Instructed Delay Discharge in Primary and Secondary Somatosensory Cortex Within the Context of a Selective Attention Task

2009 ◽  
Vol 101 (5) ◽  
pp. 2649-2667 ◽  
Author(s):  
El-Mehdi Meftah ◽  
Stéphanie Bourgeon ◽  
C. Elaine Chapman
Keyword(s):  
Somatosensory Cortex ◽  
Recent Observation ◽  
Discharge Rate ◽  
Initial Response ◽  
Common Source ◽  
Attention Task ◽  
Secondary Somatosensory Cortex ◽  
Neuronal Mechanisms ◽  
Underlying Mechanisms ◽  
Cortical Regions

The neuronal mechanisms that contribute to tactile perception were studied using single-unit recordings from the cutaneous hand representation of primate primary (S1) and secondary (S2) somatosensory cortex. This study followed up on our recent observation that S1 and S2 neurons developed a sustained change in discharge during the instruction period of a directed-attention task. We determined the extent to which the symbolic light cues, which signaled the modality (tactile, visual) to attend and discriminate, elicited changes in discharge rate during the instructed delay (ID) period of the attention task and the functional importance of this discharge. ID responses, consisting of a sustained increase or decrease in discharge during the 2-s instruction period, were present in about 40% of the neurons in S1 and S2. ID responses in both cortical regions were very similar in most respects (frequency, sign, latency, amplitude), suggesting a common source. A major difference, however, was related to attentional modulation during the ID period: attentional influences were almost entirely restricted to S2 and these effects were always superimposed on the ID response (additive effect). These findings suggest that the underlying mechanisms for ID discharge and attention are independent. ID discharge significantly modified the initial response to the standard stimuli (competing texture and visual stimuli), usually enhancing responsiveness. We also showed that tactile detection in humans is enhanced during the ID period. Together, the results suggest that ID discharge represents a priming mechanism that prepares cortical areas to receive and process sensory inputs.

scholarly journals The neuropsychology of face perception: beyond simple dissociations and functional selectivity

2011 ◽  
Vol 366 (1571) ◽  
pp. 1726-1738 ◽  
Author(s):  
Anthony P. Atkinson ◽  
Ralph Adolphs
Keyword(s):  
Somatosensory Cortex ◽  
Face Perception ◽  
Face Processing ◽  
Common Source ◽  
Subcortical Structures ◽  
Face Area ◽  
Face Categorization ◽  
Face Stimuli ◽  
Cortical Regions ◽  
Visual Cortical

Face processing relies on a distributed, patchy network of cortical regions in the temporal and frontal lobes that respond disproportionately to face stimuli, other cortical regions that are not even primarily visual (such as somatosensory cortex), and subcortical structures such as the amygdala. Higher-level face perception abilities, such as judging identity, emotion and trustworthiness, appear to rely on an intact face-processing network that includes the occipital face area (OFA), whereas lower-level face categorization abilities, such as discriminating faces from objects, can be achieved without OFA, perhaps via the direct connections to the fusiform face area (FFA) from several extrastriate cortical areas. Some lesion, transcranial magnetic stimulation (TMS) and functional magnetic resonance imaging (fMRI) findings argue against a strict feed-forward hierarchical model of face perception, in which the OFA is the principal and common source of input for other visual and non-visual cortical regions involved in face perception, including the FFA, face-selective superior temporal sulcus and somatosensory cortex. Instead, these findings point to a more interactive model in which higher-level face perception abilities depend on the interplay between several functionally and anatomically distinct neural regions. Furthermore, the nature of these interactions may depend on the particular demands of the task. We review the lesion and TMS literature on this topic and highlight the dynamic and distributed nature of face processing.

scholarly journals Descending antinociception induced by secondary somatosensory cortex stimulation in experimental neuropathy: role of the medullospinal serotonergic pathway

2017 ◽  
Vol 117 (3) ◽  
pp. 1200-1214 ◽  
Author(s):  
Boriss Sagalajev ◽  
Hanna Viisanen ◽  
Hong Wei ◽  
Antti Pertovaara
Keyword(s):  
Somatosensory Cortex ◽  
Receptor Agonist ◽  
Dynamic Range ◽  
Antinociceptive Effect ◽  
Spinal Nerve ◽  
Spinal Nerve Ligation ◽  
Secondary Somatosensory Cortex ◽  
Underlying Mechanisms ◽  
Wdr Neurons ◽  
Stimulation Of

