scholarly journals Dissociation of slow waves and fast oscillations above 200 Hz during GABA application in rat somatosensory cortex

2004 ◽  
Vol 561 (1) ◽  
pp. 205-214 ◽  
Author(s):  
Richard J. Staba ◽  
Peter C. Bergmann ◽  
Daniel S. Barth
Keyword(s):  
Somatosensory Cortex ◽  
Slow Waves ◽  
Rat Somatosensory Cortex ◽  
Fast Oscillations

Effects of Ventrobasal Lesion and Cortical Cooling on Fast Oscillations (>200 Hz) in Rat Somatosensory Cortex

2003 ◽  
Vol 89 (5) ◽  
pp. 2380-2388 ◽  
Author(s):  
Richard J. Staba ◽  
Barbara Brett-Green ◽  
Marcy Paulsen ◽  
Daniel S. Barth
Keyword(s):  
Somatosensory Cortex ◽  
Oscillatory Activity ◽  
Electrode Arrays ◽  
Subcortical Structures ◽  
Ventrobasal Thalamus ◽  
Before And After ◽  
Cortical Cooling ◽  
Rat Somatosensory Cortex ◽  
Fast Oscillations

High-frequency oscillatory activity (>200 Hz) termed “fast oscillations” (FO) have been recorded in the rodent somatosensory cortex and may reflect very rapid integration of vibrissal information in sensory cortex. Yet, while electrophysiological correlates suggest that FO is generated within intracortical networks, contributions of subcortical structures along the trigeminal pathway remain uncertain. Using surface and laminar electrode arrays, in vivo recordings of vibrissal and electrically evoked FO were made within somatosensory cortex of anesthetized rodents before and after ablation of the ventrobasal thalamus (VB) or during reversible cortical cooling. In VB-lesioned animals, vibrissal stimulation failed to evoke FO, while epicortical stimulation in lesioned animals remained effective in generating FO. In nonlesioned animals, cortical cooling eliminated vibrissal-evoked FO despite the persistence of thalamocortical input. Vibrissal-evoked FO returned with the return to physiological temperatures. Results from this study indicate that somatosensory cortex alone is able to initiate and sustain FO. Moreover, these data suggest that cortical network interactions are solely responsible for the generation of FO, while synchronized thalamocortical input serves as the afferent trigger.

Intracellular Correlates of Fast (>200 Hz) Electrical Oscillations in Rat Somatosensory Cortex

2000 ◽  
Vol 84 (3) ◽  
pp. 1505-1518 ◽  
Author(s):  
Michael S. Jones ◽  
Kurt D. MacDonald ◽  
ByungJu Choi ◽  
F. Edward Dudek ◽  
Daniel S. Barth
Keyword(s):  
Action Potential ◽  
Somatosensory Cortex ◽  
Field Potential ◽  
Oscillatory Activity ◽  
Cellular Events ◽  
Recurrent Activity ◽  
Potential Recording ◽  
Rat Somatosensory Cortex ◽  
Fast Oscillations

Oscillatory activity in excess of several hundred hertz has been observed in somatosensory evoked potentials (SEP) recorded in both humans and animals and is attracting increasing interest regarding its role in brain function. Currently, however, little is known about the cellular events underlying these oscillations. The present study employed simultaneous in-vivo intracellular and epipial field-potential recording to investigate the cellular correlates of fast oscillations in rat somatosensory cortex evoked by vibrissa stimulation. Two distinct types of fast oscillations were observed, here termed “fast oscillations” (FO) (200–400 Hz) and “very fast oscillations” (VFO) (400–600 Hz). FO coincided with the earliest slow-wave components of the SEP whereas VFO typically were later and of smaller amplitude. Regular spiking (RS) cells exhibited vibrissa-evoked responses associated with one or both types of fast oscillations and consisted of combinations of spike and/or subthreshold events that, when superimposed across trials, clustered at latencies separated by successive cycles of FO or VFO activity, or a combination of both. Fast spiking (FS) cells responded to vibrissae stimulation with bursts of action potentials that closely approximated the periodicity of the surface VFO. No cells were encountered that produced action potential bursts related to FO activity in an analogous fashion. We propose that fast oscillations define preferred latencies for action potential generation in cortical RS cells, with VFO generated by inhibitory interneurons and FO reflecting both sequential and recurrent activity of stations in the cortical lamina.

