bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential Effects of a Distant Noxious Stimulus on Hindlimb Nociceptive Withdrawal Reflexes in the Rat
Authors: Kalliomäki J. , Schouenborg J. , Dickenson A. H. 
Published: April 2006

AbstractRecent studies indicate that the nociceptive withdrawal reflexes to individual muscles are evoked by separate reflex pathways. The present study examines whether nociceptive withdrawal reflexes to different muscles are subject to differential supraspinal control in rats. A distant noxious stimulus was used to activate a bulbospinal system which selectively inhibits ‘multireceptive’ neurons (i.e. neurons receiving excitatory tactile and nociceptive inputs) in the dorsal horn of the spinal cord. Withdrawal reflexes, recorded with electromyographic techniques in single hindlimb muscles, were evoked by standardized noxious pinch. Thirty‐seven rats, anaesthetized with halothane and nitrous oxide, were used. Whereas withdrawal reflexes to the extensor digitorum longus and brevis, tibialis anterior and biceps posterior muscles were strongly inhibited, reflexes to interossei muscles were potentiated during noxious pinch of the nose. Reflexes to peronei muscles were not significantly changed. The effects on the reflexes usually had an onset latency of <0.5 s and outlasted the conditioning stimulation by up to 2 s. The monosynaptic la reflex to the deep peroneal nerve, innervating dorsiflexors of the digits and ankle, was not significantly changed during noxious pinch of the nose. Hence, the inhibitory effects on the hindlimb withdrawal reflexes induced by the conditioning stimulation were presumably exerted on reflex interneurons. It is concluded that nociceptive withdrawal reflexes to different hindlimb muscles are differentially controlled by descending pathways activated by a distant noxious stimulus. The results support our previous conclusion that there are separate nociceptive withdrawal reflex pathways to different hindlimb muscles.
Blockade of Glutamatergic Neurotransmission in the Suprachiasmatic Nucleus Prevents Cellular and Behavioural Responses of the Circadian System to Light
Authors: Vindlacheruvu R. R. , Ebling F. J. P. , Maywood E. S. , Hastings M. H. 
Published: April 2006

AbstractThe aim of this study was to test the role of glutamatergic neurotransmission in photic entrainment of the circadian oscillator of the suprachiasmatic nuclei (SCN) in the Syrian hamster. The response of the oscillator to a brief pulse of light was assessed using two independent indices, the phase shift of the free‐running activity rhythm, and the photically induced expression of the immediate‐early gene c‐fos within neurons of the SCN. The behavioural and the cellular responses to light were compared in animals which received intra‐cerebroventricular (icv) infusions into the region of the SCN of either a vehicle solution or a solution of γd‐glutamyl‐glycine (DGG), a competitive antagonist at both N‐methyl‐d‐aspartate (NMDA) and non‐NMDA types of glutamate receptor. Infusions of vehicle or DGG (200 nmol) were given 10 min before presentation of a 15‐min light pulse at either circadian time (CT) 14 or CT20 (onset of activity defined as CT12). As anticipated, animals treated with vehicle and light at CT14 exhibited phase delays in the activity rhythm, whereas animals treated at CT20 exhibited phase advances. Central infusion of DGG prior to a light pulse at CT14 blocked the phase‐delaying effect of light, and DGG delivered before a light pulse at CT20 markedly attenuated the phase‐advancing effect of light. In a separate group of animals, the expression of the immediate‐early gene c‐fos was assessed by immunocytochemical staining for its protein product Fos. Exposure of vehicle‐infused animals to light at CT14 caused extensive expression of c‐fos throughout the retinorecipient region of the SCN. However, when the light pulse was preceded by icv fusion of DGG at a dose which would block the phase‐shifting response to light, the total number of neurons immunopositive for Fos was significantly reduced (∼50%) and the expression was confined to a restricted area of the dorsolateral SCN. The precise correlation between the effects of glutamatergic blockade upon both the behavioural and the cellular responses of the circadian system to light demonstrates that effective glutamatergic neurotransmission within or adjacent to the SCN is a necessary component of the mechanism which mediates photic entrainment of the circadian clock. The results further demonstrate a pharmacological and anatomical compartmentalization of the retinorecipient zone of the SCN, consistent with the view that retinal afferents to the ventral region employ glutamate as a transmitter, whereas more dorsal input may be dependent upon non‐glutamatergic (DGG‐insensitive) pathways.
Different Types of Potassium Outward Current in Relay Neurons Acutely Isolated from the Rat Lateral Geniculate Nucleus
Authors: Budde Thomas , Mager Ralph , Pape Hans‐Christian 
Published: April 2006

