Neuronal Control of Drosophila Walking Direction

Science ◽  
2014 ◽  
Vol 344 (6179) ◽  
pp. 97-101 ◽  
Author(s):  
Salil S. Bidaye ◽  
Christian Machacek ◽  
Yang Wu ◽  
Barry J. Dickson

Most land animals normally walk forward but switch to backward walking upon sensing an obstacle or danger in the path ahead. A change in walking direction is likely to be triggered by descending “command” neurons from the brain that act upon local motor circuits to alter the timing of leg muscle activation. Here we identify descending neurons for backward walking in Drosophila—the MDN neurons. MDN activity is required for flies to walk backward when they encounter an impassable barrier and is sufficient to trigger backward walking under conditions in which flies would otherwise walk forward. We also identify ascending neurons, MAN, that promote persistent backward walking, possibly by inhibiting forward walking. These findings provide an initial glimpse into the circuits and logic that control walking direction in Drosophila.

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Kai Feng ◽  
Rajyashree Sen ◽  
Ryo Minegishi ◽  
Michael Dübbert ◽  
Till Bockemühl ◽  
...  

AbstractHow do descending inputs from the brain control leg motor circuits to change how an animal walks? Conceptually, descending neurons are thought to function either as command-type neurons, in which a single type of descending neuron exerts a high-level control to elicit a coordinated change in motor output, or through a population coding mechanism, whereby a group of neurons, each with local effects, act in combination to elicit a global motor response. The Drosophila Moonwalker Descending Neurons (MDNs), which alter leg motor circuit dynamics so that the fly walks backwards, exemplify the command-type mechanism. Here, we identify several dozen MDN target neurons within the leg motor circuits, and show that two of them mediate distinct and highly-specific changes in leg muscle activity during backward walking: LBL40 neurons provide the hindleg power stroke during stance phase; LUL130 neurons lift the legs at the end of stance to initiate swing. Through these two effector neurons, MDN directly controls both the stance and swing phases of the backward stepping cycle. These findings suggest that command-type descending neurons can also operate through the distributed control of local motor circuits.


Author(s):  
Kai Feng ◽  
Rajyashree Sen ◽  
Ryo Minegishi ◽  
Michael Dübbert ◽  
Till Bockemühl ◽  
...  

How do descending inputs from the brain control leg motor circuits to change the way an animal walks? Conceptually, descending neurons are thought to function either as command-type neurons, in which a single type of descending neuron exerts a high-level control to elicit a coordinated change in motor output, or through a more distributed population coding mechanism, whereby a group of neurons, each with local effects, act in combination to elicit a global motor response. The Drosophila Moonwalker Descending Neurons (MDNs), which alter leg motor circuit dynamics so that the fly walks backwards, exemplify the command-type mechanism. Here, we identify several dozen MDN target neurons within the leg motor circuits, and show that two of them mediate distinct and highly-specific changes in leg muscle activity during backward walking: LIN156 neurons provide the hindleg power stroke during stance phase; LIN128 neurons lift the legs at the end of stance to initiate swing. Through these two effector neurons, MDN directly controls both the stance and swing phases of the backward stepping cycle. MDN exerts these changes only upon the hindlegs; the fore-and midlegs follow passively through ground contact. These findings suggest that command-type descending neurons can also operate through the distributed control of local motor circuits.


2018 ◽  
Vol 119 (3) ◽  
pp. 1153-1165 ◽  
Author(s):  
Germana Cappellini ◽  
Francesca Sylos-Labini ◽  
Michael J. MacLellan ◽  
Annalisa Sacco ◽  
Daniela Morelli ◽  
...  

To investigate how early injuries to developing motor regions of the brain affect different forms of gait, we compared the spatiotemporal locomotor patterns during forward (FW) and backward (BW) walking in children with cerebral palsy (CP). Bilateral gait kinematics and EMG activity of 11 pairs of leg muscles were recorded in 14 children with CP (9 diplegic, 5 hemiplegic; 3.0–11.1 yr) and 14 typically developing (TD) children (3.3–11.8 yr). During BW, children with CP showed a significant increase of gait asymmetry in foot trajectory characteristics and limb intersegmental coordination. Furthermore, gait asymmetries, which were not evident during FW in diplegic children, became evident during BW. Factorization of the EMG signals revealed a comparable structure of the motor output during FW and BW in all groups of children, but we found differences in the basic temporal activation patterns. Overall, the results are consistent with the idea that both forms of gait share pattern generation control circuits providing similar (though reversed) kinematic patterns. However, BW requires different muscle activation timings associated with muscle modules, highlighting subtle gait asymmetries in diplegic children, and thus provides a more comprehensive assessment of gait pathology in children with CP. The findings suggest that spatiotemporal asymmetry assessments during BW might reflect an impaired state and/or descending control of the spinal locomotor circuitry and can be used for diagnostic purposes and as complementary markers of gait recovery.NEW & NOTEWORTHY Early injuries to developing motor regions of the brain affect both forward progression and other forms of gait. In particular, backward walking highlights prominent gait asymmetries in children with hemiplegia and diplegia from cerebral palsy and can give a more comprehensive assessment of gait pathology. The observed spatiotemporal asymmetry assessments may reflect both impaired supraspinal control and impaired state of the spinal circuitry.


