{'fraction_non_alphanumeric': 0.05400229797012639, 'fraction_numerical': 0.00995787054768288, 'mean_word_length': 5.309178743961352, '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}}
Role of apamin-sensitive k(ca) channels for reticulospinal synaptic transmission to motoneuron and for the afterhyperpolarization.

Single motoneurons and pairs of a presynaptic reticulospinal axon and a postsynaptic motoneuron were recorded in the isolated lamprey spinal cord, to investigate the role of calcium-dependent K(+) channels (K(Ca)) during the afterhyperpolarization following the action potential (AHP), and glutamatergic synaptic transmission on the dendritic level. The AHP consists of a fast phase due to transient K(+) channels (fAHP) and a slower phase lasting 100-200 ms (sAHP), being the main determinant of spike frequency regulation. We now present evidence that the sAHP has two components. The larger part, around 80%, is abolished by superfusion of Cd(2+) (blocker of voltage-dependent Ca(2+) channels), by intracellular injection of 1,2-bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA; fast Ca(2+) chelator), and by apamin (selective toxin for K(Ca) channels of the SK subtype). While 80% of the sAHP is thus due to K(Ca) channels, the remaining 20% is not mediated by Ca(2+), either entering through voltage-dependent Ca(2+) channels or released from intracellular Ca(2+) stores. This Ca(2+)-independent sAHP component has a similar time course as the K(Ca) portion and is not due to a Cl(-) conductance. It may be caused by Na(+)-activated K(+) channels. Glutamatergic excitatory postsynaptic potentials (EPSPs) evoked by single reticulospinal axons give rise to a local Ca(2+) increase in the postsynaptic dendrite, mediated in part by N-methyl-D-aspartate (NMDA) receptors. The Ca(2+) levels remain elevated for several hundred milliseconds and could be expected to activate K(Ca) channels. If so, this activation should cause a local conductance increase in the dendrite that would shunt EPSPs following the first EPSP in a spike train. We have tested this in reticulospinal/motoneuronal pairs, by stimulating the presynaptic axon with spike trains at different frequencies. We compared the first EPSP and the following EPSPs in the control and after blockade with apamin. No difference was observed in EPSP amplitude or shape before and after apamin, either in normal Ringer or in Mg(2+)-free Ringer removing the voltage-dependent block of NMDA receptors. In conclusion, the local Ca(2+) entry during reticulospinal EPSPs does not cause an activation of K(Ca) channels sufficient to affect the efficacy of synaptic transmission. Thus the integration of synaptic signals at the dendritic level in motoneurons appears simpler than would otherwise have been the case.