Stimulation of the secondary somatosensory cortex (S2) has attenuated pain in humans and inflammatory nociception in animals. Here we studied S2 stimulation-induced antinociception and its underlying mechanisms in an experimental animal model of neuropathy induced by spinal nerve ligation (SNL). Effect of S2 stimulation on heat-evoked limb withdrawal latency was assessed in lightly anesthetized rats that were divided into three groups based on prior surgery and monofilament testing before induction of anesthesia: 1) sham-operated group and 2) hypersensitive and 3) nonhypersensitive (mechanically) SNL groups. In a group of hypersensitive SNL animals, a 5-HT1A receptor agonist was microinjected into the rostroventromedial medulla (RVM) to assess whether autoinhibition of serotonergic cell bodies blocks antinociception. Additionally, effect of S2 stimulation on pronociceptive ON-cells and antinociceptive OFF-cells in the RVM or nociceptive spinal wide dynamic range (WDR) neurons were assessed in anesthetized hypersensitive SNL animals. S2 stimulation induced antinociception in hypersensitive but not in nonhypersensitive SNL or sham-operated animals. Antinociception was prevented by a 5-HT1A receptor agonist in the RVM. Antinociception was associated with decreased duration of heat-evoked response in RVM ON-cells. In spinal WDR neurons, heat-evoked discharge was delayed by S2 stimulation, and this antinociceptive effect was prevented by blocking spinal 5-HT1A receptors. The results indicate that S2 stimulation suppresses nociception in SNL animals if SNL is associated with tactile allodynia-like hypersensitivity. In hypersensitive SNL animals, S2 stimulation induces antinociception mediated by medullospinal serotonergic pathways acting on the spinal 5-HT1A receptor, and partly through reduction of the RVM ON-cell discharge. NEW & NOTEWORTHY Stimulation of S2 cortex, but not that of an adjacent cortical area, induced descending heat antinociception in rats with the spinal nerve ligation-induced model of neuropathy. Antinociception was bilateral, and it involved suppression of pronociceptive medullary cells and activation of serotonergic pathways that act on the spinal 5-HT1A receptor. S2 stimulation failed to induce descending antinociceptive effect in sham-operated controls or in nerve-ligated animals that had not developed mechanical hypersensitivity.

Propofol Anesthesia and Cerebral Blood Flow Changes Elicited by Vibrotactile Stimulation: A Positron Emission Tomography Study

2001 ◽  
Vol 85 (3) ◽  
pp. 1299-1308 ◽  
Author(s):  
V. Bonhomme ◽  
P. Fiset ◽  
P. Meuret ◽  
S. Backman ◽  
G. Plourde ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Somatosensory Cortex ◽  
Emission Tomography ◽  
Vibrotactile Stimulation ◽  
Secondary Somatosensory Cortex ◽  
Positron Emission ◽  
Level 3 ◽  
Level 1 ◽  
Cortical Regions ◽  
Level 2

We investigated the effects of the general anesthetic agent propofol on cerebral structures involved in the processing of vibrotactile information. Using positron emission tomography (PET) and the H2 15O bolus technique, we measured regional distribution of cerebral blood flow (CBF) in eight healthy human volunteers. They were scanned under five different levels of propofol anesthesia. Using a computer-controlled infusion, the following plasma levels of propofol were targeted: Level W (Waking, 0 μg/ml), Level 1 (0.5 μg/ml), Level 2 (1.5 μg/ml), Level 3 (3.5 μg/ml), and Level R (Recovery). At each level of anesthesia, two 3-min scans were acquired with vibrotactile stimulation of the right forearm either on or off. The level of consciousness was evaluated before each scan by the response of the subject to a verbal command. At Level W, all volunteers were fully awake. They reported being slightly drowsy at Level 1, they had a slurred speech and slow response at Level 2, and they were not responding at all at Level 3. The following variations in regional CBF (rCBF) were observed. During the waking state (Level W), vibrotactile stimulation induced a significant rCBF increase in the left thalamus and in several cortical regions, including the left primary somatosensory cortex and the left and right secondary somatosensory cortex. During anesthesia, propofol reduced in a dose-dependent manner rCBF in the thalamus as well as in a number of visual, parietal, and prefrontal cortical regions. At Level 1 through 3, propofol also suppressed vibration-induced increases in rCBF in the primary and secondary somatosensory cortex, whereas the thalamic rCBF response was abolished only at Level 3, when volunteers lost consciousness. We conclude that propofol interferes with the processing of vibrotactile information first at the level of the cortex before attenuating its transfer through the thalamus.

Independent Controls of Attentional Influences in Primary and Secondary Somatosensory Cortex

2005 ◽  
Vol 94 (6) ◽  
pp. 4094-4107 ◽  
Author(s):  
C. Elaine Chapman ◽  
El-Mehdi Meftah
Keyword(s):  
Somatosensory Cortex ◽  
Neuronal Responses ◽  
Directed Attention ◽  
Cell Discharge ◽  
Secondary Somatosensory Cortex ◽  
Tactile Stimuli ◽  
Neuronal Mechanisms ◽  
Additive Increase ◽  
Single Unit Recordings ◽  
Marked Suppression

