RESUMO
Human scalp-derived somatosensory evoked potentials contain a high-frequency wavelet burst, presumably reflecting repetitive synchronized population spikes. Here, the burst refractory behavior was characterized using median nerve electrostimulation with 18 frequencies (0.5-25Hz) for comparison with cellular burst characteristics. Above 10 Hz only a brief high-frequency (700 Hz) burst component remained discernible, which gradually decreased; possible generators comprise cells capable of generating spike bursts of extraordinarily high frequency, such as pyramidal 'chattering cells', cortical fast spiking inhibitory interneurons and some thalamocortical relay cells. At stimulation frequencies <4 Hz an additional late burst component appeared with only 494 Hz intraburst frequency. Comparably long refractory periods and low intraburst frequencies have been described for bursting cells driven by low-threshold calcium currents.
Assuntos
Potenciais Somatossensoriais Evocados/fisiologia , Potenciais de Ação/fisiologia , Adulto , Estimulação Elétrica , Feminino , Humanos , Masculino , Nervo Mediano/fisiologia , Nervo Radial/fisiologia , Período Refratário Eletrofisiológico/fisiologiaRESUMO
Human median nerve somatosensory evoked potentials contain a burst of high-frequency (600 Hz) wavelets superimposed on the primary cortical response (N20). These presumably reflect highly-synchronized repetitive thalamic and/or intracortical population spike bursts and are diminished in non-REM sleep with N20 persisting. Here the burst/N20 relation in awake subjects was examined by using eight different intensities of electric median nerve stimuli. In all subjects the amplitude recruitment of both N20 and burst could be modeled adequately as a sigmoidal function of stimulus intensity. While 8/10 subjects showed a parallel recruitment, 2/10 subjects required significantly higher stimulation intensities for burst than for N20 recruitment. This dampened burst recruitment possibly reflects slight vigilance fluctuations in open-eyed awake subjects; a further increase of burst thresholds could explain the burst attenuation when entering shallow sleep.