AbstractDifferent classes of potassium (K+) outward current activated by depolarization were characterized in relay neurons acutely isolated from the rat lateral geniculate nucleus (LGN), using the whole‐cell version of the patch‐clamp technique. A fast‐transient current (IA), activated at around –70 mV, declined rapidly with a voltage‐dependent time constant (τ= 6 ms at + 45 mV), was 50% steady‐state inactivated at –70 mV, and rapidly recovered from inactivation with a monoexponential time course (τ= 21 ms). IA was blocked by 4‐aminopyridine (4‐AP, 2–8 mM) and was relatively insensitive to tetraethylammonium (TEA, 2–10 mM). After elimination of IA by a conditioning prepulse (30 ms to –50 mV), a slow‐transient K+ current could be studied in isolation, and was separated into three components, IKm, IKs and a calcium (Ca2+)‐dependent current, IK[Ca]. The slow‐transient current was not consistently affected by 4‐AP (up to 8 mM), while TEA (2–10 mM) predominantly blocked IKs and IK[Ca]. The component IKm persisted in a solution containing TEA and 4‐AP, activated at around –55 mV, declined monoexponentially during maintained depolarization (τ= 98 ms at +45 mV), was 50% inactivated at –39 mV, and recovered with τ= 128 ms from inactivation. IKs activated at a similar threshold, but declined much slower with τ= 2662 ms at +45 mV. Steady‐state inactivation of IKs was half‐maximal at –49 mV, and recovery from inactivation occurred relatively fast with τ= 116 ms. From these data and additional current‐clamp recordings it is concluded that the K+ currents, due to their wide range of kinetics and dependence on membrane voltage or internal Ca2+ concentration, are capable of cooperatively controlling the firing threshold and of shaping the different states of electrophysiological behaviour in LGN relay cells.
A Quantitative Description of Low‐ and High‐threshold Ca2+ Spikes in Rat Sensory Neurons: A Perforated‐patch Study
Authors: Wanke Enzo , Becchetti Andrea , Biella Gerardo , Del Bo Roberto , Ferroni Arnaldo 
Published: April 2006

AbstractAction potentials generated by voltage‐dependent Ca2+ conductances were studied at 25°C with the perforated‐patch technique, in freshly dispersed adult rat sensory neurons perfused with Na‐free solutions containing tetraethylammonium. Brief depolarizing currents from membrane potentials negative to –75 mV always elicited long (>100 ms) plateau spikes which had different thresholds in different neurons: a low threshold around –60/–50 mV and a high‐threshold at –30/–20 mV. Stimulations from potentials positive to –55 mV, on the contrary, elicited spikes originating only in the high threshold region and sensitive to 25 μM Cd2+, designated high‐threshold spikes. In neurons which showed spikes with low threshold, addition of 25 μM Cd2+ disclosed a smaller and shorter regenerative response, the low‐threshold spike. Moreover, the classical ‘anode‐break’ stimulation from –50/–60 mV uncovered isolated low‐threshold spikes, indicating a time‐ and voltage‐dependent de‐inactivating process. From the properties of the low (LVA) and high (HVA) voltage‐activated Ca2+ currents, recorded under the same extracellular conditions, a Hodgkin–Huxley model was derived and used to reconstruct all the features of the recorded spikes. The model was also able to simulate experimental blocking of LVA channels by amiloride, modulation of HVA channels by baclofen and induced oscillatory firing. This agreement between the behaviour of recorded spikes and their mathematical description led us to conclude that the LVA and HVA Ca2+ currents underlie the low‐ and high‐threshold Ca2+ spikes, respectively. Furthermore, our data suggest that complex behaviour known to be typical of central nervous system neurons is also present in sensory peripheral neurons.
Increase in Specific Proteins and mRNAs Following Transient Anoxia‐Aglycaemia in Rat CA1 Hippocampal Slices
Authors: Charriaut‐Marlangue C. , Pollard H. , Kadri‐Hassani N. , Khrestchatisky M. , Moreau J. , Dessi F. , Kang K. I. , Ben‐Ari Y. 
Published: April 2006

