bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quasi‐reversible Photo‐axotomy Used to Investigate the Role of Extensor Muscle Tension in Controlling the Kick Motor Programme of Grasshoppers
Authors: Heitler W. J. 
Published: April 2006

AbstractThe jump and kick of the grasshopper are behaviours which are potentially critical for the survival of the animal, and whose maximal Performance depends upon optimizing the rate and level of tension development in the extensor tibiae muscle of the hind legs. In experimental conditions extensor tension control can be reduced to a single motoneuron, the fast extensor tibiae (FETi). The axon of FETi can be cut using dye‐mediated laser photo‐ axotomy without damaging the central or peripheral portions of that neuron or any other neuron innervating the leg. The axotomy can be functionally reversed (i.e. the cut axon repaired) by an electronic axonal bypass which detects FETi spikes on the proximal side of the cut and stimulates the axon on the distal side of the cut. In this way motor spikes can either be allowed to reach the muscle or prevented from doing so (by switching the bypass on or off), and the motor programmes produced with and without extensor tension can be compared. The jump and kick are normally produced by a three‐stage motor programme: (i) initial flexion brings the tibia into the fully flexed position; (ii) coactivation of extensor and flexor muscles allows the extensor muscle to develop maximal tension almost isometrically, while the simultaneous contraction of the flexor muscle holds the tibia flexed; (iii) sudden trigger inhibition of the flexor system (motoneurons and muscle) releases the tibia and allows the behaviour to be expressed. The grasshopper can produce fictive kicks with motor programmes which show each of these three major structural features of a normal kick, but without any extensor tension whatsoever. There is no significant difference in the frequency of FETi spikes, the duration of coactivation or the maximum depolarization of the flexor motoneurons between fictive and quasi‐normal (i.e. reversed axotomy) kicks. The trigger inhibition of flexor motoneurons is shallower in fictive than in quasi‐normal kicks. The significance of this is discussed in relation to the activity of the interneuron M, which is known to mediate trigger inhibition onto FlTi motoneurons. There are two main conclusions from this study. First, the CNS does not need feedback from ETi muscle tension in order to produce the three‐stage motor programme of the kick (and, by implication, the jump). Second, the CNS does not adjust the frequency or duration of FETi activity in response to unexpected changes in ETi tension. ETi tension appears to be under open‐loop control in the kick motor programme.
Evidence for a High‐affinity Uptake System for Cholecystokinin Octapeptide (CCK8) in Rat Cortical Synaptosomes
Authors: Migaud Martine , Roques Bernard P. , Durieux Christiane 
Published: April 2006

AbstractGiven the high resistance of the cholecystokinin octapeptide (CCK8) to in vivo peptidase degradation, the possible existence of a reuptake system for this peptide was investigated. Efficient accumulation of intact, tritiated propionyl CCK8 ([3H]pCC8) was observed following its incubation with rat cortical synaptosomes but not with cerebellar synaptosomes, where no cholecystokinin immunoreactivity was found. This uptake process appeared to be dependent on temperature, duration of incubation, concentration of radioligand, the presence of glucose and the integrity of the synaptosomes. A Lineweaver‐Bürk analysis indicated that the putative uptake process is characterized by a single Km value of 10.7 nM and a Vmax of 8.5 fmol/min/mg of protein. Carbonyl cyanide‐m‐chlorophenyl hydrazone, an uncoupler of oxidative phosphorylation, blocked accumulation of [3H]pCCK8, whereas ouabain did not. The uptake was found to be highly specific since, among all the cholecystokinin analogues tested, only CCb and, to a lesser extent, CCK7, were able to inhibit [3H]pCCK8 uptake. The rate of [3H]pCCK8, uptake was not affected by CCK4, CCK5, D‐Trp CCK8, BC 264, a potent and selective CCK‐B agonist, and L‐365,260, a selective CCK‐B antagonist. In addition, no accumulation of radioactivity was observed using [3H]pBC 264, a result which is not in favour of a cholecystokinin receptor‐induced internalization mechanism. The potent and selective uptake mechanism characterized in this study could participate, in conjunction with extra and intracellular degradation of CCK8 by peptidases, in the interruption of cholecystokinin‐conveyed messages in the brain.
Human Recombinant Nerve Growth Factor Replaces Deficient Neurotrophic Support in the Diabetic Rat
Authors: Fernyhough Paul , Diemel Lara T. , Hardy Jim , Brewster Wendy J. , Mohiuddin Liza , Tomlinson David R. 
Published: April 2006

