Central Pattern Generators

Note:  I'm taking a very broad view of what should be considered a CPG.  Most behavior includes adjustments at the spinal level, and this spinal level adjustment almost always involves a CPG.  So the more peripheral aspects of the behavior can be seen as elaborations of the CPG.    

Searching PubMed for "central pattern generators" yielded 667 references: 
http://www.ncbi.nlm.nih.gov/pubmed/?term=central+pattern+generators 

Searching Google for "central pattern generators" yielded 1,140,000 references: 
https://www.google.com/search?q=central+pattern+generators&ie=utf-8&oe=utf-8   


Central pattern generator (Wiki)   

Contents

    "Central pattern generators (CPGs) are biological neural networks that produce rhythmic patterned outputs without sensory feedback.[1][2] CPGs have been shown to produce rhythmic outputs resembling normal "rhythmic motor pattern production" even in isolation from motor and sensory feedback from limbs and other muscle targets.[1][2]

    To be classified as a rhythmic generator, a CPG requires:
1. "two or more processes that interact such that each process sequentially increases and decreases, and
2. that, as a result of this interaction, the system repeatedly returns to its starting condition.[1] CPGs have been found in practically all vertebrate species investigated,[3] including human.[4][5]
"

  • 1 Anatomy and physiology

    • 1.1 Localization    
    •      "The results have shown that the networks responsible for locomotion are distributed throughout the lower thoracic and lumbar regions of the spinal cord. [6] "
    •  1.2 Anatomy 
           "Neural rhythmicity can arise in two ways: "through interactions among neurons (network-based rhythmicity) or through interactions among currents in individual neurons (endogenous oscillator neurons)". [1] "
  • 2 Functions
    • 2.1 Locomotion 

    •     "
      As early as 1911, it was recognized, by the experiments of T. Graham Brown, that the basic pattern of stepping can be produced by the spinal cord without the need of descending commands from the cortex.[11][12]
      "  
          "
      The lamprey has been used as a model for vertebrate CPGs because, while its nervous system has a vertebrate organization, it shares many positive characteristics with invertebrates.  
          When removed from the lamprey, the intact spinal cord can survive for days in vitro. It also has very few neurons and can be easily stimulated to produce a fictive swimming motion indicative of a central pattern generator.  
         As early as 1983, Ayers, Carpenter, Currie and Kinch proposed that there was a basal CPG responsible for most undulating movements in the lamprey including swimming forward and backward, burrowing in the mud and crawling on a solid surface.[13] The different movements have been found to be altered by neuromodulators, including serotonin
      "
          "
      Central pattern generators also contribute to locomotion in higher animals and humans. ... As described in Neuromodulation, the human locomotive CPG is very adaptable and can respond to sensory input. It receives input from the brainstem as well as from the environment to keep the network regulated. Newer studies have not only confirmed the presence of the CPG for human locomotion, but also confirmed its robustness and adaptability.
      "   

    • 2.2 Respiration
    • 2.3 Swallowing
    • 2.4 Rhythm generators
    • 2.5 Mechanism of rhythmic generators: post-inhibitory rebound (PIR) 

    "... PIR as a robust property of CNS neurons in a wide variety of contexts." [43] This cellular property can most easily be seen in the Lamprey neural circuit. The swimming movement is produced by alternating neural activity between the left and right side of the body, causing it to bend back and forth while creating oscillating movements. While the Lamprey is bent to the left, there is reciprocal inhibition on the right side causing it to relax due to hyperpolarization. Immediately after this hyperopolarizing stimulus, the interneurons use post-inhibitory rebound to initiate activity in the right side. Depolarization of the membrane causes it to contract while reciprocal inhibition is now applied to the left side."   

  • 3 References
  • 4 External links   

    Mentioned neurotransmitters:  Serotonin. 


Searching PubMed for "central pattern generators" yielded 667 references: 
http://www.ncbi.nlm.nih.gov/pubmed/?term=central+pattern+generators  

Grillner

I noticed that many of the 667 Central Pattern Generator references listed "Grillner S" as one of the authors.  So I searched PubMed for "Grillner S".  Although Grillner doesn't mention "central pattern generators", he does talk about "locomotor networks", which are pretty much the same thing. 