AbstractIncorporation of [35S]methionine into proteins and two‐dimensional gel autoradiograms was used to characterize early post‐anoxia–aglycaemia protein synthesis in the CA1 area of rat hippocampal slices maintained in vitro. We have compared the effects of 3–4 min and 5–10 min insults, since the former but not the latter produces a reversible block of synaptic transmission (see companion paper). An insult of between 3 min 30 s and 4 min induces a transient increase in the labelled proteins during the first hour of reoxygenation, as compared to control. The increase in protein synthesis is conspicuous for several proteins, including actin, α‐tubulin and heat‐shock proteins (hsp70c and hsp90), as determined by immunoblotting. In the case of α‐tubulin, we show with in situ hybridization and polymerase chain reaction procedures that the increase in protein synthesis is associated with a marked increase in the expression of the corresponding messenger RNAs. The results demonstrate that, in addition to regulatory proteins such as hsps, the synthesis of several polypeptides, including those associated with the cytoskeleton, is altered in anoxic damage.
Evidence Against a Role for Protein Kinase C in the Inhibition of the Calcium‐activated Potassium Current IAHP by Muscarinic Stimulants in Rat Hippocampal Neurons
Authors: Sim J. A. , Gerber U. , Knöpfel T. , Brown D. A. 
Published: April 2006

AbstractThe possible role of protein kinase C activation in the inhibitory action of cholinergic transmitters on the slow Ca‐dependent afterhyperpolarizing current (IAHP) in hippocampal CA3 pyramidal neurons was investigated using hippocampal slice cultures. IAHP was inhibited reversibly by methacholine (100–600 nM) and irreversibly by the protein kinase C activator, phorbol‐12,13‐dibutyrate (PDBu, 10 nM to 1 μM). The inhibitory action of PDBu was antagonized by prior (15–60 min) exposure to staurosporin (1 μM). In contrast, the inhibitory effect of methacholine on IAHP was not reduced after up to 3 h of exposure to this compound. In addition, methacholine produced a reversible inward current at the holding potential, which was augmented by staurosporin. However, prior exposure to PDBu reduced the effect of methacholine on IAHP and occluded the methacholine‐induced inward current. This effect of PDBu was also observed in the presence of staurosporin, suggesting that it might be exerted through a protein kinase C‐independent pathway. Noradrenalin (2–5 μM) and 8‐bromo cyclic adenosine 3′,5′monophosphate (8‐Br‐cAMP, 1 mM) also produced a reversible block of IAHP. Their action was antagonized by staurosporin, probably via its effect on protein kinase A. Thus the present experiments suggest that the action of muscarinic agonists on IAHP cannot be explained by an effect on protein kinase C, but support a role for protein kinase A in mediating the action of noradrenalin.
Responses to Metabotropic Glutamate Receptor Activation in Cerebellar Purkinje Cells: Induction of an Inward Current
Authors: Staub C. , Vranesic I. , Knöpfel T. 
Published: April 2006

AbstractThe responses to activation of metabotropic glutamate receptors (mGluRs) of Purkinje cells in rat cerebellar slice cultures were investigated using intracellular recordings in single‐electrode voltage‐clamp mode combined with microfluorometric measurements of cytosolic free calcium using fura‐2. Purkinje cells were perfused with saline containing 0.5 μM tetrodotoxin and 10 μM bicuculline and voltage‐clamped at –60 mV. Bath‐applied trans‐(±)‐1‐amino‐1,3‐cyclopentanedicarboxylic acid (t‐ACPD, 50–100 μM), a selective agonist of mGluRs, induced a transient inward current that was followed by an outward current. The response induced by t‐ACPD was not affected by 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX, up to 40 μM). In contrast, inward currents caused by (RS)‐α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA, 1–2 μM) were completely abolished, while inward currents caused by quisqualate (0.25 μM) were only partially depressed by CNQX (5–40μM). The inward current induced by t‐ACPD was unaffected by external Ba2+ (1 mM), tetraethylammonium (10 mM) and Cs+ (1 mM), and was associated with an increase in apparent input conductance of the cell membrane. The extrapolated reversal potential of inward currents induced by t‐ACPD was +18 mV while Cl− currents induced by muscimol reversed at –66 mV. Inward currents induced by t‐ACPD, but not those induced by AMPA, were associated with a rise in cytosolic Ca2+ concentration and suppressed by intracellular injection of a calcium chelator. Replacement of external Na+ by choline or Li+ depressed the inward current and resulted in a slower decay of the Ca2+ signal.
Transfer of Function to a Specific Area of the Cortex After Induced Recovery from Brain Damage
Authors: Castro‐Alamancos Manuel A. , Garcia‐Segura Luis M. , Borrell José 
Published: April 2006

