Direct Current Coupled Recordings of Cortical Spreading Depression Using Silicone Probes.

Electrophysiological assessment of infraslow (<0.1 Hz) brain activities such as cortical spreading depression (SD), which occurs in a number of pathologies including migraine, epilepsy, traumatic brain injury (TBI) and brain ischemia requires direct current (DC) coupled recordings of local field potentials (LFPs). Here, we describe how DC-coupled recordings can be performed using high-density iridium electrode arrays (silicone probes). We found that the DC voltage offset of the silicone probe is large and often exceeds the amplifier input range. Introduction of an offset compensation chain at the signal ground efficiently minimized the DC offsets. Silicone probe DC-coupled recordings across layers of the rat visual and barrel cortices revealed that epipial application of KCl, dura incision or pinprick TBI induced SD which preferentially propagated through the supragranular layers and further spread to the granular and infragranular layers attaining maximal amplitudes of ~-30 mV in the infragranular layers. SD at the superficial cortical layers was nearly two-fold longer than at the deep cortical layers. Continuous epipial KCl evoked multiple recurrent SDs which always started in the supragranular layers but often failed to propagate through the deeper cortical layers. Intracortical KCl injection into the infragranular layers evoked SD which also started in the supragranular layers and spread to the granular and infragranular layers, further indicating that the supragranular layers are particularly prone to SD. Thus, DC-coupled recordings with silicone probes after offset compensation can be successfully used to explore the spatial-temporal dynamics of SD and other slow brain activities.

Preferential Initiation and Spread of Anoxic Depolarization in Layer 4 of Rat Barrel Cortex.

Anoxic depolarization (AD) is a hallmark of ischemic brain damage. AD is associated with a spreading wave of neuronal depolarization and an increase in light transmittance. However, initiation and spread of AD across the layers of the somatosensory cortex, which is one of the most frequently affected brain regions in ischemic stroke, remains largely unknown. Here, we explored the initiation and propagation of AD in slices of the rat barrel cortex using extracellular local field potential (LFP) recordings and optical intrinsic signal (OIS) recordings. We found that ischemia-like conditions induced by oxygen-glucose deprivation (OGD) evoked AD, which manifested as a large negative LFP shift and an increase in light transmittance. AD typically initiated in one or more barrels and further spread across the entire slice with a preferential propagation through L4. Elevated extracellular potassium concentration accelerated the AD onset without affecting proneness of L4 to AD. In live slices, barrels were most heavily labeled by the metabolic level marker 2,3,5-triphenyltetrazolium chloride, suggesting that the highest metabolic demand is in L4 when compared to the other layers. Thus, L4 is the layer of the barrel cortex most prone to AD, which may be due to the highest metabolic demand and cell density in this layer.