scholarly journals Short- and long-latency somatosensory neuronal responses reveal selective brain injury and effect of hypothermia in global hypoxic ischemia

2012 ◽  
Vol 107 (4) ◽  
pp. 1164-1171 ◽  
Author(s):  
Dan Wu ◽  
Wei Xiong ◽  
Xiaofeng Jia ◽  
Romergryko G. Geocadin ◽  
Nitish V. Thakor
Keyword(s):  
Brain Injury ◽  
Somatosensory Cortex ◽  
Field Potential ◽  
Cortical Activity ◽  
Neuronal Responses ◽  
Early Recovery ◽  
Long Latency Responses ◽  
Long Latency ◽  
Hypoxic Ischemia ◽  
Somatosensory Neurons

Evoked potentials recorded from the somatosensory cortex have been shown to be an electrophysiological marker of brain injury in global hypoxic ischemia (HI). The evoked responses in somatosensory neurons carry information pertaining to signal from the ascending pathway in both the subcortical and cortical areas. In this study, origins of the subcortical and cortical signals are explored by decomposing the evoked neuronal activities into short- and long-latency responses (SLR and LLR), respectively. We evaluated the effect of therapeutic hypothermia on SLR and LLR during early recovery from cardiac arrest (CA)-induced HI in a rodent model. Twelve rats were subjected to CA, after which half of them were treated with hypothermia (32–34°C) and the rest were kept at normal temperature (36–37°C). Evoked neuronal activities from the primary somatosensory cortex, including multiunit activity (MUA) and local field potential (LFP), were continuously recorded during injury and early recovery. Results showed that upon initiation of injury, LLR disappeared first, followed by the disappearance of SLR, and after a period of isoelectric silence SLR reappeared prior to LLR. This suggests that cortical activity, which primarily underlies the LLR, may be more vulnerable to ischemic injury than SLR, which relates to subcortical activity. Hypothermia potentiated the SLR but suppressed the LLR by delaying its recovery after CA (hypothermia: 38.83 ± 5.86 min, normothermia: 23.33 ± 1.15 min; P < 0.05) and attenuating its amplitude, suggesting that hypothermia may selectively downregulate cortical activity as an approach to preserve the cerebral cortex. In summary, our study reveals the vulnerability of the somatosensory neural structures to global HI and the differential effects of hypothermia on these structures.

Developmental Regulation of Plasticity in the Forepaw Representation of Ferret Somatosensory Cortex

2003 ◽  
Vol 89 (4) ◽  
pp. 2289-2298 ◽  
Author(s):  
Debra F. McLaughlin ◽  
Sharon L. Juliano
Keyword(s):  
Spatial Distribution ◽  
Somatosensory Cortex ◽  
Ulnar Nerve ◽  
Cortical Activity ◽  
Cortical Response ◽  
Nerve Lesions ◽  
Long Latency ◽  
Cortical Responses ◽  
Layer 4 ◽  
Neonatal Lesions

This study characterized the spatiotemporal responses in ferret somatosensory cortex after sensory deprivation at different phases of cortical development. We hypothesized that cortical responses to stimulation of intact superficial radial nerve in adults will vary systematically according to maturation of thalamocortical relationships at the time of an ulnar nerve transection. Depending on the age of the animal at the time of the lesion, we found differential effects on the spatial distribution of the short- and long-latency components of the cortical response. In animals lesioned at postnatal days 5–7, when thalamic projections are not yet stabilized and layer 4 is not yet formed, we found that initial (short-latency) cortical responses are widespread and fragmented. Ulnar nerve transections performed at postnatal day 20 or 21, when thalamocortical afferents are more stabilized and layer 4 is clearly identifiable, yield moderate expansions in the distribution of short- and long-latency components of the cortical response. Nerve lesions in adults lead to a wider distribution of long-latency cortical activity. Neonatal lesions broaden the spatial distribution and increase the latency of the initial cortical response; interruption of nerve input in older juveniles alters both the early and later components; and nerve lesions in adult animals expand the distribution of later cortical activity only. These findings demonstrate correlation between developmental phase at the time sensory input is interrupted and the latency of affected components of the cortical response. This supports the hypothesis that differential response changes are regulated by functional reorganization of thalamocortical connections after neonatal lesions and alteration of corticocortical dynamics after adult lesions.

Early recovery following traumatic brain injury and alcohol withdrawal management.

2018 ◽  
Vol 63 (4) ◽  
pp. 588-594
Author(s):  
Daniel W. Klyce ◽  
Kristin M. Graham ◽  
Russell W. Lacey ◽  
William E. Carter
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Alcohol Withdrawal ◽  
Early Recovery ◽  
Withdrawal Management

Human cortical potentials evoked by stimulation of the median nerve. II. Cytoarchitectonic areas generating long-latency activity

1989 ◽  
Vol 62 (3) ◽  
pp. 711-722 ◽  
Author(s):  
T. Allison ◽  
G. McCarthy ◽  
C. C. Wood ◽  
P. D. Williamson ◽  
D. D. Spencer
Keyword(s):  
Spatial Distribution ◽  
Median Nerve ◽  
Somatosensory Cortex ◽  
Sensorimotor Cortex ◽  
Preceding Paper ◽  
Short Latency ◽  
Cortical Surface ◽  
Long Latency ◽  
Area 3B ◽  
Stimulation Of