Searching PubMed for "Grillner S" identified 349 References:   
http://www.ncbi.nlm.nih.gov/pubmed/?term=grillner+s  

Note:  Combining the two searches was more difficult than I expected. 


 
1991
Co-localized GABA and somatostatin use different ionic mechanisms to hyperpolarize target neurons in the lamprey spinal cord.
http://www.ncbi.nlm.nih.gov/pubmed/1687706
    See:  Lamprey GABA


1992    618<667      

The role of heterarchical control in the evolution of central pattern generators.
http://www.ncbi.nlm.nih.gov/pubmed/1330203    
     "The acceptance of the concept of central pattern generators (CPGs) led to the perception that descending inputs initiate stereotyped movements, such as locomotion, but play relatively minor roles after the movement begins. Sensory input could entrain the CPG, and the CPG was responsive to the proper inputs for switching, etc.     Evidence is here presented that the influences of both descending and sensory inputs are two-way. Descending inputs are shown to be involved in an ongoing manner during locomotion, as it has been found that CPGs are phasically driving the same descending systems that themselves activate the CPGs.  
    Similarly, sensory inputs are being actively processed by the CPG and, here again, produce a two-way interaction between sensory input and CPGs.    
    Finally, mechanical factors are shown to be major contributors to the form of the movement.  Thus, overall the CPG can only be considered as one of several contributors to any movement; all concurrently process the flow of information."  
    Neurotransmitters
"
descending inputs initiate stereotyped movements" is interesting, but it doesn't tell us anything about the neurotransmitters. 
    112 Related citations
http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed&from_uid=1330203   


1992   
615<667 
Activation of the central pattern generators for locomotion by serotonin and excitatory amino acids in neonatal rat. 
    "1. The role of serotonin (5-HT) and excitatory amino-acids (EAAs) in the activation of the neural networks (i.e. the central pattern generators) that organize locomotion in mammals was investigated in an isolated brainstem-spinal cord preparation from the newborn rat.  
    2. The neuroactive substances were bath applied and the activity of fictive locomotion was recorded in the ventral roots.  
    3. Serotonin initiated an alternating pattern of right and left action potential bursts. The period of this rhythm was dose dependent, i.e. it decreased from around 10 s at 2 x 10(-5) M to 5 s at 10(-4) M. The effects of serotonin were blocked by a 5-HT1 antagonist (propranolol) and by 5-HT2 antagonists (ketanserin, cyproheptadine, mianserin). 5-HT3 antagonists were ineffective. The effects of methoxytryptamine, a non-selective 5-HT agonist, mimicked the 5-HT effects.  
    4. The endogenous EAAs, glutamate and aspartate, also triggered an alternating rhythmic pattern. Their effects were blocked by 2-amino-5-phosphonovaleric acid (AP-5; a N-methyl-D-aspartate (NMDA) receptor blocker) and 6,7-dinitro-quinoxaline-2,3-dione (a non-NMDA receptor blocker).  
    5. Several EAA agonists (N-methyl-D,L-aspartate (NMA) and kainate) initiated rhythmic activity." 
    Neurotransmitters
Both 5HT and glutamate triggered an alternating rhythmic activity.   


