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Motor Output (motor + output)
Selected AbstractsDecrease in cerebral oxygenation influences central motor output in humansACTA PHYSIOLOGICA, Issue 3 2009S. Perrey No abstract is available for this article. [source] The zebrafish ennui behavioral mutation disrupts acetylcholine receptor localization and motor axon stabilityDEVELOPMENTAL NEUROBIOLOGY, Issue 1 2008Louis Saint-Amant Abstract The zebrafish ennui mutation was identified from a mutagenesis screen for defects in early behavior. Homozygous ennui embryos swam more slowly than wild-type siblings but normal swimming recovered during larval stages and homozygous mutants survived until adulthood. Electrophysiological recordings from motoneurons and muscles suggested that the motor output of the CNS following mechanosensory stimulation was normal in ennui, but the synaptic currents at the neuromuscular junction were significantly reduced. Analysis of acetylcholine receptors (AChRs) in ennui muscles showed a marked reduction in the size of synaptic clusters and their aberrant localization at the myotome segment borders of fast twitch muscle. Prepatterned, nerve-independent AChR clusters appeared normal in mutant embryos and dispersed upon outgrowth of motor axons onto the muscles. Genetic mosaic analysis showed that ennui is required cell autonomously in muscle fibers for normal synaptic localization of AChRs. Furthermore, exogenous agrin failed to induce AChR aggregation, suggesting that ennui is crucial for agrin function. Finally, motor axons branched more extensively in ennui fast twitch muscles especially in the region of the myotome borders. These results suggest that ennui is important for nerve-dependent AChR clustering and the stability of axon growth. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2008 [source] Increasing stereotypy in adult zebra finch song correlates with a declining rate of adult neurogenesisDEVELOPMENTAL NEUROBIOLOGY, Issue 13 2007Carolyn L. Pytte Abstract Adult neurogenesis is often correlated with learning new tasks, suggesting that a function of incorporating new neurons is to permit new memory formation. However, in the zebra finch, neurons are added to the song motor pathway throughout life, long after the initial song motor pattern is acquired by about 3 months of age. To explore this paradox, we examined the relationship between adult song structure and neuron addition using sensitive measures of song acoustic structure. We report that between 4 and 15 months of age there was an increase in the stereotypy of fine-grained spectral and temporal features of syllable acoustic structure. These results indicate that the zebra finch continues to refine motor output, perhaps by practice, over a protracted period beyond the time when song is first learned. Over the same age range, there was a decrease in the addition of new neurons to HVC, a region necessary for song production, but not to Area X or the hippocampus, regions not essential for singing. We propose that age-related changes in the stereotypy of syllable acoustic structure and HVC neuron addition are functionally related. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007. [source] Consistent dynamics suggests tight regulation of biophysical parameters in a small network of bursting neuronsDEVELOPMENTAL NEUROBIOLOGY, Issue 14 2006Attila Szücs Abstract The neuronal firing patterns in the pyloric network of crustaceans are remarkably consistent among animals. Although this characteristic of the pyloric network is well-known, the biophysical mechanisms underlying the regulation of the systems output are receiving renewed attention. Computer simulations of the pyloric network recently demonstrated that consistent motor output can be achieved from neurons with disparate biophysical parameters among animals. Here we address this hypothesis by pharmacologically manipulating the pyloric network and analyzing the emerging voltage oscillations and firing patterns. Our results show that the pyloric network of the lobster stomatogastric ganglion maintains consistent and regular firing patterns even when entire populations of specific voltage-gated channels and synaptic receptors are blocked. The variations of temporal parameters used to characterize the burst patterns of the neurons as well as their intraburst spike dynamics do not display statistically significant increase after blocking the transient K-currents (with 4-aminopyridine), the glutamatergic inhibitory synapses (with picrotoxin), or the cholinergic synapses (with atropine) in pyloric networks from different animals. These data suggest that in this very compact circuit, the biophysical parameters are cell-specific and tightly regulated. