Properties of Convergent Thalamocortical and Intracortical Synaptic Potentials in Single Neurons of Neocortex

Gil, Ziv; Amitai, Yael

doi:10.1523/jneurosci.16-20-06567.1996

Cited by 102 publications

(75 citation statements)

References 69 publications

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“…4A3). It has been suggested that latencies Ͼ1.8 ms may represent indirect, polysynaptic connections (Gil and Amitai, 1996). Thus, our latencies could mean that OH neurons fire GABA interneurons projecting to MCH cells, presumably by releasing OH peptide since the responses persisted in glutamate receptor blockers (Fig.…”

Section: Oh Cell Firing Controls Gaba Input To Mch Cells Via Oh Recepmentioning

confidence: 93%

Optogenetic Evidence for Inhibitory Signaling from Orexin to MCH Neurons via Local Microcircuits

et al. 2015

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The lateral hypothalamus (LH) is a key regulator of multiple vital behaviors. The firing of brain-wide-projecting LH neurons releases neuropeptides promoting wakefulness (orexin/hypocretin; OH), or sleep (melanin-concentrating hormone; MCH). OH neurons, which coexpress glutamate and dynorphin, have been proposed to excite their neighbors, including MCH neurons, suggesting that LH may sometimes coengage its antagonistic outputs. However, it remains unclear if, when, and how OH actions promote temporal separation of the sleep and wake signals, a process that fails in narcolepsy caused by OH loss. To explore this directly, we paired optogenetic stimulation of OH cells (at rates that promoted awakening in vivo) with electrical monitoring of MCH cells in mouse brain slices. Membrane potential recordings showed that OH cell firing inhibited action potential firing in most MCH neurons, an effect that required GABA A but not dynorphin receptors. Membrane current analysis showed that OH cell firing increased the frequency of fast GABAergic currents in MCH cells, an effect blocked by antagonists of OH but not dynorphin or glutamate receptors, and mimicked by bath-applied OH peptide. In turn, neural network imaging with a calcium indicator genetically targeted to MCH neurons showed that excitation by bath-applied OH peptides occurs in a minority of MCH cells. Collectively, our data provide functional microcircuit evidence that intra-LH feedforward loops may facilitate appropriate switching between sleep and wake signals, potentially preventing sleep disorders.

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Section: Oh Cell Firing Controls Gaba Input To Mch Cells Via Oh Recepmentioning

confidence: 93%

Optogenetic Evidence for Inhibitory Signaling from Orexin to MCH Neurons via Local Microcircuits

et al. 2015

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“…We also observed larger excitatory amplitudes evoked by intracortical than by either sensory or thalamocortical activation. One reason could be that sensory and thalamocortical activations recruit larger feedforward inhibition than intracortical synapses (Gil and Amitai, 1996). …”

Section: Intracortical Activationmentioning

confidence: 99%

Gain Modulation of Synaptic Inputs by Network State in Auditory CortexIn Vivo

et al. 2015

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The cortical network recurrent circuitry generates spontaneous activity organized into Up (active) and Down (quiescent) states during slow-wave sleep or anesthesia. These different states of cortical activation gain modulate synaptic transmission. However, the reported modulation that Up states impose on synaptic inputs is disparate in the literature, including both increases and decreases of responsiveness. Here, we tested the hypothesis that such disparate observations may depend on the intensity of the stimulation. By means of intracellular recordings, we studied synaptic transmission during Up and Down states in rat auditory cortex in vivo. Synaptic potentials were evoked either by auditory or electrical (thalamocortical, intracortical) stimulation while randomly varying the intensity of the stimulus. Synaptic potentials evoked by the same stimulus intensity were compared in Up/Down states. Up states had a scaling effect on the stimulus-evoked synaptic responses: the amplitude of weaker responses was potentiated whereas that of larger responses was maintained or decreased with respect to the amplitude during Down states. We used a computational model to explore the potential mechanisms explaining this nontrivial stimulus-response relationship. During Up/Down states, there is different excitability in the network and the neuronal conductance varies. We demonstrate that the competition between presynaptic recruitment and the changing conductance might be the central mechanism explaining the experimentally observed stimulus-response relationships. We conclude that the effect that cortical network activation has on synaptic transmission is not constant but contingent on the strength of the stimulation, with a larger modulation for stimuli involving both thalamic and cortical networks.

