Potential Network Mechanisms Mediating Electroencephalographic Beta Rhythm Changes during Propofol-Induced Paradoxical Excitation

• DOI: 10.1523/jneurosci.3536-08.2008
• Publication Date: 2008-12-11T01:57:03Z
• Authors: Michelle M. McCarthy; Emery N. Brown; Nancy Kopell
• Keywords: Beta Rhythm; BETA (programming language)

Propofol, like most general anesthetic drugs, can induce both behavioral and electroencephalographic (EEG) manifestations of excitation, rather than sedation, at low doses. Neuronal excitation is unexpected in the presence this GABA A -potentiating drug. We construct a series network models to understand paradox. Individual neurons have ion channel conductances with Hodgkin–Huxley-type formulations. Propofol increases maximal conductance time constant decay synaptic current. Networks range size from 2 230 neurons. Population output measured as function pyramidal cell activity, electroencephalogram approximated by sum population AMPA activity between cells. These model networks suggest propofol-induced paradoxical may result membrane level interaction current an intrinsic slow potassium (M-current). This has consequences multicellular enabling switch baseline interneuron synchrony antisynchrony. Large reproduce clinical EEG changes characteristic excitation. The coincide emergence antisynchronous clusters networks. Our findings antisynchrony potential mechanism underlying generation As correlates phenomenology, these refine our understanding specific states associated anesthesia.