1994   
606<667     Free PMC Article   
GABAergic inactivation of the central pattern generators for locomotion in isolated neonatal rat spinal cord. 
    "
1. Experiments were performed using an isolated brainstem-spinal cord preparation from newborn rats, in order to study the GABAergic control of the spinal neuronal networks that generate locomotor rhythms in mammals. Locomotor-like activities were recorded in the ventral roots, and the various neurochemical compounds were added to the superfusion saline.  
    2. Bath application of GABA suppressed in a dose-dependent manner the motor activity induced by an
excitatory amino acid N-methyl-D,L-aspartate (NMA). Both the GABAA agonist muscimol and the GABAB agonist baclofen mimicked the effects of GABA, since they either slowed down or stopped the rhythmic activity.
    3. Experiments were performed in which the lumbar compartment was superfused separately from the brainstem. Chemical activation of the brainstem by NMA alone failed to induce locomotor-like activity. When GABAA (bicuculline) and GABAB (phaclofen) antagonists were simultaneously bath applied to the lumbar spinal cord, however, locomotor-like activity was induced.  
    4. The GABA uptake inhibitors nipecotic acid and guvacine suppressed the rhythmic motor pattern induced by NMA in a dose-dependent manner. The effects of nipecotic acid were reversed by bicuculline and phaclofen.  
    5. Bicuculline added during NMA-induced locomotor-like activity greatly increased both the frequency and amplitude of motor bursts, while phaclofen modified only the frequency.  
    6. The motor pattern depended on the balance between activatory and inactivatory influences, since the rhythmic patterns recorded with low doses of NMA associated with high doses of bicuculline were similar to those elicited by higher doses of NMA associated with low doses of bicuculline.. Both the GABAA agonist muscimol and the GABAB agonist baclofen mimicked the effects of GABA, since they either slowed down or stopped the rhythmic activity.  
    Neurotransmitters
GABA, agonists, antiagonists, baclofen, muscimol, bicuculline, phaclofen, nipecotic acid, guvacine   and   an excitatory amino acid N-methyl-D,L-aspartate (NMA),  
    Summary
    "
Both the GABAA agonist muscimol and the GABAB agonist baclofen mimicked the effects of GABA, since they either slowed down or stopped the rhythmic activity."  


1994     (not from PubMed search for "central pattern generators". )
Spinal pattern generation.   
http://www.ncbi.nlm.nih.gov/pubmed/7888774  
    My comment
General review.  Not very helpful. 
    176 Similar articles


Note: 

I just realized that, although I have been viewing the Grillner references in the context of central pattern generators (CPGs), none of the Grillner references mentions them.  That doesn't mean that they aren't there, he just doesn't use that label.  Instead, he discusses the connections between neurons and interneurons which comprise the CPGs without naming them as such. 

I could, of course, go back and re-review the 171 reference titles I've looked at up to this point, but I'm too lazy.  So, starting from here, I'm going to start looking for possible components of CPGs at the same time that I'm looking for afferent input into the CPGs.


1996    577<667
Spatiotemporal characteristics of 5-HT and dopamine-induced rhythmic hindlimb activity in the in vitro neonatal rat. 
    "
We conclude, that 5-HT and dopamine can activate spinal central pattern generators (CPGs) that already at birth are able to produce distinct patterns of motor activity. Modulatory inputs thus seems to be able to reconfigure the CPGs to produce specific motor outputs."  
    Neurotransmitters:   
5-HT, dopamine 


1996    170<349 
Neural networks for vertebrate locomotion.

http://www.ncbi.nlm.nih.gov/pubmed/8533066  
    See:  GABA/Glycine Inhibition  .



