{'fraction_non_alphanumeric': 0.037037037037037035, 'fraction_numerical': 0.027210884353741496, 'mean_word_length': 5.968421052631579, '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}}
Modulation of neuroventilation and central chemosensitivity: serotonergic and hypocretinergic effects

Hypocretin (HC; orexin) neurons modulate arousal state and possibly breathing. The HC system regulates dorsal raphe serotonin (5HT) neurons. Potential for HC modulation of medullary raphe 5HT neurons, putative central chemoreceptors, is unknown. We show HC receptors 1 and 2 (HC‐r1, HC‐r2) on rat medullary raphe 5HT neurons, and potential for HC modulation of chemosensitive medullary 5HT neurons. In an in situ perfused juvenile rat preparation, HC‐1 and SB‐408124 (HC‐r1 antagonist) does not alter baseline phrenic nerve firing (neuroventilation), while blocking HC‐r1 prevents hypercapnic neuroventilatory responses (chemosensitivity). Thus, endogenous HC modulation is necessary, but not sufficient, for chemosensitivity. Exogenous HC‐1 again does not alter hypoglossal neuroventilation in a neonatal rat in vitro medullary slice, or slices derived from neonatal wildtype and knockout mice (Lmx1b) which lack all central 5‐HT neurons. Lmx1b slices do not respond to acidosis, confirming that 5‐HT neurons are critical for central chemosensitivity.HC facilitate baseline neuroventilation in part through 5‐HT neurons. The impact of HC on 5‐HT neuron sensitivity to acidosis remains in question. NIH 2U54NS041069‐06A1