Biology subjects

Brette, R.

Publications and source records attributed to Brette, R..

4 recordsLinked to original sources

bioRxiv2018

Contribution of the axon initial segment to action potentials recorded extracellularly

Action potentials (APs) are electric phenomena that are recorded both intracellularly and extracellularly. APs are usually initiated in the short segment of the axon called the axon initial segment (AIS). It was recently proposed that at onset of an AP the soma and the AIS form a dipole. We study the extracellular signature (the extracellular action potential, EAP) generated by such a dipole. First, we demonstrate the formation of the dipole and its extracellular signature in detailed morphological models of a reconstructed pyramidal neuron. Then, we study the EAP waveform and its spatial dependence in models with axonal AP initiation and contrast it with the EAP obtained in models with somatic AP initiation. We show that in the models with axonal AP initiation the dipole forms between somatodendritic compartments and the AIS, and not between soma and dendrites as in the classical models. Soma-dendrites dipole is present only in models with somatic AP initiation. Our study has consequences for interpreting extracellular recordings of single-neuron activity and determining electrophysiological neuron types, but also for better understanding the origins of the high-frequency macroscopic electric fields recorded in the brain.\n\nNew & NoteworthyWe studied the consequences of the action potential (AP) initiation site on the extracellular signatures of APs. We show that: (1) at the time of AP initiation the action initial segment (AIS) forms a dipole with the soma, (2) the width but not (3) amplitude of the extracellular AP generated by this dipole increases with the soma-AIS distance. This may help to monitor dynamic changes in the AIS position in experimental in vivo recordings.

neuroscience↗

bioRxiv2017

Modeling neuron-glia interactions with the Brian 2 simulator

Despite compelling evidence that glial cells could crucially regulate neural network activity, the vast majority of available neural simulators ignores the possible contribution of glia to neuronal physiology. Here, we show how to model glial physiology and neuron-glia interactions in the Brian 2 simulator. Brian 2 offers facilities to explicitly describe any model in mathematical terms with limited and simple simulator-specific syntax, automatically generating high-performance code from the user-provided descriptions. The flexibility of this approach allows us to model not only networks of neurons, but also individual glial cells, electrical coupling of glial cells, and the interaction between glial cells and synapses. We therefore conclude that Brian 2 provides an ideal platform to efficiently simulate glial physiology, and specifically, the influence of astrocytes on neural activity.

neuroscience↗

bioRxiv2017

Is coding a relevant metaphor for the brain?

Short abstractI argue that the popular neural coding metaphor is often misleading. First, the \"neural code\" often spans both the experimental apparatus and the brain. Second, a neural code is information only by reference to something with a known meaning, which is not the kind of information relevant for a perceptual system. Third, the causal structure of neural codes (linear, atemporal) is incongruent with the causal structure of the brain (circular, dynamic). I conclude that a causal description of the brain cannot be based on neural codes, because spikes are more like actions than hieroglyphs.\n\nLong abstract\"Neural coding\" is a popular metaphor in neuroscience, where objective properties of the world are communicated to the brain in the form of spikes. Here I argue that this metaphor is often inappropriate and misleading. First, when neurons are said to encode experimental parameters, the neural code depends on experimental details that are not carried by the coding variable. Thus, the representational power of neural codes is much more limited than generally implied. Second, neural codes carry information only by reference to things with known meaning. In contrast, perceptual systems must build information from relations between sensory signals and actions, forming a structured internal model. Neural codes are inadequate for this purpose because they are unstructured. Third, coding variables are observables tied to the temporality of experiments, while spikes are timed actions that mediate coupling in a distributed dynamical system. The coding metaphor tries to fit the dynamic, circular and distributed causal structure of the brain into a linear chain of transformations between observables, but the two causal structures are incongruent. I conclude that the neural coding metaphor cannot provide a basis for theories of brain function, because it is incompatible with both the causal structure of the brain and the informational requirements of cognition.

neuroscience↗

bioRxiv2017

Mobility as the purpose of postural control

Counteracting the destabilizing force of gravity is usually considered to be the main purpose of postural control. However, from the consideration of the mechanical requirements for movement, we argue that posture is adjusted in view of providing impetus for movement. Thus, we show that the posture that is usually adopted in quiet standing in fact allows torque for potential movement. Moreover, when performing a movement - either voluntarily or in response to an external perturbation - we show that the postural adjustments are organized both spatially and temporally so as to provide the required torque for the movement. Thus, when movement is performed skillfully, the force of gravity is not counteracted but actually used to provide impetus to movement. This ability to move ones weight so as to exploit the torque of gravity seems to be dependent on development and skill learning, and is impaired in aging.

neuroscience↗