1996    (not from PubMed search for "central pattern generators". )
Neurons, networks, and motor behavior
http://www.ncbi.nlm.nih.gov/pubmed/8789940
    This is an introduction to "The International Symposium on Neurons, Networks, and Motor Behavior held in Tucson, Arizona (November 8–11, 1995)". 
     A longer summary of the conference can be found at:
http://www.sciencedirect.com/science/article/pii/S0896627300800434 .  
    Interesting observations
Neuromodulation
" Metabotropic glutamate receptors enhance the production of plateaus and produce a wind-up effect whereby repeated constant depolarizing current pulses evoke progressively more spikes per pulse.  
    N-methyl-D-aspartate (NMDA) induces oscillatory properties in spinal interneurons in several species, including lamprey, frog tadpoles , and neonatal rats. 
     Non-NMDA neuromodulatory inputs also turn on bursting properties in tadpole spinal neurons, stomatogastric neurons, and locust flight neurons  and can alter the bursting patterns produced by the mammalian respiratory rhythm in the pre-Bötzinger complex of the ventral medulla. Thus, complex oscillatory properties of neurons can be quite plastic under the influence of neuromodulatory substances."  
    "Modulatory substances alter properties of neurons in motor systems on a moment by moment basis, but they can also cause long-term developmental changes."  
    "
In lampreys, which use their entire bodies for swimming, the CPG appears to be segmental; each body segment has its own oscillator"  
    "
We have known about the mesencephalic locomotor region (MLR) for 30 years ... Despite this long history, the identity of the neurons and the nature of the command produced by the MLR have remained elusive."  
    "...
most behaviors can be initiated through a number of different pathways, and therefore no one neuron or set of neurons is likely to issue the command to produce a behavior."  
    "
There has been a revolutionary shift in thinking from hard-wired circuits to multifunctional networks."  
    The longer summary contains many active links to references, and there are also many interesting titles among the
    378 PubMed Related citations:
http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed&from_uid=8789940
    and the 5 PubMed Cited by's:
http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed_citedin&from_uid=8789940  
     My comments
1.  My  Locomotion Sequence Revision  is clearly over-simplified. 
2.  The focus on "metabotropic glutamate receptors" biases the article toward excitation.  There is no consideration of inhibition. 

Neurotransmitters
Metabotropic glutamate receptors - N-methyl-D-aspartate (NMDA) - Non-NMDA neuromodulatory inputs -


1996   
(not from PubMed search for "central pattern generators". )
Interaction between the caudal brainstem and the lamprey central pattern generator for locomotion.
http://www.ncbi.nlm.nih.gov/pubmed/8895883
    "Because of its remarkable simplicity and the robustness of the isolated preparation, the lamprey has been used as a model system to study locomotion and its central pattern generator. The function of the spinal cord is relatively well understood in this context, but the role of the brain or even the caudal brainstem remains less so.    
    We here present a study of the interaction between the caudal brainstem and the spinal pattern generator for locomotion. We show that the interaction is highly complex, with both feedforward input from the brainstem to spinal cord and feedback input from the spinal cord to brainstem playing a significant role in the motor output during locomotion. The brainstem, when diffusely stimulated pharmacologically, can initiate fictive locomotion, or it can disrupt or alter the ongoing D-glutamate initiated motor output. The nature of the disruptions vary greatly, and can induce generalized irregularity, while the alterations can include accelerating or decelerating of the bursting. All behaviors are displayed with spectrograms of the motor nerve discharge. We also show that the unstimulated brainstem can disrupt as well as slow the bursting, but in a complex fashion. Finally, a slow episodic behavior initiated from the caudal brainstem is also described. This can be elicited either by D-glutamate to the brainstem or by ascending activity from the spinal cord pattern generator.  
    Thus, we demonstrate that the interaction between the brainstem and the spinal cord during the production of locomotion is highly complex. The locomotion that is exhibited by the combined brainstem-spinal cord preparation is extremely variable. This is in striking contrast to the variability of the locomotor output pharmacologically induced in the spinal cord alone. The latter preparation exhibits remarkable regularity, or upon occasion, irregularity, but not the routine irregularity or the systemic up and down changes in frequency seen with the brainstem present. However, the pattern of frequency changes induced by the brainstem is not predictable, and remains to be understood."
    Neurotransmitters
"... D-glutamate initiated motor output ..." This may be the answer to my long-standing question.    
   250 Related citations:
http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed&from_uid=8895883
    and 2 Cited by's. 





