Vulnerability of the thalamic somatosensory pathway after prolonged global hypoxic–ischemic injury
Section snippets
Experimental procedures
All procedures were carried out with the approval of the Institute Animal Care and Use Committee of Johns Hopkins University, Baltimore, MD, USA. The experiments were carried out in accordance with the National Institute of Health (NIH) guide for the care and use of laboratory animals (NIH publications No. 80-23) revised 1978. All efforts were made to minimize animal suffering and to use only the number of animals necessary to produce reliable scientific data, and to utilize alternatives to in
Multi-unit activity in thalamus
The number of VPL neurons recorded from each animal varied between one and six. The total number of VPL neurons recorded were 17 in G1 and 18 each in G2 and G3. The number and types of units recorded at the end of each experiment were generally different from those recorded during baseline due to changes in the shape of action potentials during the experiment.
The multi-unit responses to the somatosensory stimuli recorded from the VPL consisted typically of three components: the ON response (<30
Discussions
The overall goal of this study was to investigate the acute effects of graded ischemic injury on electrophysiological indicators of function in the cortical and thalamic structures along the somatosensory pathway. We have specifically tested for differential vulnerability between the electrical indicators of somatosensory cortical and thalamic functions. We have also used the direct electrical responses of the thalamic relay neurons to somatosensory stimulus as well as the accompanying spindle
Acknowledgements
Research supported by a Grant NS24282 from the NIH. R.G. was supported by the David S. Dana Research prize.
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Multimodal assessment of recovery from coma in a rat model of diffuse brainstem tegmentum injury
2019, NeuroImageCitation Excerpt :A transient coma can be caused by administration of neuro-toxins (Sonobe et al., 2015; Sonobe and Haouzi, 2015; Tamaoki et al., 2016), anesthetics (Abulafia et al., 2009; Devor and Zalkind, 2001), or cholinergic agonists (Katayama et al., 1986), but the induced coma state is brief (e.g. 5–10 min) (Sonobe and Haouzi, 2015), dose-dependent, and associated with high fatality rates. Hypoxic-ischemic brain injury models in rats (Shoykhet et al., 2012; Manole et al., 2014; Katz et al., 1995; Jia et al., 2006; Kawai et al., 1992; Geocadin et al., 2000; Muthuswamy et al., 2002; Liachenko et al., 1998) and dogs (Leonov et al., 1990) can trigger coma, but the global neuronal injury precludes identification of specific brainstem nuclei whose lesioning causes coma and the subcortical circuits that are critical to recovery. Animal models of severe traumatic brain injury (Xiong et al., 2013) provide an opportunity to study coma but involve multifocal lesions and multiple pathophysiological processes (e.g. contusions and axonal shearing).
Study of the origin of short- and long-latency SSEP during recovery from brain ischemia in a rat model
2010, Neuroscience LettersEvolution of somatosensory evoked potentials after cardiac arrest induced hypoxic-ischemic injury
2010, ResuscitationCitation Excerpt :This potential is referred to as the N10, given its approximate latency of 10 ms. This N10 potential likely represents signal from the primary somatosensory cortex triggered by afferent stimulation relayed through the thalamic VPL nucleus, equivalent to the human N20. Previous studies have demonstrated an initial cortical response between 7 and 13 ms latency in rats.5,14–16 The amplitude of N10 is normalized to the baseline signal recorded just prior to the initiation of the CA protocol.
Coma After Global Ischemic Brain Injury: Pathophysiology and Emerging Therapies
2008, Critical Care ClinicsCitation Excerpt :“Short-latency potentials” are then sequentially lost over the ensuing minutes, first involving the thalamic potentials, then brainstem potentials. After resuscitation, short-latency potentials (brainstem and thalamus) recover over the first hour, followed by restitution of baseline amplitude in the cortical potentials over several hours [85–87]. In adult humans, persistent loss of cortical potentials beyond 48 hours accurately predicts death or the VS.
Clinical neurophysiologic monitoring and brain injury from cardiac arrest
2006, Neurologic ClinicsCitation Excerpt :In a rat model of graded injury from cardiac arrest, animals were subjected to 3, 5, and 7 minutes of arrest [54]. At the onset of asphyxia, thalamic firing was characterized by an increasingly asynchronous pattern followed by loss of firing during a 15-second span [79]. The rhythmic spindle oscillations of the VPL neurons were replaced by increased tonic firing during the first 45 seconds of asphyxia, followed by VPL silence within 1 minute [79].