“
“Estradiol (E2) modulates affective and socio-sexual behavior of female rodents. E-2′s functional effects may involve actions through alpha and beta isoforms of estrogen receptor (ERs). The importance of E2′s actions at these isoforms for anxiety ( open field, elevated Liproxstatin-1 plus maze), depression ( forced swim test), and sexual behavior ( lordosis) was investigated using an antisense oligonucleotide

(AS-ODN) strategy. If ER beta is required for anti-anxiety and antidepressant-like effects, and ER alpha is required for sexual receptivity, of E2, then intracerebroventricular administration of AS-ODNs against these ERs should attenuate these effects and reduce immunoreactivity of ERs in brain regions that mediate these behaviors, such as the hippocampus and ventral medial hypothalamus (VMH). Ovariectomized rats were primed with 17 beta-E-2 ( 10 mu g) 48 h before testing (hour 0). At hours

0, 24, and 47.5, rats were infused with saline vehicle, scrambled control AS-ODNs, or AS-ODNs targeted against ER alpha and/ or ER beta, and were tested at hour 48. Rats infused with ER beta AS-ODNs, alone, or with ERa AS-ODNs had significantly decreased open field central entries, decreased plus maze open arm time and entries, increased time spent immobile, and decreased time spent swimming in the forced swim test, and decreased ERb immunoreactivity in the brain than did rats administered ER beta AS-ODNs, buy Lapatinib vehicle, or scrambled AS-ODNs. Rats that were administered ER beta AS-ODNs, alone, or with ERb AS-ODNs had significantly decreased lordosis and decreased ER alpha immunoreactivity in the brain compared to rats administered ERb AS-ODNs, vehicle, or scrambled AS-ODNs. Thus, ER beta and ER alpha may be required for E-2′s modulation of affective and sexual behavior, respectively.”
“Prenatal Benzatropine exposure to infections represents a risk factor for the emergence of neuropsychiatric

disorders in later life, including schizophrenia and autism. However, it remains essentially unknown whether this association is primarily attributable to prenatal and/or postnatal maternal effects on the offspring. Here, we addressed this issue by dissecting the relative contributions of prenatal inflammatory events and postnatal maternal factors in an animal model of prenatal viral-like infection. Pregnant mice were exposed to the inflammatory agent polyriboinosinic-polyribocytidilic acid (Polyl:C; 5 mg/kg, i.v.) or vehicle treatment on gestation day 9, and offspring born to Polyl:C-and vehicle-treated dams were cross fostered to surrogate rearing mothers that had either experienced inflammatory or sham treatment during pregnancy. We demonstrate that a variety of dopamine- and glutamate-related pharmacological and neuroanatomical disturbances emerge after prenatal immune challenge regardless of whether neonates were raised by vehicle- or Polyl:C-exposed surrogate mothers.