AbstractManipulation of neurotrophic support is a developing strategy for new therapy aimed at neurodegenerative diseases. This study demonstrates reduced content and retrograde transport of endogenous nerve growth factor (NGF) in sciatic nerve of diabetic rats. There were also reductions in the diabetic rats in NGF protein and mRNA in skin and muscle of the hindlimb. These deficits correlated with reductions in substance P and calcitonin gene‐related peptide–both products of NGF‐influenced genes in primary afferents. These manifestations of deficient neurotrophic support were corrected by intensive insulin treatment and surmounted by administration of exogenous human recombinant NGF in a dose‐related manner. Impaired neurotrophic support may, therefore, participate in the pathogenesis of diabetic and other peripheral neuropathies.
TrkA Tyrosine Residues Involved in NGF‐induced Neurite Outgrowth of PC12 Cells
Authors: Inagaki Naoyuki , Thoenen Hans , Lindholm Dan 
Published: April 2006

AbstractThe proto‐oncogene product gp 140prototrk (TrkA) is the receptor tyrosine kinase that mediates nerve growth factor‐induced neuronal survival and differentiation. In receptor tyrosine kinases, specific intracellular tyrosine residues become phosphorylated after ligand binding and the phosphorylated tyrosines induce the cascade of signal transduction. Here we have identified intracellular tyrosine residues of TrkA involved in nerve growth factor‐induced neurite outgrowth of PC12 cells, using site‐directed mutagenesis and a PC12 cell line expressing very low levels of endogenous TrkA (PC12nnr5 cells). We analysed eight conserved intracellular tyrosine residues of TrkA while the three putative autophosphorylation sites conferring tyrosine kinase activity were left intact. Five tyrosine residues, Y499, Y643, Y704, Y760 and Y794, in rat TrkA were involved in nerve growth factor‐induced neurite outgrowth. None of these tyrosines mediated the full activity of wild‐type TrkA, and a pair of these tyrosines, Y760 and Y794, promoted neurite outgrowth in an additive manner. These data indicate that no single tyrosine is sufficient to induce complete neurite outgrowth but the five tyrosine residues Y499, Y643, Y704, Y760 and Y794 cooperate to exhibit the full activity of wild‐type TrkA.
CO2 Stimulation of the Cornea: A Comparison Between Human Sensation and Nerve Activity in Polymodal Nociceptive Afferents of the Cat
Authors: Chen Xiaojie , Gallar Juana , Pozo Miguel A. , Baeza Manuel , Belmonte Carlos 
Published: April 2006

AbstractExcitation of nociceptors by low pH has been proposed as a cause of pain following tissue injury. Here we have studied the effect of pH reductions caused by application of CO2 pulses to the cornea on the activity of corneal afferent nerves of the cat and on the magnitude of pain sensations in humans. Single‐unit activity was recorded from corneal afferent fibres in anaesthetized cats. The corneal receptive field of A‐delta or C polymodal nociceptive units was exposed for 30 s to a gas mixture with different concentrations of CO2 in air (0, 35, 50, 65, 80 and 98.5%). Responses to CO2 were evoked at a mean threshold concentration of 40 ± 3% CO2. They consisted of a discharge of impulses that decayed gradually to a tonic level. In 15% of the units the initial burst was absent. The CO2 concentration and firing frequency data could be fitted to a power function with an exponent of 1.12. Pulses of CO2 were also applied to the cornea of 16 human volunteers. Sensations experienced were measured by means of a visual analogue scale and a verbal descriptor scale. Flow was adjusted below the mechanical stimulation threshold (2.8 ± 0.5 mg). When mixtures containing 10‐90% CO2 in 5% steps were applied as 3 s pulses, threshold sensation, described as a mild stinging pain, was evoked at 33.5 ± 4.0% CO2. This sensation became overtly painful with higher CO2 concentrations (47.5 ± 3.6% CO2). For the same subject the sensory threshold was remarkably constant, though it changed with longer exposure times. The relationship between CO2 concentration and magnitude of pain could be adjusted to a power function with a power exponent of 1.12. Curves of CO2 concentration versus neural discharges in the cat and versus psychophysical sensation in humans were very similar. These results show that corneal polymodal nociceptors respond to protons, and encode changes in CO2 concentration presumably reflecting pH changes. The same stimulus evokes corneal pain sensations in humans, thus opening the possibility of using CO2 as an effective stimulus for corneal aesthesiometry.
Gamma‐range Activity Evoked by Coherent Visual Stimuli in Humans
Authors: Tallon Catherine , Bertrand Olivier , Bouchet Patrick , Pernier Jacques 
Published: April 2006

