{'fraction_non_alphanumeric': 0.0387192851824274, 'fraction_numerical': 0.018615040953090096, 'mean_word_length': 5.7537688442211055, 'pattern_counts': {'":': 0, '<': 0, '<?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}}
Cardiovascular Depressor Responses to Stimulation of the Parasubthalamic Nucleus

The parasubthamalic nucleus (PSTN) has been shown to have extensive connections to the nucleus of the solitary tract (NTS). However, the function of PSTN in cardiovascular regulation is unknown. Experiments were done in alpha‐chloralose anesthetized, paralyzed and artificially ventilated rats to investigate the effect of glutamate (Glu; 10 nl, 0.25M) stimulation of PSTN on mean arterial pressure (MAP) and heart rate (HR). Glu stimulation elicited depressor (−22±3 mmHg) and bradycardia (−31±5 bpm) responses. Administration (iv) of atropine methyl bromide attenuated the bradycardia response (−17±7 bpm), but had no effect on the MAP response (−19±5 mmHg). Subsequent iv administration of hexamethonium bromide blocked both the remaining bradycardia and depressor responses. Ipsilateral microinjection of the synaptic blocker CoCl2 (100 nl) into the caudal NTS region attenuated (60–72%) the depressor and bradycardia responses. These data indicate that activation of PSTN neurons elicit a decrease in MAP due to sympathoinhibition, while the cardiac slowing involves both sympathoinhibition and vagal excitation. In addition, these data suggest that the PSTN depressor effects on the circulation are mediated in part through a connection involving the NTS.