Effects of Bicuculline Methiodide on Fast (>200 Hz) Electrical Oscillations in Rat Somatosensory Cortex

2002 ◽  
Vol 88 (2) ◽  
pp. 1016-1025 ◽  
Author(s):  
Michael S. Jones ◽  
Daniel S. Barth
Keyword(s):  
Somatosensory Cortex ◽  
Pyramidal Cells ◽  
Oscillatory Activity ◽  
Spontaneous Discharge ◽  
Normal Brain ◽  
Bicuculline Methiodide ◽  
Epileptiform Discharges ◽  
Fast Activity ◽  
Rat Somatosensory Cortex ◽  
Fast Oscillations

Fast oscillatory activity (more than ∼200 Hz) has been attracting increasing attention regarding its possible role in both normal brain function and epileptogenesis. Yet, its underlying cellular mechanism remains poorly understood. Our prior investigation of the phenomenon in rat somatosensory cortex indicated that fast oscillations result from repetitive synaptic activation of cortical pyramidal cells originating from GABAergic interneurons ( Jones et al. 2000 ). To test this hypothesis, the effects of topical application of the γ-aminobutyric acid-A (GABAA) antagonist bicuculline methiodide (BMI) on fast oscillations were examined. At subconvulsive concentrations (∼10 μM), BMI application resulted in a pronounced enhancement of fast activity, in some trials doubling the number of oscillatory cycles evoked by whisker stimulation. The amplitude and frequency of fast activity were not affected by BMI in a statistically significant fashion. At higher concentrations, BMI application resulted in the emergence of recurring spontaneous slow-wave discharges resembling interictal spikes (IIS) and the eventual onset of seizure. High-pass filtering of the IIS revealed that a burst of fast oscillations accompanied the spontaneous discharge. This activity was present in both the pre- and the postictal regimes, in which its morphology and spatial distribution were largely indistinguishable. These data indicate that fast cortical oscillations do not reflect GABAergic postsynaptic currents. An alternate account consistent with results observed to date is that this activity may instead arise from population spiking in pyramidal cells, possibly mediated by electrotonic coupling in a manner analogous to that underlying 200-Hz ripple in the hippocampus. Additionally, fast oscillations occur within spontaneous epileptiform discharges. However, at least under the present experimental conditions, they do not appear to be a reliable predictor of seizure onset nor an indicator of the seizure focus.

Fractal properties of neurophysiologic signals in rat somatosensory cortex

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S186-S186
Author(s):  
Peter Herman ◽  
Shaun A Wahab ◽  
Andras Eke ◽  
Fahmeed Hyder
Keyword(s):  
Somatosensory Cortex ◽  
Fractal Properties ◽  
Rat Somatosensory Cortex

Removal of a compressive mass causes a transient disruption of blood-brain barrier but a long-term recovery of spiny stellate neurons in the rat somatosensory cortex

2021 ◽  
pp. 1-17
Author(s):  
Tzu-Yin Yeh ◽  
Pei-Hsin Liu
Keyword(s):  
Somatosensory Cortex ◽  
Blood Brain Barrier ◽  
Dendritic Spines ◽  
Late Onset ◽  
Brain Barrier ◽  
Blood Brain ◽  
Afferent Fibers ◽  
Prolonged Recovery ◽  
Rat Somatosensory Cortex

Background: In the cranial cavity, a space-occupying mass such as epidural hematoma usually leads to compression of brain. Removal of a large compressive mass under the cranial vault is critical to the patients. Objective: The purpose of this study was to examine whether and to what extent epidural decompression of the rat primary somatosensory cortex affects the underlying microvessels, spiny stellate neurons and their afferent fibers. Methods: Rats received epidural decompression with preceding 1-week compression by implantation of a bead. The thickness of cortex was measured using brain coronal sections. The permeability of blood-brain barrier (BBB) was assessed by Evans Blue and immunoglobulin G extravasation. The dendrites and dendritic spines of the spiny stellate neurons were revealed by Golgi— Cox staining and analyzed. In addition, the thalamocortical afferent (TCA) fibers in the cortex were illustrated using anterograde tracing and examined. Results: The cortex gradually regained its thickness over time and became comparable to the sham group at 3 days after decompression. Although the diameter of cortical microvessels were unaltered, a transient disruption of the BBB was observed at 6 hours and 1 day after decompression. Nevertheless, no brain edema was detected. In contrast, the dendrites and dendritic spines of the spiny stellate neurons and the TCA fibers were markedly restored from 2 weeks to 3 months after decompression. Conclusions: Epidural decompression caused a breakdown of the BBB, which was early-occurring and short-lasting. In contrast, epidural decompression facilitated a late-onset and prolonged recovery of the spiny stellate neurons and their afferent fibers.

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