{'fraction_non_alphanumeric': 0.021479713603818614, 'fraction_numerical': 0.00477326968973747, 'mean_word_length': 5.321608040201005, '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}}
Thyrotropin-releasing hormone causes excitation of rat hypoglossal motoneurons in vitro.

A brainstem slice preparation and conventional intracellular recording techniques were used to study the effects of the neuropeptide thyrotropin-releasing hormone (TRH) on adult rat hypoglossal motoneurons (HMs) in vitro. We found that TRH (0.1-10 microM) had two effects: 1) it caused depolarization of HMs and 2) decreased their input conductance. We tested the effects of TRH on HMs using a sinusoidal current injection paradigm to approximate the rhythmic activity of HMs in vivo. Waves of injected current that elicited only subthreshold behavior in control conditions caused repetitive firing in the presence of TRH. Compensating for the TRH-induced depolarization by hyperpolarizing direct current injection revealed the consequences of decreased input conductance in isolation. Under these conditions, the spike-firing of HMs at the peak of the sinusoid was still enhanced. In addition, the maximal hyperpolarization at the nadir of the current wave was also increased. This suggests that in the presence of TRH, the effects of both excitatory and inhibitory synaptic inputs on HMs are enhanced and the contrast between excitation and inhibition is sharpened.