AbstractWe tested the hypothesis of a role of gamma‐range synchronized oscillatory activity in visual feature binding by recording evoked potentials from 12 subjects to three stimuli: two coherent ones (a Kanizsa triangle and a real triangle) and a non‐coherent one (a Kanizsa triangle in which the inducing disks had been rotated so that no triangle could be perceived). The evoked potentials were analysed by convoluting the signal for each subject and each stimulation type by Gabor wavelets centred from 28 up to 46 Hz, providing a continuous measure of frequency‐specific power over time. A first peak of activity was found around 38 Hz and 100 ms with a maximum at electrode Cz in each experimental condition. A second peak of activity occurred around 30 Hz and 230 ms, with a maximum at O1 in response to the real triangle and a maximum at Cz in the case of the illusory triangle. At 100 ms we did not find any variations of the gamma‐band component of the evoked potential with stimulation type, but the power of the 30 Hz component of the evoked potential between 210 and 290 ms differed from noise only in the case of a coherent triangle, no matter whether real or illusory. We thus found a 30 Hz component whose power correlates with stimulus coherency, which supports the hypothesis of a functional role of high‐frequency synchronization in feature binding. Moreover, this correlation seemed specific to the gamma‐frequency range, as neither the power of the low‐frequency components (0–25 Hz) nor the power of the electromyogram range components (60–80 Hz) showed the same effect.
Ultrastructural Changes in the Hydropic Cochlea of the Guinea‐pig
Authors: Horner K. C. , Guilhaume A. 
Published: April 2006

AbstractTransmission electron microscopy of the cochlear organ of Corti in experimental endolymphatic hydrops revealed two principal features. Starting 1 month after induction of hydrops, osmiophilic inclusions thought to represent lipofuscin accumulation were frequently observed in the subcuticular cytoplasm of the outer hair cells along the length of the cochlea. Starting 3 months after induction of hydrops the efferent terminals on the outer hair cells appeared to be vacuolated. These data suggest that oxidative insult is likely to contribute to the pathology associated with endolymphatic hydrops and thus that free radical scavengers might be useful in the treatment of Menière's disease patients. In addition the early modification of the efferent innervation of the hydropic cochlea might underlie the known hypersensitivity to various insults, including noise stimulation, glycerol administration and hypoxia.
Inhibitors of Cyclooxygenases produce Amnesia for a Passive Avoidance Task in the Chick
Authors: Hölscher Christian 
Published: April 2006

AbstractArachidonic acid is a putative messenger in synaptic transmission which presumably plays a role in learning and memory. Previous experiments showed that inhibitors of phospholipase A2‐dependent release of arachidonic acid cause amnesia in a one‐trial passive avoidance task in the chick. To test if arachidonic acid is metabolized to other messengers, the effects of inhibitors of enzymes which metabolize arachidonic acid were tested in the same task. The cyclooxygenase inhibitors indomethacin, naproxen and ibuprofen caused amnestic effects at all concentrations tested when injected intracerebrally before training. Injections were 5 μl of 5–20 mmolar solutions per hemisphere. The onset of amnestic effects was always 2 h after training, independently of drug type, concentration, and injection time before training. The delay of 2 h after training suggests that the drugs prevent induction of cyclooxygenase synthesis. Post‐training injections had no effect. Control tests showed little effect of the drugs on motor control and motivation. Caffeic acid and esculetin, inhibitors of lipoxygenases, and sodium furegrelate, a thromboxane synthase inhibitor, had no effect on performance of chicks in the task at all concentrations or time points tested. The results indicate that cyclooxygenase products, but not lipoxygenase or thromboxane synthase products, play a role in memory consolidation in the chick when learning this task.
Calmodulin and In Vitro Regenerating Frog Sciatic Nerves: Release and Extracellular Effects
Authors: Remgård Pär , Ekström Per A. R. , Wiklund Peter , Edström Anders 
Published: April 2006

