Thalamocortical responses of mouse somatosensory (barrel) cortexin vitro

Agmon, Ariel; Connors, Barry W.

doi:10.1016/0306-4522(91)90333-j

Cited by 665 publications

(534 citation statements)

References 42 publications

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“…The origin of P1 from SI-specific thalamocortical inputs is well established (Mitzdorf, 1985). N1 is associated with the slow, long latency sink in layers I/II (Agmon and Connors, 1991;Kulics and Cauller, 1986) and is generated by excitatory cortical events (Cauller and Kulics, 1991). N1 is reduced during deep anesthesia (Arezzo et al, 1981) and slow-wave sleep (Cauller and Kulics, 1988).…”

Section: Introductionmentioning

confidence: 99%

Coupling between somatosensory evoked potentials and hemodynamic response in the rat

Franceschini

Nissilä

et al. 2008

NeuroImage

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We studied the relationship between somatosensory evoked potentials (SEP) recorded with scalp electroencephalography (EEG) and hemoglobin responses recorded non-invasively with diffuse optical imaging (DOI) during parametrically varied electrical forepaw stimulation in rats. Using these macroscopic techniques we verified that the hemodynamic response is not linearly coupled to the somatosensory evoked potentials, and that a power or threshold law best describes the coupling between SEP and the hemoglobin response, in agreement with the results of most invasive studies. We decompose the SEP response in three components (P1, N1, and P2) to determine which best predicts the hemoglobin response. We found that N1 and P2 predict the hemoglobin response significantly better than P1 and the input stimuli (S). Previous electrophysiology studies reported in the literature show that P1 originates in layer IV directly from thalamocortical afferents, while N1 and P2 originate in layers I and II and reflect the majority of local cortico-cortical interactions. Our results suggest that the evoked hemoglobin response is driven by the cortical synaptic activity and not by direct thalamic input. The N1 and P2 components, and not P1, need to be considered to correctly interpret neurovascular coupling.

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Section: Introductionmentioning

confidence: 99%

Coupling between somatosensory evoked potentials and hemodynamic response in the rat

Franceschini

Nissilä

et al. 2008

NeuroImage

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“…Here the authors investigate the cellular basis of this missing inhibition using in vitro electrophysiological recordings in the mouse thalamocortical slice 11 . This preparation leaves thalamocortical connections intact, and the authors perform a set of beautiful experiments that show that the neonatal thalamocortical microcircuit is incomplete in several ways.…”

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confidence: 99%

It's about time for thalamocortical circuits

Hull

Scanziani

2007

Nat Neurosci

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The timing of thalamocortical excitation and inhibition is critical to local microcircuits. Two new papers shed light on the development and performance of a somatosensory microcircuit that regulates the integration of thalamic inputs.The timing of sensory stimuli is a fundamental parameter used by the neocortex to construct representations of the external world. In the somatosensory system, the timing of cortical spikes can accurately follow the pattern of stimuli generated while touching an object 1 . This temporal precision is likely to be essential for proper tactile discrimination. To enforce precise timing, the cortex uses a simple circuit that is activated by thalamic afferents 2 . These thalamocortical afferents provide the main input to the somatosensory cortex and form excitatory, glutamatergic synapses onto a subset of cortical neurons. In this issue, two papers examine the development and function of a microcircuit activated by thalamocortical afferents. Daw et al. show that the ontogeny of this thalamocortical microcircuit involves a set of rapid, coordinated steps that transform it into a precise coincidence detector 3 . Once the circuit is mature, Cruikshank and colleagues demonstrate that it relies on divergent kinetics and strength of excitation from thalamocortical afferents for reliable performance 4 .Upon entering the cortex, individual thalamocortical afferents contact both excitatory projection neurons (glutamatergic principal cells) and local inhibitory interneurons (GABAergic cells). Thus, somatosensory information is immediately distributed to both excitatory and inhibitory cells. Surprisingly though, thalamocortical synapses onto inhibitory interneurons are much stronger than those onto excitatory principal cells 2,5,6 . By contacting both inhibitory and excitatory cells, thalamocortical afferents lay the foundation for a simple disynaptic circuit that provides powerful, local feedforward inhibition (Fig. 1).In the somatosensory cortex, thalamocortical afferents initiate feedforward inhibition by activating so-called fast-spiking interneurons, a subtype of GABAergic interneuron. Because these fast-spiking interneurons synapse onto the same excitatory principal cells that are directly contacted by thalamocortical afferents, thalamic activity results in both excitation and inhibition of cortical principal cells.Because excitation is direct, whereas inhibition is delayed by one synapse, disynaptic feedforward inhibition lags monosynaptic thalamocortical excitation by 1-2 ms. The short latency between the onset of thalamocortical excitation and the onset of feedforward inhibition presents a temporal 'window of opportunity' for principal neurons to integrate

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“…The possible contribution of these factors to tactile stimulus response measured in vivo can be delineated with simultaneous pair recordings from pre-and postsynaptic cells in vitro. Feldmeyer used neocortex slices [1], allowing visualization of individual columns and making simultaneous recordings from cells located in the granular and supragranular layers (Fig. 3c).…”

Section: Resultsmentioning

confidence: 99%