1998   
148<349
Intrinsic function of a neuronal network - a vertebrate central pattern generator.
http://www.ncbi.nlm.nih.gov/pubmed/9651523   
    "The cellular bases of vertebrate locomotor behaviour is reviewed using the lamprey as a model system. Forebrain and brainstem cell populations initiate locomotor activity via reticulospinal fibers activating a spinal network comprised of glutamatergic and glycinergic interneurons. The role of different subtypes of Ca2+ channels, Ca2+ dependent K+ channels and voltage dependent NMDA channels at the neuronal and network level is in focus as well as the effects of different metabotropic, aminergic and peptidergic modulators that target these ion channels. This is one of the few vertebrate networks that is understood at a cellular level."  
    My comment
" Forebrain and brainstem cell populations initiate locomotor activity via reticulospinal fibers activating a spinal network comprised of glutamatergic and glycinergic interneurons."   
    This implies that the interneurons may be either glutamatergic or glycinergic, but it doesn't say anything about the neurotransmitter employed by the cell populations which initiate the locomotor activity.         
    Neurotransmitters
"glutamatergic and glycinergic interneurons"
    24 Cited by's: 
http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed_citedin&from_uid=9651523 
    CPG rather than input  



2002    496<667      Free full text   
The requirement of presynaptic metabotropic glutamate receptors for the maintenance of locomotion.
    "
Spinal circuits known as central pattern generators maintain vertebrate locomotion. In the lamprey, the contralaterally alternating ventral root activity that defines this behavior is driven by ipsilateral glutamatergic excitation (Buchanan and Grillner, 1987) coupled with crossed glycinergic inhibition (Buchanan, 1982; Alford and Williams, 1989). These mechanisms are distributed throughout the spinal cord. Glutamatergic excitatory synapses activate AMPA and NMDA receptors known to be necessary for the maintenance of the locomotor rhythm. Less is known of the role and location of metabotropic glutamate receptors (mGluRs), although group I mGluRs enhance transmitter release at giant synapses in the lamprey spinal cord, whereas group II/III receptors may inhibit release.  
    In this study we show that group I mGluR antagonists block fictive locomotion, a neural correlate of locomotion, by acting at the presynaptic terminal. Under physiological conditions, synaptically released glutamate activates presynaptic group I mGluRs (autoreceptors) during the repetitive activation of glutamatergic terminals. The resulting rise in [Ca2+]i caused by the release from presynaptic intracellular stores is coincident with an enhancement of synaptic transmission. Thus, blocking mGluRs reduces glutamate release during the repetitive activity that is characteristic of locomotion, leading to the arrest of locomotor activity. We found the effects of group I mGluRs on locomotion to be inconsistent with a postsynaptic effect on the central pattern generator. Consequently, the activation of metabotropic glutamate autoreceptors is necessary to maintain rhythmic motor output. Our results demonstrate the role of presynaptic mGluRs in the physiological control of movement for the first time."  
    Neurotransmitters
"ipsilateral glutamatergic excitation  coupled with crossed glycinergic inhibition" 
"Glutamatergic excitatory synapses activate AMPA and NMDA receptors"   
"
metabotropic glutamate receptors (mGluRs) ... group I mGluRs"  
"
group II/III receptors"     "group I mGluR antagonists
"
synaptically released glutamate activates presynaptic group I mGluRs (autoreceptors) "  


2003   
481<667 
The pharmacology of vertebrate spinal central pattern generators.
    "
Activation and excitation of activity is driven by descending, sensory, and intraspinal glutamatergic neurons. NMDA receptor activation may also lead to the activation of oscillatory properties in individual neurons that depend on an array of ion channels situated in those neurons. Coordination across joints or the midline of the animal is driven primarily by glycinergic inhibition. In addition to these processes, numerous modulatory mechanisms alter the function of the central pattern generator. These include metabotropic amino acid receptors activated by rhythmic release of glutamate and GABA as well as monoamines, ACh, and peptides."  
    Neurotransmitters
"
descending, sensory, and intraspinal glutamatergic neurons"  
"
NMDA receptor activation
"
glycinergic inhibition"  
"
metabotropic amino acid receptors activated by rhythmic release of glutamate and GABA as well as monoamines, ACh, and peptides."  

KEY POINT

    "
Activation and excitation of activity is driven by descending, sensory, and intraspinal glutamatergic neurons." 