AbstractAlthough calmodulin (CaM) is commonly considered to be an intracellular protein, it has been suggested lately that it is released and exerts functions extracellularly. In the present investigation this was studied in in vitro regenerating adult frog (Rana temporaria) sciatic nerves. Using a multi‐compartment incubation chamber, the non‐neuronal cells in the outgrowth region of such nerves were radiolabelled with amino acid precursors. Based on immunological criteria, these cells were shown to release CaM. When the nerves were treated with CaM, both the outgrowth of sensory axons and the injury‐induced proliferation of non‐neuronal cells were partially inhibited. The inhibitory effects occurred even when the incubation medium contained as little as 30 pM CaM. Furthermore, treatment with anti‐CaM antibodies resulted in reduced outgrowth, which suggested that during normal conditions extracellular CaM is kept at an optimal concentration. Finally, conditioned medium was found to contain several CaM‐binding proteins. The present findings may reflect an earlier unknown function of extracellular CaM in controlling various growth mechanisms in integrated tissues.
Truncated and Catalytic Isoforms of trkB are Co‐expressed in Neurons of Rat and Mouse CNS
Authors: Armanini M. P. , McMahon S. B. , Sutherland J. , Shelton D. L. , Phillips H. S. 
Published: April 2006

AbstractLocalization of mRNA encoding trkB indicates that two truncated isoforms of trkB, T1trkB and T2trkB, are differentially distributed in the rodent nervous system, and that each of these transcripts is co‐expressed with catalytic trkB (TK+trkB) in adult motor neurons. In contrast to the prominent expression of T1trkB by non‐neuronal cells, T2trkB expression appeared to be restricted to neurons and demonstrated significant overlap with the pattern of TK+trkB distribution. In developing spinal cord ventral horn, an age‐related increase in hybridization was observed for truncated isoforms. These findings suggest that truncated trkB may modulate neuronal responses to neurotrophins which act via trkB.
Orienting Behaviour and Superior Colliculus Sensory Representations in Mice with the Vibrissae Bent into the Contralateral Hemispace
Authors: Benedetti F. 
Published: April 2006

AbstractWhen a tactile stimulus touches the body on one side, animals show an orienting response toward that side with the eyes, the head or the entire body. This movement requires the transformation of sensory information into motor commands. The superior colliculus is supposed to be a fundamental part of the brain where this sensorimotor transformation occurs and where one of the possible mechanisms could be the alignment among sensory and motor topographies. We changed the body shape of mice in order to analyse the development of new orienting responses following tactile stimulation. To do this, we bent the left vibrissae from left to right such that they were located in the right portion of the visual hemifield. If left‐right inversion was performed in adults, tactile stimulation of the left vibrissae performed from the right produced wrong orienting movements to the left. Conversely, if left—right inversion was performed in newborns, mice learned to respond correctly to the right. By recording from superior colliculus multisensory neurons of mice whose vibrissae were displaced at birth, we found a shift of visual and auditory receptive fields from left to right in those multisensory neurons receiving tactile input from the displaced vibrissae. These results show the strict relation existing between the neuronal modifications in the superior colliculus and the changes in orienting behaviour. These findings also suggest two important conclusions. First, sensory mapping in the superior colliculus depends on sensory inputs coming from the same portion of space. Second, since the neuronal modifications we found involved sensory representations, the observed motor learning seems to be due, at least in part, to sensory changes, and the superior colliculus appears therefore to be an important brain region where the internal schema of the body is specified.
Human Motor Planning, Motor Programming, and Use of New Task‐relevant Information with Different Apraxic Syndromes
Authors: Platz T. , Mauritz K.‐H. 
Published: April 2006