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006 [source] Parasitoid wasp sting: A cocktail of GABA, taurine, and ,-alanine opens chloride channels for central synaptic block and transient paralysis of a cockroach hostDEVELOPMENTAL NEUROBIOLOGY, Issue 8 2006Eugene L. Moore Abstract The wasp Ampulex compressa injects venom directly into the prothoracic ganglion of its cockroach host to induce a transient paralysis of the front legs. To identify the biochemical basis for this paralysis, we separated venom components according to molecular size and tested fractions for inhibition of synaptic transmission at the cockroach cercal-giant synapse. Only fractions in the low molecular weight range (<2 kDa) caused synaptic block. Dabsylation of venom components and analysis by HPLC and MALDI-TOF-MS revealed high levels of GABA (25 mM), and its receptor agonists ,-alanine (18 mM), and taurine (9 mM) in the active fractions. Each component produces transient block of synaptic transmission at the cercal-giant synapse and block of efferent motor output from the prothoracic ganglion, which mimics effects produced by injection of whole venom. Whole venom evokes picrotoxin-sensitive chloride currents in cockroach central neurons, consistent with a GABAergic action. Together these data demonstrate that Ampulex utilizes GABAergic chloride channel activation as a strategy for central synaptic block to induce transient and focal leg paralysis in its host. © 2006 Wiley Periodicals, Inc. © 2006 Wiley Periodicals, Inc. J Neurobiol, 2006 [source] Persistent rhythmic oscillations induced by nicotine on neonatal rat hypoglossal motoneurons in vitroEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2006Nerijus Lamanauskas Abstract Patch-clamp recording from hypoglossal motoneurons in neonatal Wistar rat brainstem slices was used to investigate the electrophysiological effects of bath-applied nicotine (10 µm). While nicotine consistently evoked membrane depolarization (or inward current under voltage clamp), it also induced electrical oscillations (3,13 Hz; lasting for , 8.5 min) on 40% of motoneurons. Oscillations required activation of nicotinic receptors sensitive to dihydro-,-erythroidine (0.5 µm) or methyllycaconitine (5 nm), and were accompanied by enhanced frequency of spontaneous glutamatergic events. The slight voltage dependence of oscillations and their block by the gap junction blocker, carbenoxolone, suggest they originate from electrically coupled neurons. Network nicotinic receptors desensitized more slowly than motoneuron ones, demonstrating that network receptors remained active longer to support heightened release of the endogenous glutamate necessary for enhancing the network excitability. The ionotropic glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and the group I metabotropic receptor antagonist, (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), suppressed oscillations, while the NMDA receptor antagonist, d -amino-phosphonovaleriate (APV), produced minimal depression. Nicotine-evoked oscillations constrained spike firing at low rates, although motoneurons could still generate high-frequency trains of action potentials with unchanged gain for input depolarization. This is the first demonstration that persistent activation of nicotinic receptors could cause release of endogenous glutamate to evoke sustained oscillations in the theta frequency range. As this phenomenon likely represented a powerful process to coordinate motor output to tongue muscles, our results outline neuronal nicotinic acetylcholine receptors (nAChRs) as a novel target for pharmacological enhancement of motoneuron output in motor dysfunction. [source] Intermittent hypoxia and respiratory plasticity in humans and other animals: does exposure to intermittent hypoxia promote or mitigate sleep apnoea?EXPERIMENTAL PHYSIOLOGY, Issue 3 2009Jason H. Mateika This review focuses on two phenomena that are initiated during and after exposure to intermittent hypoxia. The two phenomena are referred to as long-term facilitation and progressive augmentation of respiratory motor output. Both phenomena are forms of respiratory plasticity. Long-term facilitation is characterized by a sustained elevation in respiratory activity after exposure to intermittent hypoxia. Progressive augmentation is characterized by a gradual increase in respiratory activity from the initial to the final hypoxic exposure. There is much speculation that long-term facilitation may have a significant role in individuals with sleep apnoea because this disorder is characterized by periods of upper airway collapse accompanied by intermittent hypoxia, one stimulus