Reticular formation

Summary

The reticular formation is a set of interconnected nuclei that are located throughout the brainstem. It is not anatomically well defined, because it includes neurons located in different parts of the brain. The neurons of the reticular formation make up a complex set of networks in the core of the brainstem that extend from the upper part of the midbrain to the lower part of the medulla oblongata. The reticular formation includes ascending pathways to the cortex in the ascending reticular activating system (ARAS) and descending pathways to the spinal cord via the reticulospinal tracts. Neurons of the reticular formation, particularly those of the ascending reticular activating system, play a crucial role in maintaining behavioral arousal and consciousness. The overall functions of the reticular formation are modulatory and premotor, involving somatic motor control, cardiovascular control, pain modulation, slee

Official source

https://en.wikipedia.org/wiki/Reticular_formation

About this result

This page is automatically generated and may contain information that is not correct, complete, up-to-date, or relevant to your search query. The same applies to every other page on this website. Please make sure to verify the information with EPFL's official sources.

Related publications (42)

Related publications

Related people (4)

Related people

Related units (2)

Related units

Related concepts (54)

Related concepts

Related courses (6)

Related courses

Related lectures (8)

Related lectures

Motor Control in the Mouse Whisker System

Varun Sreenivasan

The motor systems of the mammalian brain are a remarkable product of many millions of years of evolution. It is the motor systems that make us and other mammals mobile, that guide our actions in response to sensory information and conversely modulate the very nature of the sensory input that our brain receives. The mystacial vibrissae or whiskers present on the face of mice are important sensors that provide high resolution tactile information to the brain. Whereas the pathways that are involved in signaling and processing sensory information from the whiskers have been the subject of intense investigation for many years, we know relatively little about how whisker movements are controlled by the brain. In the first part of the thesis, I present evidence for two parallel pathways originating from the neocortex that control antagonistic movements of the whiskers. I first describe whisker movements elicited upon Channelrhodopsin-2 (ChR2) stimulation of whisker somatosensory cortex (wS1) and whisker motor cortex (wM1). At short latencies, optogenetic stimulation of wS1 drove whisker retraction while optogenetic stimulation of wM1 drove rhythmic whisker protraction. Next, using recent developments in Rabies virus retrograde tracing, I mapped the location of the motor neurons in the facial nucleus, finding two distinct neuron pools for the extrinsic (retractor) muscle Nasolabialis and the intrinsic (protractor) follicular muscle. These distinct motor neuron populations received premotor input from different sources in the brainstem. While the premotor neurons of the extrinsic muscle were located more densely in the spinal trigeminal nucleus (Sp5), the premotor neurons of the intrinsic muscle were located more densely in the reticular formation (Rt). Anterograde tracing from wS1 and wM1 cortex revealed a complementary distribution of axons in the brainstem. Whereas wS1 strongly innervated Sp5, wM1 innervated the Rt. These data therefore begin to unravel the circuitry from the neocortex to the whisker motor neurons. In the second part of the thesis, I investigated the subthreshold and spiking correlates of whisker movements using whole-cell current clamp recordings of individual excitatory neurons in wM1. Brief 1 ms optogenetic stimulation of wS1 elicited rhythmic whisking after long latencies which was abolished upon pharmacological inactivation of wM1. Whole-cell recordings in wM1 during wS1 stimulation showed that the long-range synaptic input from wS1 to wM1 is encoded as a bi-phasic membrane potential response with an early depolarizing post-synaptic potential (Dep. PSP), followed by a hyperpolarizing post-synaptic potential (Hyp. PSP) in individual wM1 neurons. Approximately 150 ms after the wS1 stimulus, the Vm showed a rebound depolarization, which, on most trials, was followed by late rhythmic whisking. Whole-cell recordings during self-generated whisker movements showed that upon whisking, wM1 undergoes a profound cortical state change, where the mean Vm is more depolarized, slow fluctuations of the Vm are reduced and spike rates in layer 5 increase. Aligning the membrane potential trajectories to the onset of whisker movement epochs revealed that changes in Vm occurred almost 100 ms before movement onset. Finally, an examination of the Vm dynamics during rhythmic whisking showed that the Vm of individual wM1 neurons is modulated by the phase of the whisk cycle. This modulation is stronger in layer 2/3 compared to layer 5.

