Biomedical subjects
Publications and source records attributed to G L Tribble.
We describe a circuit that compensates for a slowly drifting baseline without distorting the signal of interest. Implementation of this non-linear filter is quite simple; total cost of components is less than $20.00. The baseline stabilizer should be especially useful for intracellular recording and for recording evoked surface potentials.
The reduction of postsynaptic inhibition tolerated before initiation of intrinsic spinal seizures was assessed using intracellular recording from lumbar motoneurons in spinal cats anesthetized by pentobarbital or alpha-chloralose or decerebrated and unanesthetized. The amplitude of antagonist group Ia and recurrent (Renshaw) IPSPs was monitored while incremental doses of the specific glycine antagonist, strychnine, were injected until seizures developed. Both kinds of IPSPs were reduced to less than 25% of control at seizure onset, independent of anesthesia. Assuming the recorded pathways were representative of all glycine-mediated spinal pathways, the results suggested that postsynaptic inhibition could be virtually eliminated before intrinsic spinal seizures were triggered. These results place a constraint on theories of spinal seizures initiation due to reduction of postsynaptic inhibition.
The reduction of GABA-mediated postsynaptic inhibition tolerated before seizure initiation was assessed using the GABA-mediated, disynaptic, inhibitory pathway from the ipsilateral vestibular nerve to trochlear motoneurons in pentobarbital-anesthetized cats. The amplitude of intracellularly recorded IPSPs or the corresponding extracellular field potential was monitored while incremental doses of the specific GABA antagonist, bicuculline, were injected intravenously. Cortical seizures (measured by ECoG activity) and spontaneous trochlear motoneuron bursting occurred at bicuculline doses which reduced inhibitory vestibular-trochlear field potentials by 10% or less. After midbrain transection trochlear motoneurons no longer participated in the cortical seizures. Rather, a widespread, paroxysmal increase of intrinsic brain stem activity, including motoneuron bursting, occurred after injection of additional bicuculline sufficient to reduce the vestibular-trochlear inhibition to 25% of control or less. Thus, postsynaptic inhibition could be virtually eliminated before intrinsic brain stem seizures were triggered, but the brain stem could participate in cortical seizures in spite of the integrity of inhibitory brain stem pathways. Because the cortex seized when inhibitory potentials were only slightly reduced in the brain stem, we suggest that factors such as different GABA receptor properties or altered membrane properties may contribute to the greater sensitivity of cortex to bicuculline.
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