The neuronal mechanisms underlying enhanced perception of tactile stimuli with directed attention were investigated using single-unit recordings from primary (S1, n = 53) and secondary (S2, n = 50) somatosensory cortex in macaque monkeys. Neuronal responses to textures scanned under the digit tips (spatial periods, SP, of 2, 3.7 or 4.7 mm) were recorded while attention was directed either to discriminating a change in texture or to the reward and also in a neutral no-task condition. Cell discharge was quantified in three periods of the trials: salient Δ texture (directed attention), postreward, and static (both cases, attention directed to the reward). S1 texture- and non-texture-sensitive cells, as well as S2 non-texture-sensitive cells, showed a modest enhancement of discharge during the salient Δ texture period (∼25%) but no change in response gain, consistent with an additive increase in neuronal responsiveness with directed attention. In contrast, S2 texture-related cells showed a larger enhancement with directed attention to salient inputs (82%) and increased response gain, suggesting that directed attention produces a multiplicative increase in S2 responsiveness. During the postreward period, and also in no-task testing, S1 texture-sensitive cells preserved their sensitivity to SP. In contrast, S2 texture-, but not non-texture-, sensitive cells showed a marked suppression of discharge and decreased gain after the discrimination response. Together, the results support the notion that S2 discharge reflects stimulus parameters in relation to ongoing behavioral demands. The results also support the existence of two independent attentional mechanisms in somatosensory cortex, one generalized (S1 and S2), and the other focused on S2 texture-related cells.

Adaptation to hypercapnia vs. intracellular pH in cat carotid body: responses in vitro

1996 ◽  
Vol 80 (4) ◽  
pp. 1090-1099 ◽  
Author(s):  
S. Lahiri ◽  
R. Iturriaga ◽  
A. Mokashi ◽  
F. Botre ◽  
D. Chugh ◽  
...  
Keyword(s):  
Steady State ◽  
Intracellular Ph ◽  
Baseline Level ◽  
Discharge Rate ◽  
Initial Response ◽  
Extracellular Ph ◽  
Carotid Bodies ◽  
Initial Peak ◽  
Initial Change

The hypotheses that the chemosensory discharge rate parallels the intracellular pH (pHi) during hypercapnia and that the initial change in pHi (delta pHi) is always more than the stead-state delta pHi were studied by using cat carotid bodies in vitro at 36.5 degrees C in the absence and presence of methazolamide (30-100 mg/l). Incremental acidic hypercapnia was followed by an incremental initial peak response and a greater adaptation. A given acidic hypercapnia elicited a rapid initial response followed by a slower adaptation; isohydric hypercapnia produced an equally rapid initial response but of smaller magnitude that returned to near-baseline level; alkaline hypercapnia induced a similar rapid initial response but one of still smaller magnitude that decreased rapidly to below the baseline. Methazolamide eliminated the initial overshoot, which also suggested involvement of the initial rapid pHi in the overshoot. These results show that the initial delta pHi is always greater than the steady-state delta pHi and during hypercapnia. Also, the steady-state chemoreceptor activity varied linearly with the extracellular pH, indicating a linear relationship between extracellular pH and pHi.

scholarly journals A supragranular nexus for the effects of neocortical beta events on human tactile perception

2019 ◽  
Author(s):  
Robert G. Law ◽  
Sarah Pugliese ◽  
Hyeyoung Shin ◽  
Danielle Sliva ◽  
Shane Lee ◽  
...  
Keyword(s):  
Somatosensory Cortex ◽  
Spectral Power ◽  
Sensory Information ◽  
Sensory Perception ◽  
Higher Order ◽  
Beta Band ◽  
Top Down ◽  
Sensory Suppression ◽  
Neuronal Mechanisms ◽  
Event Rates

AbstractTransient neocortical events with high spectral power in the 15–29Hz beta band are among the most reliable predictors of sensory perception: High prestimulus beta event rates in primary somatosensory lead to sensory suppression, most effective at 100–300ms prestimulus latency. However, the synaptic and neuronal mechanisms inducing beta’s perceptual effects have not been completely localized. We combined human MEG with neural modeling designed to account for these macroscale signals to interpret the cellular and circuit mechanisms that underlie the influence of beta on tactile detection. Extending prior studies, we modeled the hypothesis that higher-order thalamic bursts, sufficient for beta event generation in cortex, recruit supragranular GABAB inhibition acting on a 300ms time scale to suppress sensory information. Consistency between model and MEG data supported this hypothesis and led to a further prediction, validated in our data, that stimuli are perceived when beta events occur simultaneously with tactile stimulation. The post-event suppressive mechanism explains an array of studies that associate beta with decreased processing, while the during-event mechanism may demand a reinterpretation of the role of beta events in the context of coincident timing.Significance statementSomatosensory beta events – transient 15-29Hz oscillations in electromagnetic recordings – are thought to be generated when “top-down” bursts of spikes presumably originating in higher-order thalamus arrive in upper layers of somatosensory cortex. Physiological evidence had shown that the immediate action of these top-down projections should be excitatory; however, after a beta event, sensory perception is noticeably inhibited for approximately 300ms. The source of this post-event sensory suppression, in particular, had been unresolved. Using a detailed computational model of somatosensory cortex, we find evidence for the hypothesis that these bursts couple indirectly to GABAB inhibition in upper layers of cortex, and that beta events first briefly disinhibit sensory relay before a longer period of inhibition.

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