1. The anatomic generators of human median nerve somatosensory evoked potentials (SEPs) in the 40 to 250-ms latency range were investigated in 54 patients by means of cortical-surface and transcortical recordings obtained during neurosurgery. 2. Contralateral stimulation evoked three groups of SEPs recorded from the hand representation area of sensorimotor cortex: P45-N80-P180, recorded anterior to the central sulcus (CS) and maximal on the precentral gyrus; N45-P80-N180, recorded posterior to the CS and maximal on the postcentral gyrus; and P50-N90-P190, recorded near and on either side of the CS. 3. P45-N80-P180 inverted in polarity to N45-P80-N180 across the CS but was similar in polarity from the cortical surface and white matter in transcortical recordings. These spatial distributions were similar to those of the short-latency P20-N30 and N20-P30 potentials described in the preceding paper, suggesting that these long-latency potentials are generated in area 3b of somatosensory cortex. 4. P50-N90-P190 was largest over the anterior one-half of somatosensory cortex and did not show polarity inversion across the CS. This spatial distribution was similar to that of the short-latency P25-N35 potentials described in the preceding paper and, together with our and Goldring et al. 1970; Stohr and Goldring 1969 transcortical recordings, suggest that these long-latency potentials are generated in area 1 of somatosensory cortex. 5. SEPs of apparently local origin were recorded from several regions of sensorimotor cortex to stimulation of the ipsilateral median nerve. Surface and transcortical recordings suggest that the ipsilateral potentials are generated not in area 3b, but rather in other regions of sensorimotor cortex perhaps including areas 4, 1, 2, and 7. This spatial distribution suggests that the ipsilateral potentials are generated by transcallosal input from the contralateral hemisphere. 6. Recordings from the periSylvian region were characterized by P100 and N100, recorded above and below the Sylvian sulcus (SS) respectively. This distribution suggests a tangential generator located in the upper wall of the SS in the second somatosensory area (SII). In addition, N125 and P200, recorded near and on either side of the SS, suggest a radial generator in a portion of SII located in surface cortex above the SS. 7. In comparison with the short-latency SEPs described in the preceding paper, the long-latency potentials were more variable and were more affected by intraoperative conditions.

scholarly journals A zebrafish and mouse model for selective pruritus via direct activation of TRPA1

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Kali Esancy ◽  
Logan Condon ◽  
Jing Feng ◽  
Corinna Kimball ◽  
Andrew Curtright ◽  
...  
Keyword(s):  
Mouse Model ◽  
Allyl Isothiocyanate ◽  
Neuronal Responses ◽  
Zebrafish Larvae ◽  
Direct Activation ◽  
Neuron Response ◽  
Tlr7 Agonist ◽  
Lower Vertebrates ◽  
Somatosensory Neurons ◽  
Noxious Stimuli

Little is known about the capacity of lower vertebrates to experience itch. A screen of itch-inducing compounds (pruritogens) in zebrafish larvae yielded a single pruritogen, the TLR7 agonist imiquimod, that elicited a somatosensory neuron response. Imiquimod induced itch-like behaviors in zebrafish distinct from those induced by the noxious TRPA1 agonist, allyl isothiocyanate. In the zebrafish, imiquimod-evoked somatosensory neuronal responses and behaviors were entirely dependent upon TRPA1, while in the mouse TRPA1 was required for the direct activation of somatosensory neurons and partially responsible for behaviors elicited by this pruritogen. Imiquimod was found to be a direct but weak TRPA1 agonist that activated a subset of TRPA1 expressing neurons. Imiquimod-responsive TRPA1 expressing neurons were significantly more sensitive to noxious stimuli than other TRPA1 expressing neurons. Together, these results suggest a model for selective itch via activation of a specialized subpopulation of somatosensory neurons with a heightened sensitivity to noxious stimuli.

scholarly journals Cholinergic upregulation by optogenetic stimulation of nucleus basalis after photothrombotic stroke in forelimb somatosensory cortex improves endpoint and motor but not sensory control of skilled reaching in mice

2020 ◽  
Author(s):  
Behroo Mirza Agha ◽  
Roya Akbary ◽  
Arashk Ghasroddashti ◽  
Mojtaba Nazari-Ahangarkolaee ◽  
Ian Q. Whishaw ◽  
...  
Keyword(s):  
Somatosensory Cortex ◽  
Sensorimotor Integration ◽  
Motor Behavior ◽  
Field Potential ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Optogenetic Stimulation ◽  
Photothrombotic Stroke ◽  
Skilled Reaching ◽  
Stimulation Of

AbstractA network of cholinergic neurons in the basal forebrain innerve the forebrain and are proposed to contribute to a variety of functions including attention, and cortical plasticity. This study examined the contribution of the nucleus basalis cholinergic projection to the sensorimotor cortex on recovery on a skilled reach-to-eat task following photothrombotic stroke in the forelimb region of the somatosensory cortex. Mice were trained to perform a single-pellet skilled reaching task and their pre and poststroke performance, from Day 4 to Day 28 poststroke, was assessed frame-by-frame by video analysis with end point, movement and sensorimotor integration measures. Somatosensory forelimb lesions produced impairments in endpoint and movement component measures of reaching and increased the incidence of fictive eating, a sensory impairment in mistaking a missed reach for a successful reach. Upregulated acetylcholine (ACh) release, as measured by local field potential recording, elicited via optogenetic stimulation of the nucleus basalis improved recovery of reaching and improved movement scores but did not affect a sensorimotor integration impairment poststroke. The results show that the mouse cortical forelimb somatosensory region contributes to forelimb motor behavior and suggest that ACh upregulation could serve as an adjunct to behavioral therapy for the acute treatment of stroke.

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