AbstractPatients with ideomotor apraxia (n= 2) or ideational apraxia (n= 2) after left brain stroke and patients with constructional apraxia (n= 2) after cerebrovascular accident of the right hemisphere, as well as 16 non‐brain‐damaged control subjects, were given a standardized simple motor task: they were asked to make triangular arm movements of specific size, configuration and spatial orientation without visual control. Motion was analysed three‐dimensionally in great detail prior to and after kinaesthetic training using a triangular stencil, and 1 day later. The experiment was conceptualized to assess three aspects of motor behaviour: (i) motor planning, operationalized as specification of content parameters of the movement as a whole; (ii) motor programming, the specification of spatiotemporal parameters of movement segments; and (iii) the ability to make use of task‐relevant information provided by the training. Patients with ideational apraxia showed signs of impaired motor planning: they had difficulty in selecting the body parts to be moved, and movement concept and configurational aspects were deficient. The kinaesthetic sensorimotor training given seemed not adequate to reduce behavioural deficits. Kinematic peculiarities of patients with ideomotor apraxia can be understood as deficits in programming movement elements. Submovements were more segmented, showed irregularities as well as additional, not‐requested elements. Their impairments could be reduced by task‐specific sensorimotor training. Patients suffering from visuoconstructive apraxia after right brain damage might have difficulties in making use of new sensorimotor information relevant for spatial‐motor aspects, as suggested by training‐induced behavioural impairment with a severely constructional apraxic patient.
Corticosteroid Regulation of Gene Expression and Binding Characteristics of Vasopressin Receptors in the Rat Brain
Authors: Patchev Vladimir K. , Almeida Osborne F. X. 
Published: April 2006

AbstractArginine‐vasopressin (AVP) plays significant roles in neuroendocrine and autonomic regulation, and in processing of cognitive information. Its synthesis and secretion are subject to control by circulating glucocorticoids. The lateral septum and subdivisions of the hippocampus are innervated by AVP‐ergic fibres and, together with AVP‐producing neurons in the hypothalamic paraventricular nucleus, are major neural targets of glucocorticoid negative feedback. In this study, we investigated the effects of chronic adrenalectomy (ADX) and subsequent treatment with supraphysiological doses of corticosterone (B) on the gene expression of AVP receptors of the V1a subtype in the septum, hippocampus and hypothalamic arcuate (ARC) nucleus using semiquantitative in situ hybridization histochemistry. Adrenalectomy did not alter AVP receptor expression in any of the structures studied. Supplementation with B significantly decreased AVP receptor expression in the lateral septum and hippocampus, whereas receptor mRNA levels in the ARC were indistinguishable from those measured in controls. In a complementary study, we investigated the binding characteristics of V1 AVP receptors in membrane preparations from the hippocampus. Adrenalectomy significantly decreased the number of AVP binding sites, and chronic corticosteroid treatment was associated with a further suppression of AVP receptor concentrations in this structure. These results indicate that the gene transcription of V1a AVP receptors in the brain is regulated by circulating glucocorticoids in a site‐specific fashion that largely reflects the corticosteroid sensitivity of the corresponding structure. The comparison between corticosteroid‐induced changes in receptor binding and gene transcription in the hippocampus suggests that two separate mechanisms may be operational in the regulation of AVP receptors by glucocorticoids: increased AVP release probably accounts for the observed down‐regulation in receptor binding following ADX, whereas increased corticosteroid levels interfere with AVP receptor expression.
The Unique Characteristics of Inflammatory Responses in Mouse Brain are Acquired During Postnatal Development
Authors: Lawson Linda J. , Perry V. Hugh 
Published: April 2006

AbstractThe kinetics of leukocyte recruitment during acute inflammation in adult mouse brain differ from the stereotyped response occurring in non‐CNS tissues; neutrophil recruitment is minimal and monocyte recruitment occurs after a 48 h delay. One aspect of the CNS microenvironment which may contribute to restricted leukocyte recruitment is the highly differentiated nature of resident CNS macrophages, the microglia. Thus we studied the inflammatory response to intracerebral injections of endotoxin in neonates in which microglia are less differentiated and resemble more closely macrophages of non‐CNS tissues. Mice injected with endotoxin on the day of birth exhibited both neutrophil and monocyte recruitment to the parenchyma, but the response differed from that occurring in non‐CNS tissues such as skin. Leukocyte recruitment was very slow, the mononuclear phagocyte response peaking 14 days after endotoxin injection. This sluggish inflammatory response was reminiscent of that previously described in fetal wounds. However, when endotoxin was injected into brains of 7‐day‐old neonates the inflammatory response resembled that seen in non‐CNS tissues; i.e. prolific neutrophil recruitment and a brisk mononuclear phagocyte response. Thus the unusual inflammatory cell kinetics are a property of the mature CNS microenvironment; all signals necessary to support typical leukocyte recruitment are present in the brain by 7 days of age but the brain becomes able to restrict leukocyte immigration during subsequent postnatal development. Developmental changes in the host response to identical inflammatory challenges suggest a window during which the brain may be particularly vulnerable to inflammatory bystander damage.