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“…Intracortical synaptic interactions in the barrel cortex are dependent, in large part, on activation of glutamatergic NMDA receptors (Gil and Amitai, 1996b;Thomson and Deuchars, 1997;Huang et al, 1998). We therefore reasoned that activation of these receptors may augment intracortical synaptic interactions and enhance the spatial spread of activity in the barrel cortex.…”

Section: Nmda Receptors Mediate Spread Of Activitymentioning

confidence: 99%

Thalamic-Evoked Synaptic Interactions in Barrel Cortex Revealed by Optical Imaging

2000

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We used optical imaging of voltage-sensitive dye signals to study the spatiotemporal spread of activity in the mouse barrel cortex, evoked by stimulation of thalamocortical afferents in an in vitro slice preparation. Stimulation of the thalamus, at low current intensity, results in activity largely restricted to a single barrel, and to the border between layers Vb and VI. Low concentrations of the GABA A receptor antagonist bicuculline increase the amplitude of the optical signals, without affecting their spatiotemporal propagation. Higher concentrations of bicuculline result in paroxysmal activity, which propagates via intracolumnar and intercolumnar excitatory pathways. Enhancing the activity of NMDA receptors, by removing Mg 2ϩ from the extracellular solution, dramatically alters the spatiotemporal pattern of excitation: activity spreads to supragranular and infragranular layers and adjacent barrel columns. This enhanced propagation is suppressed by the NMDA receptor antagonist AP5. A similar enhancement of activity propagation can be produced by stimulating the thalamus with a short, high-frequency pulse train. Application of AP5 suppresses the frequency-dependent spread of activity. These findings indicate that the spatiotemporal spread of activity in the barrel cortex is altered by varying the temporal patterns of thalamic inputs, via an NMDA receptor-mediated mechanism, and suggest that a similar process occurs during repetitive whisking activity. Key words: somatosensory cortex; voltage-sensitive dyes; glutamate; NMDA; GABA; epilepsy; temporal coding; mouseProcessing of sensory information in the cerebral cortex can be described as a hierarchical process, in which inputs from "specific" thalamic nuclei are integrated by their postsynaptic cortical targets, which, in turn, provide inputs to neurons in other layers of the same functional column and subsequently to adjacent columns (Gilbert, 1992;Keller, 1995;Rauschecker et al., 1997). Although this hierarchical scheme is oversimplified in that it omits factors such as parallel processing and feedback interactions, it is thought to faithfully represent at least the initial stages of cortical sensory processing (Stone et al., 1979;Felleman and Van Essen, 1991;Iwamura, 1993).To understand the mechanisms underlying cortical sensory processing, it is necessary to determine how thalamic inputs are integrated by their postsynaptic cortical neurons and propagated via intracolumnar and intercolumnar cortical pathways. This requires methods to identify discrete functional columns and to reveal the spatiotemporal propagation of thalamic inputs within and among these columns. In the present study we took advantage of a functional imaging approach (see Orbach and Cohen, 1983;Cinelli and Salzberg, 1987;Yuste et al., 1997;Keller et al., 1998) to investigate intracortical processing of thalamic inputs in the somatosensory cortex and its modulation by glutamatergic and GABAergic processes.The somatosensory cortex of certain rodent species contains representations of the my...

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Properties of Convergent Thalamocortical and Intracortical Synaptic Potentials in Single Neurons of Neocortex

Cited by 102 publications

References 69 publications

Optogenetic Evidence for Inhibitory Signaling from Orexin to MCH Neurons via Local Microcircuits

Optogenetic Evidence for Inhibitory Signaling from Orexin to MCH Neurons via Local Microcircuits

Gain Modulation of Synaptic Inputs by Network State in Auditory CortexIn Vivo

Thalamic-Evoked Synaptic Interactions in Barrel Cortex Revealed by Optical Imaging

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