known to induce long-term facilitation. It has been suggested that activation of long-term facilitation may serve to mitigate apnoea by facilitating ventilation and, more importantly, upper airway muscle activity. We examine the less discussed but equally plausible situation that exposure to intermittent hypoxia might ultimately lead to the promotion of apnoea. There are at least two scenarios in which apnoea might be promoted following exposure to intermittent hypoxia. In both scenarios, long-term facilitation of upper airway muscle activity is initiated but ultimately rendered ineffective because of other physiological conditions. Thus, one of the primary goals of this review is to discuss, with support from basic and clinical studies, whether various forms of respiratory motor neuronal plasticity have a beneficial and/or a detrimental impact on breathing stability in individuals with sleep apnoea. [source] Improving functional magnetic resonance imaging motor studies through simultaneous electromyography recordingsHUMAN BRAIN MAPPING, Issue 9 2007Bradley J. MacIntosh Abstract Specially designed optoelectronic and data postprocessing methods are described that permit electromyography (EMG) of muscle activity simultaneous with functional MRI (fMRI). Hardware characterization and validation included simultaneous EMG and event-related fMRI in 17 healthy participants during either ankle (n = 12), index finger (n = 3), or wrist (n = 2) contractions cued by visual stimuli. Principal component analysis (PCA) and independent component analysis (ICA) were evaluated for their ability to remove residual fMRI gradient-induced signal contamination in EMG data. Contractions of ankle tibialis anterior and index finger abductor were clearly distinguishable, although observing contractions from the wrist flexors proved more challenging. To demonstrate the potential utility of simultaneous EMG and fMRI, data from the ankle experiments were analyzed using two approaches: 1) assuming contractions coincided precisely with visual cues, and 2) using EMG to time the onset and offset of muscle contraction precisely for each participant. Both methods produced complementary activation maps, although the EMG-guided approach recovered more active brain voxels and revealed activity better in the basal ganglia and cerebellum. Furthermore, numerical simulations confirmed that precise knowledge of behavioral responses, such as those provided by EMG, are much more important for event-related experimental designs compared to block designs. This simultaneous EMG and fMRI methodology has important applications where the amplitude or timing of motor output is impaired, such as after stroke. Hum Brain Mapp 2006. © 2006 Wiley-Liss, Inc. [source] Ultrastructure of the tentacle nerve plexus and putative neural pathways in sea anemonesINVERTEBRATE BIOLOGY, Issue 3 2002Jane A. Westfall Abstract. Neurons of sea anemone tentacles receive stimuli via sensory cells and process and transmit information via a plexus of nerve fibers. The nerve plexus is best revealed by scanning electron microscopy of epidermal peels of the tentacles. The nerve plexus lies above the epidermal muscular layer where it appears as numerous parallel longitudinal and short interconnected nerve fibers in Calliactis parasitica. Bipolar and multipolar neurons are present and neurites form interneuronal and neuromuscular synaptic contacts. Transmission electron microscopy of cross sections of tentacles of small animals, both C. parasitica and Aiptasia pallida, reveals bundles of 50,100 nerve fibers lying above groups of longitudinal muscle fibers separated by intrusions of mesoglea. Smaller groups of 10,50 slender nerve fibers are oriented at right angles to the circular muscle formed by the bases of the digestive cells. The unmyelinated nerve fibers lack any glial wrapping, although some bundles of epidermal fibers are partially enveloped by cytoplasmic extensions of the muscle cells; small gastrodermal nerve bundles lie between digestive epithelial cells above their basal myonemes. A hypothetical model for sensory input and motor output in the epidermal and gastrodermal nerve plexuses of sea anemones is proposed. [source] Sensory functions in dystonia: Insights from behavioral studies,,MOVEMENT DISORDERS, Issue 10 2009Michele Tinazzi MD Abstract The pathophysiology of primary dystonia is thought to involve dysfunction of the basal ganglia cortico-striatal-thalamo-cortical motor circuits. In the past, emphasis was placed on the role of the basal ganglia in controlling movements; in more recent times, however, it has also become clear that they play an important part in sensory as well as cognitive functions. Here, we