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Spinal Cord Preparation (spinal + cord_preparation)
Selected AbstractsAltered sensorimotor development in a transgenic mouse model of amyotrophic lateral sclerosisEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2004Julien Amendola Abstract Most neurodegenerative diseases become manifest at an adult age but abnormalities or pathological symptoms appear earlier. It is important to identify the initial mechanisms underlying such progressive neurodegenerative disease in both humans and animals. Transgenic mice expressing the familial amyotrophic lateral sclerosis (ALS)-linked mutation (G85R) in the enzyme superoxide dismutase 1 (SOD1) develop motor neuron disease at 8,10 months of age. We address the question of whether the mutation has an early impact on spinal motor networks in postnatal mutant mice. Behavioural tests showed a significant delay in righting and hind-paw grasping responses in mutant SOD1G85R mice during the first postnatal week, suggesting a transient motor deficit compared to wild-type mice. In addition, extracellular recordings from spinal ventral roots in an in vitro brainstem,spinal cord preparation demonstrated different pharmacologically induced motor activities between the two strains. Rhythmic motor activity was difficult to evoke with N -methyl- dl -aspartate and serotonin at the lumbar levels in SOD1G85R mice. In contrast to lumbar segments, rhythmic activity was similar in the sacral roots from the two strains. These results strongly support the fact that the G85R mutation may have altered lumbar spinal motor systems much earlier than previously recognized. [source] Differential maturation of motoneurons innervating ankle flexor and extensor muscles in the neonatal ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2000L Vinay Abstract The first postnatal week is a critical period for the development of posture in the rat. The use of ankle extensor muscles in postural reactions increases during this period. Changes in excitability of motoneurons are probably an important factor underlying this maturation. The aim of this study was to identify whether variations in the maturation exist between motor pools innervating antagonistic muscles. Intracellular recordings in the in vitro brain stem,spinal cord preparation of neonatal rats (from postnatal day 0,5) were used to examine the developmental changes in excitability of motoneurons innervating the ankle flexors (F-MNs) and the antigravity ankle extensors (E-MNs). No significant difference in resting potential, action potential threshold, input resistance or rheobase was observed at birth. The age-related increase in rheobase was more pronounced for F-MNs than for E-MNs. The development of discharge properties of E-MNs lagged behind that of F-MNs. More F-MNs than E-MNs were able to fire repetitively in response to current injection at birth. F-MNs discharged at a higher frequency than E-MNs at all ages. Differences in the duration of action potential afterhyperpolarization accounted, at least partly, for the differences in discharge frequency between E-MNs and F-MNs at birth, and for the age-related increase in firing rate. These results suggest that E-MNs are more immature at birth than F-MNs and that there is a differential development of motoneurons innervating antagonistic muscles. This may be a critical factor in the development of posture and locomotion. [source] Pre- and postsynaptic modulation of monosynaptic reflex by GABAA receptors on turtle spinal cordTHE JOURNAL OF PHYSIOLOGY, Issue 14 2010Wendy Bautista There is growing evidence that activation of high affinity extrasynaptic GABAA receptors in the brain, cerebellum and spinal cord substantia gelatinosa results in a tonic inhibition controlling postsynaptic excitability. The aim of the present study was to determine if GABAA receptors mediating tonic inhibition participate in the modulation of monosynaptic reflex (MSR) in the vertebrate spinal cord. Using an in vitro turtle lumbar spinal cord preparation, we show that conditioning stimulation of a dorsal root depressed the test monosynaptic reflex (MSR) at long condition,test intervals. This long duration inhibition is similar to the one seen in mammalian spinal cord and it is dependent on GABAA as it was completely blocked by 20 ,m picrotoxin (PTX) or bicuculline (BIC) or 1 ,m gabazine, simultaneously depressing the dorsal root potential (DRP) without MSR facilitation. Interestingly 100 ,m picrotoxin or BIC potentiated the MSR, depressed the DRP, and produced a long lasting motoneurone after-discharge. Furosemide, a selective antagonist of extrasynaptic GABAA receptors, affects receptor subtypes with ,4/6 subunits, and in a similar way to higher concentrations of PTX or