AbstractDifferent methods of inducing recovery after brain damage and different mechanisms that might mediate the induced recovery have been proposed. One possible mechanism involves the ability of one part of the brain to take over the function of another. We show here in rats that (1) bar‐pressing behaviour to eliminate an aversive stimulus, which becomes dramatically impaired after bilateral lesion of the frontal primary motor ‐ sensory cortex, is recovered when the animals receive an electrical intracranial stimulation in the ventral tegmental nucleus of the brain contingent on an adequate response during performance in the behavioural task, (2) in recovered animals an area in the posterior primary motor – sensory cortex, the hindlimb motor ‐ sensory cortex, shows a 35% increase in the number of fos‐like immunoreactive cells compared to non‐recovered animals, and (3) a bilateral lesion of this area in recovered animals reinstates the impairment in the performance of the behavioural task. These results indicate that an area of the cerebral cortex is able to assume the role of another area after induced recovery from brain damage.
Striatal Graft‐Associated Recovery of a Lesion‐Induced Performance Deficit in the Rat Requires Learning to Use The Transplant
Authors: Mayer E. , Brown V. J. , Dunnett S. B. , Robbins T. W. 
Published: April 2006

AbstractPeformance in a prelearned choice reaction time task was studied 6 months after surgery in rats with ibotenate‐induced lesions of the striatum either with or without striatal grafts, and in sham‐operated controls. The long postoperative interval allowed full transplant maturation and the establishment of appropriate connections by the transplants. The animals were trained prior to surgery on a visual choice reaction time task which requires that a movement is made away from stimuli signalling reward. The use of multiple measures allowed a thorough analysis of several aspects of the animals' performance. Whilst sham‐operated control animals recovered normal (preoperative) performance rapidly, the lesioned animals had a severe performance deficit. Although the transplanted animals were initially at least as deficient in performance as the lesioned group, repeated testing led to an amelioration of the lesion‐induced deficit according to two distinct measures of spatial bias and reaction time. On a third measure, latency to complete the lateralized movement, the grafted group were initially worse than the lesioned group but repeated testing resulted in significant recovery. These results suggest that postoperative training may help to optimize the efficacy of graft‐induced recovery, and that animals may need to learn to use a transplant in order for it to confer functional benefit in complex prelearned tasks.
Hydrogen Ion Regulation in Rat Cerebellar Granule Cells Studied by Single‐Cell Fluorescence Microscopy
Authors: Pocock G. , Richards C. D. 
Published: April 2006

AbstractThe internal pH (pHi) regulatory mechanisms of individual rat cerebellar granule cells maintained in tissue culture have been investigated using the fluorescent indicator BCECF (2,7’bis carboxyethyl 5,6 carboxyfluorescein) and quantitative fluorescence microscopy. The steady‐state pH, was estimated as 7.27 ± 0.25 in bicarbonate‐buffered media and 7.49 ± 0.35 in HEPES‐buffered media. Buffering power was estimated at about 8 mM/pH unit from the peak alkalinization and acidification transients seen on addition and removal of NH4CI. Bicarbonate did not appear to contribute to the buffering power estimated in this way. Following an acid load imposed by the ammonium prepulse technique, pHi recovered to steady‐state values with first‐order kinetics. Recovery was absolutely dependent upon extracellular sodium and, in about half of the cells tested, bicarbonate ions. In cells that did not require bicarbonate for pHi recovery, amiloride (1 mM) inhibited pHi recovery. Removal of extracellular chloride produced a reversible alkalinization of pHi in a third of the cells studied. This alkalinization persisted even when extracellular sodium had been reduced to zero. Removal of extracellular chloride did not inhibit bicarbonate‐dependent pHi recovery following an acid load. These results are best explained by the existence of three independent pHi regulatory mechanisms: Na+/H+ exchange, Na+/HCO3− cotransport and Cl−/HCO3− exchange.
Extra‐ and Intracellular pH in the Brain During Ischaemia, Related to Tissue Lactate Content in Normo‐and Hypercapnic rats
Authors: Katsura Kenichiro , Asplund Barbro , Ekholm Anders , Siesjö Bo K. 
Published: April 2006