review evidence for dysfunction of sensory processing in patients with dystonia, and speculate that this may lead to abnormalities in a crucial role of the basal ganglia that links sensory information to appropriate motor output. Sensory function, particularly in the somatosensory domain, has been shown to be compromised in patients with primary dystonia, both in adult onset focal dystonia and in genetically characterized DYT1 dystonia. Given that nonaffected DYT1 gene carriers may show similar abnormalities to clinically affected individuals, sensory deficits could constitute a subclinical endophenotypic trait of disease that precedes overt clinical manifestations. Whether they can trigger primary dystonia or are an epiphenomenon is an issue warranting further study, but the fact that a number of different neurorehabilitative approaches explicitly manipulate somatosensory inputs to improve motor function suggests there may be a causal link between them. We believe that in future, randomized, blind and controlled studies in large patient populations should address this issue, providing efficient strategies to aid functional recovery, particularly in focal hand dystonia, where the available medical treatments offer little benefit. © 2009 Movement Disorder Society [source] Mechanisms underlying mirror movements in Parkinson's disease: A transcranial magnetic stimulation studyMOVEMENT DISORDERS, Issue 7 2006Massimo Cincotta MD Abstract The neural mechanisms underlying unintended mirror movements (MMs) of one hand during unimanual movements of the other hand in patients with Parkinson's disease (PD) are largely unexplored. Here we used surface electromyographic (EMG) analysis and focal transcranial magnetic stimulation (TMS) to investigate the pathophysiological substrate of MMs in four PD patients. Surface EMG was recorded from both abductor pollicis brevis (APB) and first dorsal interosseous (FDI) muscles. Cross-correlation EMG analysis revealed no common motor drive to the two APBs during intended unimanual tasks. Focal TMS of either primary motor cortex (M1) elicited normal motor-evoked potentials (MEPs) in the contralateral APB, whereas MEPs were not seen in the ipsilateral hand. During either mirror or voluntary APB contraction, focal TMS of the contralateral M1 produced a long-lasting silent period (SP), whereas stimulation of the ipsilateral M1 produced a short-lasting SP. During either mirror or voluntary finger tapping, 5 Hz repetitive TMS (rTMS) of the contralateral M1 disrupted EMG activity in the target FDI, whereas the effects of rTMS of the ipsilateral M1 were by far slighter. During either mirror or voluntary APB contraction, paired-pulse TMS showed a reduction of short-interval intracortical inhibition in the contralateral M1. These findings provide converging evidence that, in PD, MMs do not depend on unmasking of ipsilateral projections but are explained by motor output along the crossed corticospinal projection from the mirror M1. © 2006 Movement Disorder Society [source] Transient improvement induced by motor fatigue in focal occupational dystonia: The handgrip testMOVEMENT DISORDERS, Issue 6 2001Alessandra Pesenti MD Abstract Muscle fatigue induced by a previous sustained contraction temporarily decreases the motor output, transiently worsening motor performance. Whether muscle fatigue alters motor performance also in dystonia,a disorder whose main pathophysiological abnormality is motor overflow,remains unknown. To assess the effects of muscle fatigue in patients with focal occupational upper limb dystonia, we studied the effect of a previous maximum fatiguing voluntary contraction on motor performance in 10 musicians with focal occupational dystonia, in 3 musicians with hand motor impairment due to non-dystonic disorders, and in 5 normal musicians. The fatiguing task consisted of grasping a spring handgrip as long as possible until the task failed. In dystonic musicians, a fatiguing contraction significantly improved motor performance. The improvement lasted less than 5 minutes and appeared only after fatigue of the affected upper limb. In contrast, in musicians with non-dystonic motor impairment, motor performance remained unchanged or worsened, and normal musician performance consistently worsened. © 2001 Movement Disorder Society. [source] Fluctuations in isometric muscle force can be described by one linear projection of low-frequency components of motor unit discharge ratesTHE JOURNAL OF PHYSIOLOGY, Issue 24 2009Francesco Negro The aim of the study was to investigate the relation between linear transformations of motor unit discharge rates and muscle force. Intramuscular (wire electrodes) and high-density surface EMG (13 × 5 electrode grid) were recorded from the abductor digiti minimi muscle of eight healthy men during 60 s contractions at 5%, 7.5% and 10% of the maximal force. Spike trains of a total of 222 motor units were identified from the EMG recordings with decomposition algorithms. Principal component analysis of the smoothed motor unit discharge rates indicated that one component (first common component, FCC) described 44.2 ± 7.5% of the total variability of the smoothed discharge rates when computed over the entire contraction interval and 64.3 ± 10.2% of the variability when computed over 5 s intervals. When the FCC was computed from four or more motor units per contraction, it correlated with the force produced by the muscle (62.7 ± 10.1%) by a greater degree (P < 0.001) than the smoothed discharge rates of individual motor units (41.4 ± 7.8%). The correlation between FCC and the force signal increased up to 71.8 ± 13.1% when the duration and the shape of the smoothing window for discharge rates were similar to the average motor unit twitch force. Moreover, the coefficients of variation (CoV) for the force and for the FCC signal were correlated in all subjects (R2 range = 0.14,0.56; P < 0.05) whereas the CoV for force was correlated to the interspike interval variability in only one subject (R2= 0.12; P < 0.05). Similar results were further obtained from measures on the tibialis anterior muscle of an additional eight subjects during contractions at forces up to 20% of the maximal force (e.g. FCC explained 59.8 ± 11.0% of variability of the smoothed discharge rates). In conclusion, one signal captures most of the underlying variability of the low-frequency components of motor unit discharge rates and explains large part of the fluctuations in the motor output during isometric contractions. [source] Serotonin 5-HT2 receptor activation induces a long-lasting amplification of spinal reflex actions in the ratTHE JOURNAL OF PHYSIOLOGY, Issue 1 2001D. W. Machacek 1C-fibre activation induces a long-term potentiation (LTP) in the spinal flexion reflex in mammals, presumably to provide enhanced reflexive protection of damaged tissue from further injury. Descending monoaminergic pathways are thought to depress sensory input but may also amplify spinal reflexes; the mechanisms of this modulation within the spinal cord remain to be elucidated. 2We used electrical stimulation of primary afferents and recordings of motor output, in the rat lumbar spinal cord maintained in vitro, to demonstrate that serotonin is capable of inducing a long-lasting increase in reflex strength at all ages examined (postnatal days 2,12). 3Pharmacological analyses indicated an essential requirement for activation of 5-HT2C receptors while 5-HT1A/1B, 5-HT7 and 5-HT2A receptor activation was not required. In addition, primary afferent-evoked synaptic potentials recorded in a subpopulation of laminae III-VI spinal neurons were similarly facilitated by 5-HT. Thus, serotonin receptor-evoked facilitatory actions are complex, and may involve alterations in neuronal properties at both motoneuronal and pre-motoneuronal levels. 4This study provides the first demonstration of a descending transmitter producing a long-lasting amplification in reflex strength, accomplished by activating a specific serotonin receptor subtype. It is suggested that brain modulatory systems regulate reflex pathways to function within an appropriate range of sensori-motor gain, facilitating reflexes in behavioural situations requiring increased sensory responsiveness. [source] Visual and non-visual control of landing movements in humansTHE JOURNAL OF PHYSIOLOGY, Issue 1 2001Marco Santello 1The role of vision in controlling leg muscle activation in landing from a drop was investigated. Subjects (n= 8) performed 10 drops from four heights (0.2, 0.4, 0.6 and 0.8 m) with and without vision. Drop height was maintained constant throughout each block of trials to allow adaptation. The aim of the study was to assess the extent to which proprioceptive and vestibular information could substitute for the lack of vision in adapting landing movements to different heights. 2At the final stages of the movement, subjects experienced similar peak centre of body mass (CM) displacements and joint rotations, regardless of the availability of vision. This implies that subjects were able to adapt the control of landing to different heights. The amplitude and timing of electromyographic signals from the leg muscles scaled to drop height in a similar fashion with and without vision. 