BIC, also potentiated the MSR but did not affect the DRP, suggesting the presence of ,4/6 GABAA receptors at motoneurones. Our results suggest that (1) the turtle spinal cord has a GABAA mediated long duration inhibition similar to presynaptic inhibition observed in mammals, (2) GABAA receptors located at the motoneurones and primary afferents might produce tonic inhibition of monosynaptic reflex, and (3) GABAA receptors modulate motoneurone excitability reducing the probability of spurious and inappropriate activation. [source] Synaptic Control Of Motoneuron Excitability In Rodents: From Months To MillisecondsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2000Gd Funk SUMMARY 1. Motoneurons (MN) shape motor patterns by transforming inputs into action potential output. This transformation, excitability, is determined by an interaction between synaptic inputs and intrinsic membrane properties. Excitability is not static, but changes over multiple time scales. The purpose of the present paper is to review our recent data on synaptic factors important in the dynamic control of MN excitability over time scales ranging from weeks to milliseconds. 2. Developmental changes in modulation of MN excitability are well established. Noradrenergic potentiation of hypoglossal (XII) MN inspiratory activity in rhythmically active medullary slice preparations from rodents increases during the first two postnatal weeks. This is due to increasing ,1 - and ,-adrenoceptor excitatory mechanisms and to a decreasing inhibitory mechanism mediated by ,2 -adrenoceptors. Over a similar period, ATP potentiation of XII inspiratory activity does not change. 3. Motoneuron excitability may also change on a faster time scale, such as between different behaviours or different phases of a behaviour. Examination of this has been confounded by the fact that excitatory synaptic drives underlying behaviour can obscure smaller concurrent changes in excitability. Using the rhythmically active neonatal rat brain-stem,spinal cord preparation, we blocked excitatory inspiratory drive to phrenic MN (PMN) to reveal a reduction in PMN excitability specific to the inspiratory phase that: (i) arises from an inhibitory GABAergic input; (ii) is not mediated by recurrent pathways; and (iii) is proportional to and synchronous with the excitatory inspiratory input. We propose that the proportionality of the concurrent inhibitory and excitatory drives provides a means for phase- specific modulation of PMN gain. 4. Modulation across such diverse time scales emphasizes the active role that synaptic factors play in controlling MN excitability and shaping behaviour. [source] Developmental changes in the modulation of respiratory rhythm generation by extracellular K+ in the isolated bullfrog brainstemDEVELOPMENTAL NEUROBIOLOGY, Issue 3 2003Rachel E. Winmill Abstract This study tested the hypothesis that voltage-dependent, respiratory-related activity in vitro, inferred from changes in [K+]o, changes during development in the amphibian brainstem. Respiratory-related neural activity was recorded from cranial nerve roots in isolated brainstem,spinal cord preparations from 7 premetamorphic tadpoles and 10 adults. Changes in fictive gill/lung activity in tadpoles and buccal/lung activity in adults were examined during superfusion with artificial CSF (aCSF) with [K+]o ranging from 1 to 12 mM (4 mM control). In tadpoles, both fictive gill burst frequency (fgill) and lung burst frequency (flung) were significantly dependent upon [K+]o (r2 > 0.75; p < 0.001) from 1 to 10 mM K+, and there was a strong correlation between fgill and flung (r2 = 0.65; p < 0.001). When [K+]o was raised to 12 mM, there was a reversible abolition of fictive breathing. In adults, fictive buccal frequency (fbuccal), was significantly dependent on [K+]o (r2 = 0.47; p < 0.001), but [K+]o had no effect on flung (p > 0.2), and there was no significant correlation between fbuccal and flung. These data suggest that the neural networks driving gill and lung burst activity in tadpoles may be strongly voltage modulated. In adults, buccal activity, the proposed remnant of gill ventilation in adults, also appears to be voltage dependent, but is not correlated with lung burst activity. These results suggest that lung burst activity in amphibians may shift from a "voltage-dependent" state to a "voltage-independent" state during development. This is consistent with the hypothesis that the fundamental mechanisms generating respiratory rhythm in the amphibian brainstem change during development. We hypothesize that lung respiratory rhythm generation in amphibians undergoes a developmental change from a pacemaker to network-driven process. © 2003 Wiley Periodicals, Inc. J Neurobiol 55: 278,287, 2003 [source] | ||||||||||