Maternal deprivation induces persistent adaptations in putative dopamine neurons in rat ventral tegmental area: in vivo
- PDF / 833,396 Bytes
- 8 Pages / 595.276 x 790.866 pts Page_size
- 17 Downloads / 166 Views
RESEARCH ARTICLE
Maternal deprivation induces persistent adaptations in putative dopamine neurons in rat ventral tegmental area: in vivo electrophysiological study Hossein Masrouri1 · Maryam Azadi1 · Saeed Semnanian1 · Hossein Azizi1 Received: 28 February 2020 / Accepted: 13 July 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Early life aversive experiences can trigger persistent deficits in neuronal signaling within the mesolimbic pathway, most notably in the dopamine (DA) neurons of the ventral tegmental area (VTA). The identity of such cellular mechanisms currently appears as an important issue. To address this concern, we investigated whether early life maternal deprivation (MD) would affect the electrical activity of VTA DA neurons, via in vivo extracellular single-unit recording. Male Wistar rats were deprived of their dams for 3 h per day from postnatal days (PND) 1–14. Thereafter, the adult animals (PND 70–80) were tested for the discharge activity of putative VTA DA neurons. The VTA DA neurons displayed a decrease in firing rate and an increase in the variability of baseline discharge activity in deprived animals. MD also caused a decrease in burst firing of VTA DA neurons compared to control subjects. In summary, early life MD induces a hypoactive VTA DA system, which may contribute to lifespan psychopathologies. Keywords Maternal deprivation · Ventral tegmental area dopamine neurons · Extracellular single-unit recording
Introduction Brain functions of adults are considerably affected by their environment during the postnatal developmental period (Ploj and Nylander 2003; Ploj et al. 2003b; Chocyk et al. 2011; Salmanzadeh et al. 2020). Early life adverse events have been shown to lead to future vulnerability to a variety of affective and addictive disorders (Huot et al. 2001; Matthews and Robbins 2003; Ploj et al. 2003a; Moffett et al. 2007; Der-Avakian and Markou 2010; Pachenari et al. 2018; Azadi et al. 2019). Compelling evidence has documented the role of epigenetic mechanisms as an underlying cause of such delayed consequences. Epigenetics causes stable changes in gene expression without altering the DNA sequence (Bird 2007). Indeed, early life environmental perturbations alter the epigenetic programming of brain development, resulting
Communicated by Thomas Deller. * Hossein Azizi [email protected] 1
Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
in long-lasting neural plasticity (Rodrigues et al. 2011; Schwarz et al. 2011; Maccari et al. 2014). The reward circuit that has been best characterized is the DA neurons originate in the ventral tegmental area (VTA) of the midbrain and project to limbic structures and the medial prefrontal cortex (Beier et al. 2015). The VTA DA neurons show two distinct firing patterns, fast bursting activity and slow single-spike firing, with the likelihood of switching between these patterns (Floresco et al. 2003). Burst activity causes an enhanced DA efflux into the synaptic cleft,
Data Loading...
