Article

Sherman, S. M. Tonic and burst firing: dual modes of thalamocortical relay. Trends Neurosci. 24, 122-126

Department of Neurobiology, State University of New York, Stony Brook, New York, NY 11794-5230, USA.
Trends in Neurosciences (Impact Factor: 13.56). 03/2001; 24(2):122-6. DOI: 10.1016/S0166-2236(00)01714-8
Source: PubMed

ABSTRACT

All thalamic relay cells exhibit two distinct response modes--tonic and burst--that reflect the status of a voltage-dependent, intrinsic membrane conductance. Both response modes efficiently relay information to the cortex in behaving animals, but have markedly different consequences for information processing. The lateral geniculate nucleus, which is the thalamic relay of retinal information to cortex, provides a reasonable model for all of thalamus. Compared with burst mode, geniculate relay cells that are firing in tonic mode exhibit better linear summation, but have poorer detectability for visual stimuli. The switch between the response modes can be controlled by nonretinal, modulatory afferents to these cells, such as the feedback pathway from cortex. This allows the thalamus to provide a dynamic relay that affects the nature and format of information that reaches the cortex.

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    • "Thus, two-third of synapses contacting a single TC neuron are related directly or indirectly to the activity of layer 6 corticothalamic (CT) axons. The CT feedback has long been considered as having a strong influence on the control of sensory information transfer by thalamocortical cells (Sherman and Koch, 1986; Koch, 1987; Ahissar, 1997; Sherman, 2001; Sillito and Jones, 2002) and could be involved in selective attention (O'Connor et al., 2002; Casagrande et al., 2005; Saalmann and Kastner, 2009), with recent evidences pointing out that corticothalamic feedback alters orientation-selectivity in human LGN during attention (Ling et al., 2015) and is involved in goal-directed attention in the mouse, via the disynaptic pathway involving the NRT (Ahrens et al., 2014). However, the mechanisms of cortically-driven attention in the thalamus remain an intriguing open question. "
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    ABSTRACT: A reason why the thalamus is more than a passive gateway for sensory signals is that two-third of the synapses of thalamocortical neurons are directly or indirectly related to the activity of corticothalamic axons. While the responses of thalamocortical neurons evoked by sensory stimuli are well characterized, with ON- and OFF-center receptive field structures, the prevalence of synaptic noise resulting from neocortical feedback in intracellularly recorded thalamocortical neurons in vivo has attracted little attention. However, in vitro and modeling experiments point to its critical role for the integration of sensory signals. Here we combine our recent findings in a unified framework suggesting the hypothesis that corticothalamic synaptic activity is adapted to modulate the transfer efficiency of thalamocortical neurons during selective attention at three different levels: First, on ionic channels by interacting with intrinsic membrane properties, second at the neuron level by impacting on the input-output gain, and third even more effectively at the cell assembly level by boosting the information transfer of sensory features encoded in thalamic subnetworks. This top-down population control is achieved by tuning the correlations in subthreshold membrane potential fluctuations and is adapted to modulate the transfer of sensory features encoded by assemblies of thalamocortical relay neurons. We thus propose that cortically-controlled (de-)correlation of subthreshold noise is an efficient and swift dynamic mechanism for selective attention in the thalamus.
    Preview · Article · Dec 2015 · Frontiers in Neural Circuits
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    • "Using depolarizing current pulses above threshold, the LGMD response showed a bimodal interspike interval (ISI), supporting a bursting behavior (Gabbiani and Krapp, 2006). Bursting neurons occur in many sensory systems, including mammalian auditory (Eggermount and Smith, 1996) and visual (Sherman, 2001) systems, weakly electric fishes (Krahe and Gabbiani, 2004), and auditory neurons in insects, such as crickets (Marsat and Pollack, 2006) and locusts (Eyherabide et al., 2008). Information within a burst signal can be more precise compared to a single action potential and may reliably transmit a signal from one neuron to another, avoiding synaptic transmission failure (Chen et al., 2009). "

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    • "PH is hypothesized to result from brainstem damage in regions that modulate the lateral geniculate nucleus (LGN) (Manford & Andermann, 1998). Overlapping brainstem nuclei control thalamic state shifts and coordinate REM sleep (McCarley, Benoit, & Barrionuevo, 1983; Manford & Andermann, 1998; Sherman, 2001). Manford and Andermann (1998) proposed that in addition to causing sleep disturbance, a brainstem lesion could produce complex visual hallucinations via thalamic inhibition by impairing LGN transmission and reducing the fidelity of retinoegeniculateeoccipital signaling. "
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    ABSTRACT: Brainstem lesions causing peduncular hallucinosis (PH) produce vivid visual hallucinations occasionally accompanied by sleep disorders. Overlapping brainstem regions modulate visual pathways and REM sleep functions via gating of thalamocortical networks. A 66-year-old man with paroxysmal atrial fibrillation developed abrupt-onset complex visual hallucinations with preserved insight and violent dream enactment behavior. Brain MRI showed restricted diffusion in the left rostrodorsal pons suggestive of an acute ischemic stroke. REM sleep behavior disorder (RBD) was diagnosed on polysomnography. We investigated the integrity of ponto-geniculate-occipital circuits with seed-based resting-state functional connectivity MRI (rs-fcMRI) in this patient compared to 46 controls. Rs-fcMRI revealed significantly reduced functional connectivity between the lesion and lateral geniculate nuclei (LGN), and between LGN and visual association cortex compared to controls. Conversely, functional connectivity between brainstem and visual association cortex, and between visual association cortex and prefrontal cortex (PFC) was significantly increased in the patient. Focal damage to the rostrodorsal pons is sufficient to cause RBD and PH in humans, suggesting an overlapping mechanism in both syndromes. This lesion produced a pattern of altered functional connectivity consistent with disrupted visual cortex connectivity via de-afferentation of thalamocortical pathways.
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