Dataset Information

In Vivo Ca(2+) Imaging Reveals that Decreased Dendritic Excitability Drives Startle Habituation.

ABSTRACT: Exposure to repetitive startling stimuli induces habitation, a simple form of learning. Despite its simplicity, the precise cellular mechanisms by which repeated stimulation converts a robust behavioral response to behavioral indifference are unclear. Here, we use head-restrained zebrafish larvae to monitor subcellular Ca(2+) dynamics in Mauthner neurons, the startle command neurons, during startle habituation in vivo. Using the Ca(2+) reporter GCaMP6s, we find that the amplitude of Ca(2+) signals in the lateral dendrite of the Mauthner neuron determines startle probability and that depression of this dendritic activity rather than downstream inhibition mediates glycine and N-methyl-D-aspartate (NMDA)-receptor-dependent short-term habituation. Combined, our results suggest a model for habituation learning in which increased inhibitory drive from feedforward inhibitory neurons combined with decreased excitatory input from auditory afferents decreases dendritic and Mauthner neuron excitability.

SUBMITTER: Marsden KC

PROVIDER: S-EPMC4680997 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature

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In Vivo Ca(2+) Imaging Reveals that Decreased Dendritic Excitability Drives Startle Habituation.

Marsden Kurt C KC Granato Michael M

Cell reports 20151119 9

Exposure to repetitive startling stimuli induces habitation, a simple form of learning. Despite its simplicity, the precise cellular mechanisms by which repeated stimulation converts a robust behavioral response to behavioral indifference are unclear. Here, we use head-restrained zebrafish larvae to monitor subcellular Ca(2+) dynamics in Mauthner neurons, the startle command neurons, during startle habituation in vivo. Using the Ca(2+) reporter GCaMP6s, we find that the amplitude of Ca(2+) signa ...[more]

PMID: 26655893

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Project description:Neurological examination of non-communicating patients relies on a few decisive items that enable the crucial distinction between vegetative state (VS)-also coined unresponsive wakefulness syndrome (UWS)-and minimally conscious state. Over the past 10 years, this distinction has proven its diagnostic value as well as its important prognostic value on consciousness recovery. However, clinicians are currently limited by three factors: (i) the current behavioural repertoire of minimally conscious state items is limited and restricted to a few cognitive domains in the goldstandard revised version of the Coma Recovery Scale; (ii) a proportion of ∼15-20% clinically VS/UWS patients are actually in a richer state than VS/UWS as evidenced by functional brain imaging; and (iii) the neurophysiological and cognitive interpretation of each minimally conscious state item is still unclear and debated. In the current study we demonstrate that habituation of the auditory startle reflex (hASR) tested at bedside constitutes a novel, simple and powerful behavioural sign that can accurately distinguish minimally conscious state from VS/UWS. In addition to enlarging the minimally conscious state items repertoire, and therefore decreasing the low sensitivity of current behavioural measures, we also provide an original and rigorous description of the neurophysiological basis of hASR through a combination of functional (high density EEG and 18F-fluorodeoxyglucose PET imaging) and structural (diffusion tensor imaging MRI) measures. We show that preservation of hASR is associated with the functional and structural integrity of a brain-scale fronto-parietal network, including prefrontal regions related to control of action and inhibition, and meso-parietal areas associated with minimally conscious and conscious states. Lastly, we show that hASR predicts 6-month improvement of consciousness. Taken together, our results show that hASR is a cortically-mediated behaviour, and suggest that it could be a new clinical item to clearly and accurately identify non-communicating patients who are in the minimally conscious state.

Project description:A mild traumatic brain injury is a neurological disturbance of transient or/and chronic nature after a direct blow of the head/neck or exposure of the body to impulsive biomechanical forces, indirectly affecting the brain. The neuropathological events leading to the clinical signs, symptoms and functional disturbances are still elusive due to a lack of sensitive brain-screening tools. Animal models offer the potential to study neural pathomechanisms in close detail. We recently proposed a non-invasive protocol for inducing concussion-like symptoms in larval zebrafish via exposure to rapid linearly accelerating-decelerating body motion. By mean of auditory 'startle reflex habituation' assessments-an established neurophysiological health index-we probed acute and chronic effects that mirror human concussion patterns. This study aimed at expanding our previous work by assessing the ensuing effects with visual-as opposed to auditory-'startle reflex habituation' quantifications, by using the same methodology. We observed that immediately after impact exposure, the fish showed impaired sensory reactivity and smaller decay constant, possibly mirroring acute signs of confusion or loss of consciousness in humans. By 30-min post-injury, the fish display temporary signs of visual hypersensitivity, manifested as increased visuomotor reactivity and a relatively enlarged decay constant, putatively reflecting human post-concussive sign of visual hypersensitivity. In the following 5-24 h, the exposed fish progressively develop chronic signs of CNS dysfunction, in the form of low startle responsivity. However, the preserved decay constant suggests that neuroplastic changes may occur to restore CNS functioning after undergoing the 'concussive procedure'. The observed findings expand our previous work providing further behavioural evidence for the model. Limitations that still require addressment are discussed, advancing further behavioural and microscopic analyses that would be necessary for the validation of the model in its putative relatability with human concussion.

Dataset Information

In Vivo Ca(2+) Imaging Reveals that Decreased Dendritic Excitability Drives Startle Habituation.

Publications

In Vivo Ca(2+) Imaging Reveals that Decreased Dendritic Excitability Drives Startle Habituation.

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