3However, variables measured throughout the execution of the movement indicated important differences. Without vision, landings were characterised by 10 % larger ground reaction forces, 10 % smaller knee joint rotations, different time lags between peak joint rotations, and more variable ground reaction forces and times to peak CM displacement. 4We conclude that non-visual sensory information (a) could not fully compensate for the lack of continuous visual feedback and (b) this non-visual information was used to reorganise the motor output. These results suggest that vision is important for the very accurate timing of muscle activity onset and the kinematics of landing. [source] Pattern Formation And Rhythm Generation In The Ventral Respiratory GroupCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2000Donald R McCrimmon SUMMARY 1. There is increasing evidence that the kernel of the rhythm-generating circuitry for breathing is located within a discrete subregion of a column of respiratory neurons within the ventrolateral medulla referred to as the ventral respiratory group (VRG). It is less clear how this rhythm is transformed into the precise patterns appearing on the varied motor outflows. 2. Two different approaches were used to test whether subregions of the VRG have distinct roles in rhythm or pattern generation. In one, clusters of VRG neurons were activated or inactivated by pressure injection of small volumes of neuroactive agents to activate or inactivate groups of respiratory neurons and the resulting effects on respiratory rhythm and pattern were determined. The underlying assumption was that if rhythm and pattern are generated by neurons in different VRG subregions, then we should be able to identify regions where activation of neurons predominantly alters rhythm with little effect on pattern and other regions where pattern is altered with little effect on rhythm. 3. Based on the pattern of phrenic nerve responses to injection of an excitatory amino acid (DL -homocysteate), the VRG was divided into four subdivisions arranged along the rostrocaudal axis. Injections into the three rostral regions elicited changes in both respiratory rhythm and pattern. From rostral to caudal the regions included: (i) a rostral bradypnoea region, roughly associated with the Bötzinger complex; (ii) a dysrhythmia/tachypnoea area, roughly associated with the pre-Bötzinger complex (PBC); (iii) a second caudal bradypnoea area; and, most caudally, (iv) a region from which no detectable change in respiratory motor output was elicited. 4. In a second approach, the effect of unilateral lesions of one subregion, the PBC, on the Breuer,Hering reflex changes in rhythm were determined. Activation of this reflex by lung inflation shortens inspiration and lengthens expiration (TE). 5. Unilateral lesions in the PBC attenuated the reflex lengthening of TE, but did not change baseline respiratory rhythm. 6. These findings are consistent with the concept that the VRG is not functionally homogeneous, but consists of rostrocaudally arranged subregions. Neurons within the so-called PBC appear to have a dominant role in rhythm generation. Nevertheless, neurons within other subregions contribute to both rhythm and pattern generation. Thus, at least at an anatomical level resolvable by pressure injection, there appears to be a significant overlap in the circuitry generating respiratory rhythm and pattern. [source] Convergence of multisensory inputs in Xenopus tadpole tectumDEVELOPMENTAL NEUROBIOLOGY, Issue 14 2009Masaki Hiramoto Abstract The integration of multisensory information takes place in the optic tectum where visual and auditory/mechanosensory inputs converge and regulate motor outputs. The circuits that integrate multisensory information are poorly understood. In an effort to identify the basic components of a multisensory integrative circuit, we determined the projections of the mechanosensory input from the periphery to the optic tectum and compared their distribution to the retinotectal inputs in Xenopus laevis tadpoles using dye-labeling methods. The peripheral ganglia of the lateral line system project to the ipsilateral hindbrain and the axons representing mechanosensory inputs along the anterior/posterior body axis are mapped along the ventrodorsal axis in the axon tract in the dorsal column of the hindbrain. Hindbrain neurons project axons to the contralateral optic tectum. The neurons from anterior and posterior hindbrain regions project axons to the dorsal and ventral tectum, respectively. While the retinotectal axons project to a superficial lamina in the tectal neuropil, the hindbrain axons project to a deep neuropil layer. Calcium imaging showed that multimodal inputs converge on tectal neurons. The layer-specific projections of the hindbrain and retinal axons suggest a functional segregation of sensory inputs to proximal and distal tectal cell dendrites, respectively. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009 [source] The Kölliker-Fuse nucleus gates the postinspiratory phase of the respiratory cycle to control inspiratory off-switch and upper airway resistance in ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2006Mathias Dutschmann Abstract Lesion or pharmacological manipulation of the dorsolateral pons can transform the breathing pattern to apneusis (pathological prolonged inspiration). Apneusis reflects a disturbed inspiratory off-switch mechanism (IOS) leading to a delayed phase transition from inspiration to expiration. Under intact conditions the IOS is irreversibly mediated via activation of postinspiratory (PI) neurons within the respiratory network. In parallel, populations of laryngeal premotoneurons manifest the IOS by a brief glottal constriction during the PI phase. We investigated effects of pontine excitation (glutamate injection) or temporary lesion after injection of a GABA-receptor agonist (isoguvacine) on the strength of PI-pool activity determined from respiratory motor outputs or kinesiological measurements of laryngeal resistance in a perfused brainstem preparation. Glutamate microinjections into distinct parts of the pontine Kölliker-Fuse nucleus (KF) evoked a tonic excitation of PI-motor activity or sustained laryngeal constriction accompanied by prolongation of the expiratory phase. Subsequent isoguvacine microinjections at the same loci abolished PI-motor or laryngeal constrictor activity, triggered apneusis and established a variable and decreased breathing frequency. In summary, we revealed that excitation or inhibition of defined areas within the KF activated and blocked PI activity and, consequently, IOS. Therefore, we conclude, first, that descending KF inputs are essential to gate PI activity required for a proper pattern formation and phase control within the respiratory network, at least during absence of pulmonary stretch receptor activity and, secondly, that the KF contains large numbers of laryngeal PI premotor neurons that might have a key role in the regulation of upper airway resistance during reflex control and vocalization. [source] Activation of MAP Kinase in Lumbar Spinothalamic Cells Is Required for EjaculationTHE JOURNAL OF SEXUAL MEDICINE, Issue 7 2010Michael D. Staudt MSc ABSTRACT Introduction., Ejaculation is a reflex controlled by a spinal ejaculation generator located in the lumbosacral spinal cord responsible for the coordination of genital sensory with autonomic and motor outputs that regulate ejaculation. In the male rat, a population of lumbar spinothalamic cells (LSt cells) comprises an essential component of the spinal ejaculation generator. LSt cells are activated with ejaculation, but the nature of the signal transduction pathways involved in this activation is unknown. Moreover, it is unknown if LSt cell activation is required for expression of ejaculation. Aim., The current study tested the hypothesis that ejaculatory reflexes are triggered via activation of the mitogen-activated protein (MAP) kinase signaling pathway in the LSt cells. Methods., Expression of phosphorylated extracellular signal-related kinases 1 and 2 (pERK) was investigated following mating behavior, or following ejaculation induced by electrical stimulation of the dorsal penile nerve (DPN) in anesthetized, spinalized male rats. Next, the effects of intrathecal or intraspinal delivery of Mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitor U0126 on DPN stimulation-induced ejaculation was examined. Main Outcome Measures., Expression of pERK in LSt cells and associated areas was analyzed. Electromyographic recordings of the bulbocavernosus muscle were recorded in anesthetized, spinalized rats. Results., Results indicate that the MAP kinase signaling pathway is activated in LSt cells following ejaculation in mating animals or induced by DPN stimulation in anesthetized, spinalized animals. Moreover, ERK activation in LSt cells is an essential trigger for ejaculation, as DPN stimulation-induced reflexes were absent following administration of MEK inhibitor in the L3-L4 spinal area. Conclusion., These data provide insight into the nature of the signal transduction pathways involved in the activation of ejaculation through LSt cells. The data demonstrate that ERK activation in LSt cells is essential for ejaculation and contribute to a more detailed understanding of the spinal generation of ejaculation. Staudt MD, de Oliveira CVR, Lehman MN, McKenna KE, and Coolen LM. Activation of MAP kinase in lumbar spinothalamic cells is required for ejaculation. 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