2004    467<667     Free Article   
Central pattern generators deciphered by molecular genetics. 
http://www.ncbi.nlm.nih.gov/pubmed/14766172   
    Note:  The diagram and explanation, below, are from the free Full Text Article, not the Abstract.
    "The assembly of ion channels and their distribution in the membrane of CPG neurons will dictate how they react to and interpret synaptic inputs from other neurons in the network. In addition, neuromodulators such as glutamate acting on metabotropic glutamate receptors will affect the intrinsic membrane properties and may reconfigure the motor output.   



http://www.cell.com/cms/attachment/572217/4233342/gr1_lrg.jpg


Figure 1

Schematic Model of the Basic Connectivity Pattern in the Lamprey CPG

Each segment along the spinal cord is thought to contain a CPG network with neurons on the left and right side of the cord. The segmental CPG networks are connected with fibers running along the cord (not shown in the figure). The CPG activity is turned on by activity in glutamatergic fibers originating from neurons in the reticular formation. These descending fibers are acting on NMDA and non-NMDA receptors. Excitatory ipsilaterally projecting neurons (E) provide the rhythmic excitation of motor neurons (M) and other Es. The commissural interneurons (Is) that have axons crossing the midline inhibit all CPG neurons and MNs on the other side of the cord, ensuring that when one side is active the other is shot off. Adapted from Grillner, 2003.


KEY POINT

    "
The CPG activity is turned on by activity in glutamatergic fibers originating from neurons in the reticular formation."  

    Neurotransmitters
glutamate,  metabotropic glutamate receptors


2004    743<1206 
Defense reaction mediated by NMDA mechanisms in the inferior colliculus is modulated by GABAergic nigro-collicular pathways.  
http://www.ncbi.nlm.nih.gov/pubmed/14746929            
    See:  Fear  for full Abstract, Related citations and Cited by's.   



2004    740<1206 
Mechanisms and significance of reduced activity and responsiveness in resting frog tadpoles.   
http://www.ncbi.nlm.nih.gov/pubmed/14978054       
    "This leads to tonic GABA inhibition that reduces tadpole activity and responses, and leads to fewer attacks by predators."  
    See:  GABA/Glycine Inhibition  for full Abstract, Related citations, Cited by's and Full Free Text.  


2004   739<1206 
Brainstem control of activity and responsiveness in resting frog tadpoles: tonic inhibition.    
http://www.ncbi.nlm.nih.gov/pubmed/14991305      
    "We provide evidence supporting the hypothesis that long-term reduced responsiveness in attached tadpoles results from tonic activity in the reticulospinal GABAergic pathway mediating the stopping response."  
    See:   Reticulospinal Transmission   for full Abstract, Related citations and Cited by's.   




2006   
428<667
Tuning and playing a motor rhythm: how metabotropic glutamate receptors orchestrate generation of motor patterns in the mammalian central nervous system.     
Free PMC Article   
    "
One emerging mechanism is activation of glutamate metabotropic receptors (mGluRs) belonging to group I, while group II and III mGluRs appear to play an inhibitory function on sensory inputs."  
    Neurotransmitters
glutamate metabotropic receptors 

2007    404<667 
GABAergic output of the basal ganglia.
    See:  Basal Ganglia  for full Abstract, Related citations and Cited by's. 
    Neurotransmitter:    GABA 


2007   
395<667       Free PMC Article   
Muscarinic receptor activation elicits sustained, recurring depolarizations in reticulospinal neurons.   

http://www.ncbi.nlm.nih.gov/pubmed/17344371   
    "
In lampreys, brain stem reticulospinal (RS) neurons constitute the main descending input to the spinal cord and activate the spinal locomotor central pattern generators. Cholinergic nicotinic inputs activate RS neurons, and consequently, induce locomotion.  Cholinergic muscarinic agonists also induce locomotion when applied to the brain stem of birds. "  
    "
We propose that unilateral mAchR activation on specific cells in the caudal rhombencephalon activates a circuit that generates synchronous sustained, recurring depolarizations in bilateral populations of RS neurons."  
    Neurotransmitter:    Acetylcholine 


