Oestradiol Regulates Neuropeptide Y Release and Gene Coupling with the GABAergic and Glutamatergic Synapses in the Adult Female Rat Dentate Gyrus

Abstract

Neuropeptide Y (NPY) is an endogenous modulator of neuronal activity affecting both GABAergic and glutamatergic transmission. Previously, we found that oestradiol modifies the number of NPY immunoreactive neurones in the hippocampal dentate gyrus. In the present study, we investigated which oestrogen receptor type is responsible for these changes in the number of NPY-positive neurones. Furthermore, we determined the effects of oestrogen receptor activation on NPY release. Finally, we examined the contribution of oestrogen toward the remodelling of the GABAergic and glutamatergic gene networks in terms of coupling with Npy gene expression in ovariectomised rats. We found that activation of either oestrogen receptor type (ERα or ERβ) increases the number of NPY-immunopositive neurones and enhances NPY release in the dentate gyrus. We also found that, compared to oestrogen-lacking ovariectomised rats, oestrogen replacement increases the probability of synergistic/antagonistic coupling between the Npy and GABAergic synapse genes, whereas the glutamatergic synapse genes are less likely to be coupled with Npy under similar conditions. The data together suggest that oestrogens play a critical role in the regulation of NPY system activity and are also involved in the coupling/uncoupling of the Npy gene with the GABAergic and glutamatergic synapses in the female rat dentate gyrus.

Sex Differences in the Neuropeptide Y System and Implications for Stress Related Disorders

“…Females have less NPY expression than males in unstressed conditions within many stress-related brain regions and in plasma [ 64 , 65 , 70 , 71 ], with the estrogen playing a potential role in its regulation [ 57 , 118 , 119 , 120 ].…”

“…Estrogen is known to play a regulatory role in NPY expression. Estrogen increases the number of NPY neurons, amount of NPY in pre-synaptic boutons and NPY release in the hippocampus [ 57 , 118 ]. Furthermore, estrogen increases NPY mRNA expression in the hippocampus and caudate nucleus [ 119 ].…”

Powerful quantifiers for cancer transcriptomics

“…As proved in numerous studies, a major problem in the transcriptomic signature is that the expression profile is modulated by factors such as: Genetic background[ 18 ], sex[ 19 ], age[ 20 ], medical history[ 21 ], hormonal activity[ 22 ], diet[ 23 ], cellular environment[ 24 ], exposure to toxins[ 25 ], hypoxia[ 26 ], life style[ 27 ] etc . Owing to the unique combination and fluctuations of such factors, although a trained pathologist can identify common phenotypes, each human has a unique transcriptome whose features and dynamics are never exactly repeated in another human being.…”

ACTH and PMX53 recover synaptic transcriptome alterations in a rat model of infantile spasms

“…We proved recently 29 that gene networks associated with glutamatergic transmission depend on species (mouse, rat), sex, brain region (hypothalamic arcuate nucleus, striatum and prefrontal cortex) and are affected by the prenatal exposure to betamethasone. We have shown also that neuropeptide Y coupling to glutamatergic and GABAergic transmission genes is strongly dependent on the sex hormones 44 . Transcriptomic networks (that may cross the cell’s boundaries) 45 ensure the “transcriptomic stoichiometry” of the functional pathways so that the participating genes are expressed in the right proportions 46 .…”