| Background:Propofol, an emulsion formulation of 2,6 diisopropylphenol, is a rapid-onset and short-acting intravenous anesthetics and has been applied to clinic for several decades,the research on its interaction mechanisms is still under debate. It has proved that propofol could modulate GABAA receptor, but in the system level especially in the thalamocortical network, the contribution of GABAA receptor to propofol is uncertain. In this study, we examine the spontaneous activity and evoke potential, investigate the effect of antagonists/agonists of GABAA receptor to the activity, and analyze the contribution of GABAA receptor in thalamocortical network in response to propofol.Methods:The extracellular tungsten electrodes was slowly inserted into S1 for recording spontaneous local field potentials (sLFPs),whiskers-stimulation-evoked somatosensory evoked potentials (SEPs), and their change after local injection of GABAAreceptor blocker or agonist in thalamus or in S1. According to the injection site, the animals were divided into the VPM's group and the S1's group. Each group contains control group and the experiment group. The control group was microinjected saline; the experiment group was given bicuculline or muscimol. Whisker stimuli were executed by deflections of the optimal whisker on the contralateral face. Firstly record the spontaneous activities for 600s, then record the evoked activity for 1000s with stimulated the whisker every 4 s, the duration of stimulation was 50 ms. Anesthesia levels were modulated by the infusion rate of propofol administrated from tail vein. At each depth of anesthesia, spontaneous LFPs was band-pass-filtered toδ,θ,α,βandγfrequency bands; SEPs and peri-stimulus time histograms (PSTHs) were extracted and averaged from responses to whisker stimuli.Results:All the recordings of somatosensory activity were under propofol anesthesia:1.The spontaneous activity in S1 was weakened under propofol anesthesia, while the spontaneous activity of S1 were strengthen by given bicuculline in VPM and weakened by given muscimol; All powers of spontaneous activity in S1 were weakened, no mater microinjection of muscimol or bicuculline in S1.2. The amplitude of evoked potential of S1 was remarkably increased after local administration of bicuculline in VPM; otherwise, the amplitude decreased remarkably after microinjection of muscimol in S1; after microinjection of muscimol or bicuculline in S1, the amplitude of the evoked potential reduced significantly.3. Microinjection the bicuculline in VPM, the amplitude of Spontaneous spindle wave was instensified its frequency was slow; following muscimol, the amplitude was smaller, the spontaneous rhythms was disappear; eiyher microinjection bicuculline or muscimol in S1, the spindle wave amplitude was smaller, but the frequency was constant.Conclusions:The results showed:1. Propofol inhibits the spontaneous activity of S1:the bicuculline could reverse the effect, administration of bicuculline in VPM could completely reverse, but in S1, it could not; the muscimol could strengthen the inhibition of propofol, both given muscimol in the VPM or the S1, the activity of S1 was weakened. They implied propofol generate the inhibition to thalamocortical network by GABAA receptor in thalamus.2. The main action site of propofol induced suppression of thalamic somatosensory information transfer was thalamus,propofol strengthen the GABAergic inhibition may play an important role in the process.3. Spindle wave was originated in Thalamus, where local injection GABAA receptor antagonists could overturn the influence of the propofol to the rhythmic and the frequency of spindle wave. |
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