{'fraction_non_alphanumeric': 0.03606853020739405, 'fraction_numerical': 0.020739404869251576, 'mean_word_length': 5.7272727272727275, '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}}
Whole‐cell clamp analysis of the effects of the anti‐malarial drug, CHLOROQUINE, on several components of the action current in differentiated NG108‐15 cells

We examined the pharmacological effects of chloroquine (10 – 100μM) on NG 108‐15 cells, a cultured mouse neuroblastoma/rat glioma hybrid cell line, using the whole‐cell patch clamp technique. In current clamp recordings, chloroquine at concentrations above 50 μM reduced the peak amplitude of the action potential. The action potential was also prolonged in a concentration‐dependent manner. The resting membrane potential increased gradually as the concentration of chloroquine increased from 10 to 100 μM. Voltage‐clamp recordings revealed that the reductions in amplitude and increase in duration of the action potential were due to the block of several inward and outward membrane currents, including the sodium, the transient (T‐type) calcium, and the A‐type and the Ca2+‐activated potassium currents. In contrast, chloroquine did not affect the delayed rectifying potassium, the neuronal (N‐type) and the long‐lasting (L‐type) calcium channels.