{'fraction_non_alphanumeric': 0.06306306306306306, 'fraction_numerical': 0.05045045045045045, 'mean_word_length': 4.907801418439717, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Chronic Estradiol Exposure Increases Interleukin‐1 Beta and Nitrate Levels in the Arcuate Nucleus

Chronic exposure to low levels of estradiol‐17β (E2) affects tuberoinfundibular dopaminergic (TIDA) neuronal function resulting in decreased dopamine (DA) synthesis and hyperprolactinemia. We hypothesized that this effect is mediated by cytokines such as IL‐1β, and elevating nitric oxide (NO) and associated free radicals. Young (Y; 3–4 mo) and middle‐aged (MA; 10–12 mo) female Sprague Dawley rats were either ovariectomized (OVX) or left intact. They were sham implanted or implanted s.c. with slow release E2 pellets (20ng/day for 90 days). At the end of treatment, animals were sacrificed and the brains were frozen and sectioned. The arcuate nucleus (AN) and substantia nigra (SN) were collected and analyzed for IL‐1β and nitrate concentrations. E2 exposure increased IL‐1β levels (pg/μg protein; Mean±SE) in the AN of Y, E2‐treated animals whether they were intact (32.11±8.03) or OVX (29.73±6.88) compared to controls (9.78±2.6 and 15.03±4.96 intact and OVX respectively; p<0.05). Similar differences between E2‐treated and control animals were observed in MA animals. Nitrate levels (μM/μg±SE) were higher in intact E2‐treated (3.81±0.9 and 4.97±1.22; Y and MA respectively) animals compared to the controls (1.93±0.4 and 1.59±0.3; Y and MA respectively; p<0.05). There were no significant differences in IL‐1β or nitrate levels in the SN. These results indicate that chronic E2 exposure increases IL‐1β and NO levels in the AN of Y and MA rats. This may contribute to TIDA neuronal dysfunction and subsequent hyperprolactinemia. Supported by NIH AG027697.