AbstractThe objective of the present study was to assess the relationship between the amount of lactate accumulated during complete ischaemia and the ensuing changes in extra‐ and intracellular pH (pHe and pHi respectively). The preischaemic plasma glucose concentration of anaesthetized rats was varied by administration of glucose or insulin, pHe was determined in neocortex with ion‐sensitive microelectrodes, and tissue lactate and CO2 contents were measured, tissue CO2 tension being known from separate experiments. The experiments were carried out in both normocapnic [arterial CO2 tension (PaCO2) ‐40 mm Hg] and hypercapnic (PaCO2 ‐80 mm Hg) animals. Irrespective of the preischaemic CO2 tension, δpHe was linearly related to tissue lactate content. Depending on the preischaemic glucose concentration, δpHe varied from <0.4 to >1.4 units. The results thus fail to confirm previous results that the changes in pHe describe two plateau functions (δ pHe‐0.5 and 1.1, respectively), with a transition zone at tissue lactate contents of 17–20 mmol kg−1. Changes in pH; given in this study are based on the assumption of a uniform intracellular space. The pH, changed from a normal value of ‐7.0 to 6.5, 6.1 and 5.8 at tissue lactate contents of 10, 20 and 30 mmol kg‐1. The intrinsic (non‐bicarbonate) buffer capacity, derived from these figures, was 23 mmol kg −1 pH−1. Some differences in pH and in HCO3− concentration between extra‐ and intracellular fluids persisted in the ischaemic tissue. These differences were probably caused by a persisting membrane potential in the ischaemic cells.
Cell Survival in the Uncrossed Projection of the Mammalian Retina is Independent of Birthdate
Authors: Reese B. E. , Colello R. J. , Thompson W. F. 
Published: April 2006

AbstractNaturally occurring cell loss in the retinal ganglion cell population of one eye can be interrupted by removal of the other eye in newborn rodents. Many of the rescued retinal ganglion cells which project ipsilaterally reside in the nasal retina, that part of the retina normally giving rise to primarily crossed optic axons. Their naturally occurring elimination has been attributed to their hypothesized late neurogenesis and the consequent delayed time of arrival of their axons in the target visual nuclei, thereby placing them at a competitive disadvantage with other, early arriving, optic axons. By combining the technique of tritiated thymidine autoradiography with the retrograde axonal transport of horseradish peroxidase in rats that had been enucleated on the day of birth, we report here that rescued cells in the nasal retina which project ipsilaterally are generated at the same time as their neighbours in the temporal retina. Time of genesis does not distinguish them; consequently, their axons should not differ in their arrival times within the target visual nuclei. Since their only obvious anomaly is one of pathway choice at the optic chiasm, their place of arrival, rather than their time, may ultimately determine their naturally occurring elimination.
Lack of Exuberance in Clustered Intrinsic Connections in the Striate Cortex of One‐month‐old Kitten
Authors: Lübke Joachim , Albus Klaus 
Published: April 2006

AbstractThe topographies of the intrinsic tangential connections in layers II ‐ IVab of one‐month‐old and adult cat's striate cortex were compared by plotting the distribution of retrogradely labelled neurons following injection of small amounts of wheat‐germ agglutinin ‐ horseradish peroxidase. In both cortices, the tracer reveals the characteristic cluster‐like arrangement of intrinsic tangential connections. No differences were found between the two age groups in terms of either the numbers of cell clusters, their periodicities or their profiles, nor was there any difference in the lateral extent of the tangential connections. We conclude that one month postnatally, tangentially projecting intrinsic networks in the upper layers of the cat striate cortex lack exuberance and have an adult‐like topography.