2009    674<1465 
Neuroethological approach to frontolimbic epileptic seizures and parasomnias 
https://www.ncbi.nlm.nih.gov/pubmed/19733874  
    "
CPG are located at the subcortical level (mainly in the brain stem and spinal cord)"   


2009   
323<667      Free PMC Article   
Optogenetic dissection of a behavioural module in the vertebrate spinal cord   

    "Locomotion relies on neural networks called central pattern generators (CPGs) that generate periodic motor commands for rhythmic movements.  
    In vertebrates, the excitatory synaptic drive for inducing the spinal CPG can originate from either supraspinal glutamatergic inputs or from within the spinal cord. Here we identify a spinal input to the CPG that drives spontaneous locomotion using a combination of intersectional gene expression and optogenetics in zebrafish larvae.  
    The photo-stimulation of one specific cell type was sufficient to induce a symmetrical tail beating sequence that mimics spontaneous slow forward swimming. This neuron is the Kolmer-Agduhr cell, which extends cilia into the central cerebrospinal-fluid-containing canal of the spinal cord and has an ipsilateral ascending axon that terminates in a series of consecutive segments. Genetically silencing Kolmer-Agduhr cells reduced the frequency of spontaneous free swimming, indicating that activity of Kolmer-Agduhr cells provides necessary tone for spontaneous forward swimming. Kolmer-Agduhr cells have been known for over 75 years, but their function has been mysterious. Our results reveal that during early development in zebrafish these cells provide a positive drive to the spinal CPG for spontaneous locomotion."  
    Neurotransmitter:   Glutamate   

Key Point:   

    "the excitatory synaptic drive for inducing the spinal CPG can originate from either supraspinal glutamatergic inputs ..."  



2010     308<667
Activation of groups of excitatory neurons in the mammalian spinal cord or hindbrain evokes locomotion. 
    "
Our results indicate that glutamatergic neurons in the spinal cord are critical for initiating or maintaining the rhythm and that activation of hindbrain areas containing the locomotor command regions is sufficient to directly activate the spinal locomotor network."  
    Neurotransmitter
Glutamate     


2012 
Evolution of the basal ganglia: dual-output pathways conserved throughout vertebrate phylogeny. 
http://www.ncbi.nlm.nih.gov/pubmed/22351244
    See:   GABA/Glycine Inhibition  . 



2013    23<349 
Independent circuits in the basal ganglia for the evaluation and selection of actions.   
See:  Basal Ganglia for full Abstract, Related citations, Cited by's and  
 - Free PMC Article



2013     18<349
The evolutionary origin of the vertebrate basal ganglia and its role in action selection.
   
See:  Basal Ganglia for full Abstract, Related citations, Cited by's and  
 Free PMC Article .    


2014
  112>667
Serotonergic modulation of post-synaptic inhibition and locomotor alternating pattern in the spinal cord. 
   
Free PMC Article   
    "
Experiments aimed at either reducing the endogenous level of serotonin in the spinal cord or blocking the activation of 5-HT2 receptors.  
    We then describe recent evidence that the action of 5-HT2 receptors is mediated, at least in part, through a modulation of chloride homeostasis. The postsynaptic action of GABA and glycine depends on the intracellular concentration of chloride ions which is regulated by a protein in the plasma membrane, the K(+)-Cl(-) cotransporter (KCC2) extruding both K(+) and Cl(-) ions. Absence or reduction of KCC2 expression leads to a depolarizing action of GABA and glycine and a marked reduction in the strength of postsynaptic inhibition."  
    Neurotransmitters
5-HT, GABA, glycine, K(+)-Cl(-) cotransporter (KCC2) 


2014
  85<667
GABAergic and glycinergic inputs modulate rhythmogenic mechanisms in the lamprey respiratory network.      Free PMC Article   
    "
We have previously shown that GABA and glycine modulate respiratory activity in the in vitro brainstem preparations of the lamprey and that blockade of GABAA and glycine receptors restores the respiratory rhythm during apnoea caused by blockade of ionotropic glutamate receptors. "   
    Neurotransmitters
GABA, glycine, ionotropic glutamate receptors 