Author(s):  
J. Eric Ahlskog

As a prelude to the treatment chapters that follow, we need to define and describe the types of problems and symptoms encountered in DLB and PDD. The clinical picture can be quite varied: problems encountered by one person may be quite different from those encountered by another person, and symptoms that are problematic in one individual may be minimal in another. In these disorders, the Lewy neurodegenerative process potentially affects certain nervous system regions but spares others. Affected areas include thinking and memory circuits, as well as movement (motor) function and the autonomic nervous system, which regulates primary functions such as bladder, bowel, and blood pressure control. Many other brain regions, by contrast, are spared or minimally involved, such as vision and sensation. The brain and spinal cord constitute the central nervous system. The interface between the brain and spinal cord is by way of the brain stem, as shown in Figure 4.1. Thought, memory, and reasoning are primarily organized in the thick layers of cortex overlying lower brain levels. Volitional movements, such as writing, throwing, or kicking, also emanate from the cortex and integrate with circuits just below, including those in the basal ganglia, shown in Figure 4.2. The basal ganglia includes the striatum, globus pallidus, subthalamic nucleus, and substantia nigra, as illustrated in Figure 4.2. Movement information is integrated and modulated in these basal ganglia nuclei and then transmitted down the brain stem to the spinal cord. At spinal cord levels the correct sequence of muscle activation that has been programmed is accomplished. Activated nerves from appropriate regions of the spinal cord relay the signals to the proper muscles. Sensory information from the periphery (limbs) travels in the opposite direction. How are these signals transmitted? Brain cells called neurons have long, wire-like extensions that interface with other neurons, effectively making up circuits that are slightly similar to computer circuits; this is illustrated in Figure 4.3. At the end of these wire-like extensions are tiny enlargements (terminals) that contain specific biological chemicals called neurotransmitters. Neurotransmitters are released when the electrical signal travels down that neuron to the end of that wire-like process.


1961 ◽  
Vol 16 (5) ◽  
pp. 827-830 ◽  
Author(s):  
Y. K. Byon ◽  
E. F. Adolph

An oxygen electrode and a thermistor were placed in the brain stem, leg muscle, or abdomen of a rat cooled to 17—15 C. When the rat was thereafter kept at 16∘the electrode usually showed a steady current. At 13—11∘ the apparent Po2 of tissue in most instances diminished during 2—3 hr unless artificial breathing was given. Forced breathing of air or oxygen ordinarily raised the Po2; of nitrogen usually, but not always, lowered the Po2. When the apparent Po2 was not thus raised or lowered, the flow of blood to the one tissue being examined, but not necessarily to all tissues, was evidently inadequate. The heart could be stopped reversibly by further cooling to 9—5∘; brain Po2 diminished only gradually at that low temperature. Survival was assured by a Po2 that was high and steady, but often occurred also after a diminishing or zero Po2. In the hypothermic rat, either pulmonary ventilation or systemic blood flow or an unidentified factor could limit the rat's survival. Submitted on October 26, 1960


2001 ◽  
Vol 86 (4) ◽  
pp. 1764-1772 ◽  
Author(s):  
Yin Fang ◽  
Vlodek Siemionow ◽  
Vinod Sahgal ◽  
Fuqin Xiong ◽  
Guang H. Yue

Despite abundant evidence that different nervous system control strategies may exist for human concentric and eccentric muscle contractions, no data are available to indicate that the brain signal differs for eccentric versus concentric muscle actions. The purpose of this study was to evaluate electroencephalography (EEG)-derived movement-related cortical potential (MRCP) and to determine whether the level of MRCP-measured cortical activation differs between the two types of muscle activities. Eight healthy subjects performed 50 voluntary eccentric and 50 voluntary concentric elbow flexor contractions against a load equal to 10% body weight. Surface EEG signals from four scalp locations overlying sensorimotor-related cortical areas in the frontal and parietal lobes were measured along with kinetic and kinematic information from the muscle and joint. MRCP was derived from the EEG signals of the eccentric and concentric muscle contractions. Although the elbow flexor muscle activation (EMG) was lower during eccentric than concentric actions, the amplitude of two major MRCP components—one related to movement planning and execution and the other associated with feedback signals from the peripheral systems—was significantly greater for eccentric than for concentric actions. The MRCP onset time for the eccentric task occurred earlier than that for the concentric task. The greater cortical signal for eccentric muscle actions suggests that the brain probably plans and programs eccentric movements differently from concentric muscle tasks.


2020 ◽  
Author(s):  
Adam J. Lundquist ◽  
Tyler J. Gallagher ◽  
Giselle M. Petzinger ◽  
Michael W. Jakowec

AbstractL-lactate is an energetic and signaling molecule that is key to the metabolic and neuroplastic connection between astrocytes and neurons and may be involved in exercise-induced neuroplasticity. This study sought to explore the role of L-lactate in astrocyte reactivity and neuroplasticity. Using in vitro cultures of primary astrocytes, we show L-lactate increased expression of plasticity-related genes, including neurotrophic factors, Bdnf, Gdnf, Cntf and the immediate early gene cFos. L-lactate’s promotion of neurotrophic factor expression may be mediated in part by the lactate receptor HCAR1 since application of the HCAR1 agonist 3,5-DHBA also increased expression of Bdnf in primary astrocytes. In vivo L-lactate administration to healthy mice caused a similar increase in the expression of plasticity-related genes as well as increased astrocyte morphological complexity in a region-specific manner, with increased astrocytic response found in the striatum but not the ectorhinal cortex, regions of the brain where increases in regional cerebral blood flow are increased or unaltered, respectively, with motor behavior. Additionally, L-lactate administration did not cause synaptogenesis or improve motor behavior based on the latency to fall on the accelerating rotarod, suggesting that L-lactate administration can initiate astrocyte-specific gene expression, but the activation of motor circuits is necessary to initiate striatal neuroplasticity. These results suggest that peripheral L-lactate is likely an important molecular component of exercise-induced neuroplasticity by acting in an astrocyte-specific manner to prime the brain for neuroplasticity.


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