescent rats

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Języki publikacji
Prenatal maternal stress (PS) adversely influences the development of the central nervous system. Its effects become evident later in life and may lead to mental and neurological disorders. The dorsal raphe nucleus (DRN) is a major source of serotonin in the mammalian brain. DRN plays a key role in regulation of the stress response and is involved in the development of stress-related psychiatric disorders. Little is known of the effect of prenatal stress on the DRN. In particular, it is not known how PS influences excitatory and inhibitory synaptic transmission and the properties of neurons in the DRN. The aim of this study was to determine the effects of prenatal stress on glutamatergic and GABAergic inputs to DRN serotonergic neurons of the rat. Pregnant Sprague-Dawley rats were subjected daily to three restraint stress sessions, from 14th day of pregnancy until the delivery. The effects of this treatment were studied in slices of the DRN prepared from adolescent male offspring of control and stressed mothers. Whole-cell recordings were carried out from putative serotonergic neurons in DRN slices. Spontaneous excitatory (sEPSCs) and inhibitory (sIPSCs) postsynaptic currents were recorded to assess glutamatergic and GABA-ergic transmission, respectively. Prenatal stress caused an increase in the frequency of sEPSCs and a decrease in the frequency of sIPSCs. Basic electrophysiological properties of serotonergic neurons in rat dorsal raphe nucleus, such as resting membrane potential, input resistance and excitability were not changed after prenatal stress. These results suggest that prenatal maternal stress causes an enhancement of glutamatergic transmission and an attenuation of GABAergic transmission in the DRN of adolescent offspring rats. These effects are likely to affect the function of the serotonergic system. FINANCIAL SUPPORT: This study was supported by grant 2015/17/N/NZ4/02455, National Science Centre Poland. Joanna Sowa is a holder of scholarship from the KNOW sponsored by Ministry of Science and Higher Education, Republic of Poland.
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Opis fizyczny
  • Institute of Pharmacology Polish Academy of Sciences, Department of Physiology, Cracow, Poland
  • Institute of Pharmacology Polish Academy of Sciences, Department of Physiology, Cracow
  • Jagiellonian University, Institute of Zoology and Biomedical Research, Cracow, Poland
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