2014    77<667
The motor output of hindlimb innervating segments of the spinal cord is modulated by cholinergic activation of rostrally projecting sacral relay neurons. 
    "
Cholinergic networks have been shown to be involved in generation and modulation of the locomotor rhythmic pattern produced by the mammalian central pattern generators. Here, we show that changes in the endogenous levels of acetylcholine in the sacral segments of the isolated spinal cord of the neonatal rat modulate the locomotor-related output produced by stimulation of sacrocaudal afferents in muscarinic receptor-dependent mechanisms."   
    Neurotransmitters
Acetylcholine, muscarinic receptor 


2014
     73<667    
Free PMC Article   
Neural control and modulation of swimming speed in the larval zebrafish. 
    "
Vertebrate locomotion at different speeds is driven by descending excitatory connections to central pattern generators in the spinal cord."    


2014   
64<667
Neuroanatomical basis for cholinergic modulation of locomotor networks by sacral relay neurons with ascending lumbar projections.
 
    "
Thus, pharmacological manipulations of the sacral cholinergic system may be used to modulate the locomotor-related motor output in the absence of descending supraspinal control."  
    Neurotransmitter
Acetylcholine 


2014   62<667
Differential modulation of descending signals from the reticulospinal system during reaching and locomotion   
http://www.ncbi.nlm.nih.gov/pubmed/25143539   
    "We tested the hypothesis that the same spinal interneuronal pathways are activated by the reticulospinal system during locomotion and reaching. If such were the case, we expected that microstimulation within the pontomedullary reticular formation (PMRF) would evoke qualitatively similar responses in muscles active during both behaviors. To test this, we stimulated in 47 sites within the PMRF during both tasks.  
    Stimulation during locomotion always produced a strongly phase-dependent, bilateral pattern of activity in which activity in muscles was generally facilitated or suppressed during one phase of activity (swing or stance) and was unaffected in the other.  
    During reaching, stimulation generally activated the same muscles as during locomotion, although the modulation of the magnitude of the evoked responses was less limb dependent than during locomotion. An exception was found for some forelimb flexor muscles that were strongly facilitated by stimulation during the swing phase of locomotion but were not influenced by stimulation during the transport phase of the reach.  
     We suggest that during locomotion the activity in interneuronal pathways mediating signals from the reticulospinal system is subject to strong modulation by the central pattern generator for locomotion. During reach, we suggest that, for most muscles, the same spinal interneuronal pathways are used to modify muscle activity but are not as strongly gated according to limb use as during locomotion. Finally, we propose that the command for movement during discrete voluntary movements suppresses the influence of the reticulospinal system on selected forelimb flexor muscles, possibly to enhance fractionated control of movement. "     



2016   2<667 
Evolution of central pattern generators and rhythmic behaviours   
http://www.ncbi.nlm.nih.gov/pubmed/26598733   
    "Comparisons of rhythmic movements and the central pattern generators (CPGs) that control them uncover principles about the evolution of behaviour and neural circuits. Over the course of evolutionary history, gradual evolution of behaviours and their neural circuitry within any lineage of animals has been a predominant occurrence. Small changes in gene regulation can lead to divergence of circuit organization and corresponding changes in behaviour. However, some behavioural divergence has resulted from large-scale rewiring of the neural network. Divergence of CPG circuits has also occurred without a corresponding change in behaviour. When analogous rhythmic behaviours have evolved independently, it has generally been with different neural mechanisms. Repeated evolution of particular rhythmic behaviours has occurred within some lineages due to parallel evolution or latent CPGs. Particular motor pattern generating mechanisms have also evolved independently in separate lineages.  
    The evolution of CPGs and rhythmic behaviours shows that although most behaviours and neural circuits are highly conserved, the nature of the behaviour does not dictate the neural mechanism and that the presence of homologous neural components does not determine the behaviour. This suggests that although behaviour is generated by neural circuits, natural selection can act separately on these two levels of biological organization. "   
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