EPFL2015

First human trials involving neuroprosthetic rehabilitation demonstrated recently that significant functional benefits can be achieved with lumbosacral neuromodulation and reorganized spared projections. However, complete spinal cord injuries (SCI) wholly isolate infralesional circuits from any supraspinal control, leading to irreversible motor deficits that neuroprosthetics still fails to address. As axons fail to regrow across the lesion site, neuroregenerative research after SCI has been dogmatically focusing attention on minimizing the environmental inhibitions to axon regeneration. In the present work, we demonstrate that spontaneous axon regeneration failure can be reversed, and that propriospinal axons are able to grow across complete non-neural lesion cores when the required facilitators are provided. We identified three mechanisms needed for propriospinal regrowth : i) enhancing neuronal intrinsic growth capacities using viral technologies, ii) remodeling the lesion core with growth factors, in order to densify permissive substrates, and iii) guiding axons chemically across the SCI site. Propriospinal neurons - that coordinate different spinal segments in healthy conditions - are known to support recovery of locomotion in incomplete models of spinal cord injury. However, restoring a robust descending bridge of propriospinal axons does not by itself promote any functional benefit. We hypothesize that a lack of somatosensory feedback to the motor cortex (M1), together with insufficient descending motor control, may prevent coherent exchange of information between lumbosacral and cortical motor centers. Therefore, we explored the neuroregenerative potential of reticulospinal axons - which are projected from the brainstem to the spinal cord - as a second relay for the descending motor cortical command. Together with axon guidance and lesion remodeling, our viral manipulation of intrinsic growth programs induced limited yet significant reticulospinal regeneration into the lesion core. In order to enhance this reticulospinal regrowth, we explored activity-dependent mechanisms of neurite growth control. As we observed that activity does not recruit growth programs after SCI, we revealed a possible divergence between the mechanisms that underly reticulospinal axon regrowth and neurite sprouting. In the mean time, we are developing a somatosensory interface that aims at restoring sensory feedback to the motor cortex after complete SCI. Based on hindlimb electromyographic activity, we linked locomotion to optogenetic neuromodulation of the motor thalamus, and were able to evoke responses in M1 by selectively activating thalamocortical projections, both before and after complete spinal lesion. Such technology enables a direct recruitment of thalamic nuclei that gate motor learning and motor planning at a cortical level. Coming experiments will test wether a strategy combining propriospinal regeneration with locomotion-dependent thalamocortical modulation is sufficient to restore voluntary stepping after complete SCI.

EPFL2019

A computational biophysical model of thalamic and reticular nucleus microcircuitry: from neurons to emergent network dynamics

Elisabetta Iavarone

The thalamus, once believed to be a simple relay station between the body periphery and the neocortex, has started to be recognized as a key player in higher-order functions, such as attention. It participates in the transition between brain states, such as sleep and wakefulness, and thalamocortical oscillations. Many of these functions involve the reticular nucleus (Rt), an inhibitory brain structure that surrounds the thalamus and where thalamocortical and corticothalamic axons establish synaptic contacts. Recent technical advances have made possible the study of thalamic activity in vivo and its contributions to cortical processing and behavior. However, a unified understanding of how network dynamics in the thalamus and the thalamocortical system is shaped by its neurons and synapses is still lacking. To address these challenges, we developed biophysically-detailed computational models of thalamic and reticular neurons. We then incorporated them in a large-scale model of thalamo-reticular microcircuitry, whose connectivity was directly constrained by three-dimensional reconstructions of neuronal morphologies. We included intrathalamic connections through chemical synapses, gap junctions and synapses from the sensory periphery and the neocortex. A large part of the data used to build and validate the model was extracted from the literature and leveraged a framework for its systematic and collaborative curation. This framework allowed us to keep track of parameter values used in the model, along with metadata describing the species, brain regions and experimental conditions. As a first validation of the model at the network level, we studied the generation of spindle-like oscillations. We found that external inputs are necessary to initiate this rhythm, while its termination can be sustained by the synaptic interplay alone, with a key role of mutual inhibition between reticular neurons. We found that that waxing-and-waning oscillations have a clear spatial component, that reflected the connectivity through chemical synapses as well as gap junctions. Finally, we investigated how differential depolarization in reticular and thalamocortical neurons influence the properties of spindle-like oscillations and predicted conditions where they are less easy to evoke. Taken together this thesis demonstrates how a bottom-up modelling approach can be successfully applied to reconstruct and simulate thalamic microcircuitry, which shows emergent network behavior compatible with experimental findings, and paves the way for understanding the role of the thalamus in thalamocortical functions.

EPFL2020