bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cells that Express Brain‐Derived Neurotrophic Factor mRNA in the Developing Postnatal Rat Brain
Authors: Friedman Wilma J. , Olson Lars , Persson Håkan 
Published: April 2006

AbstractBrain‐derived neurotrophic factor (BDNF) is a member of a family of related neurotrophic proteins which includes nerve growth factor (NGF) and hippocampus‐derived neurotrophic factor/neurotrophin‐3 (NT‐3). To obtain information regarding possible roles for BDNF during postnatal brain development, we have examined the temporal and spatial expression of this trophic factor using in situ hybridization. In specific neocortical regions BDNF mRNA‐expressing cells were seen at 2 weeks of age and thereafter. One particular neuronal cell type strikingly labelled was the inverted pyramidal cell population in the deep layers of parietotemporal cortex. In pyriform and cingulate cortices, BDNF mRNA was detected at postnatal day 1 and 1 week of age, respectively, with increasing levels during ontogeny. Several forebrain regions, including the thalamic anterior paraventricular nucleus, hypothalamic ventromedial nucleus as well as the preoptic area, contained moderate levels of BDNF mRNA throughout development. BDNF mRNA was detected transiently in several brainstem structures, notably in the substantia nigra and interpeduncular nucleus. Expression of this trophic factor in hippocampus was relatively low in the early neonatal brain, but attained high levels in the CA3 and CA4 regions as well as in the dentate gyrus by 2 weeks of age. At this early age, which is still during the period of neurogenesis in the dentate gyrus, labelling was restricted to the outer layer, which contained cells with a more mature appearance. However, by 3 weeks of age labelling was distributed throughout the granule cell layer. Our results show both transient and persistent expression of BDNF mRNA in various regions of the developing rat brain and suggest that there is a caudal to rostral gradient of BDNF expression during postnatal brain development, which may be correlated to neuronal maturation.
Nerve Growth Factor is Required for Induction of c‐Fos Immunoreactivity by Serum, Depolarization, Cyclic AMP or Trauma in Cultured Rat Sympathetic Neurons
Authors: Buckmaster A. , Nobes C. D. , Edwards S. N. , Tolkovsky A. M. 
Published: April 2006

AbstractNerve growth factor (NGF) induces transient Fos‐immunoreactivity (Fos‐IR) independently of any other factor, both in newly isolated rat sympathetic neurons and in established cultures after NGF deprivation. The same proportion of neurons that express Fos‐IR in response to NGF also survive. In addition to direct stimulation of Fos‐IR expression, the presence or recent exposure to NGF is required to obtain Fos‐IR expression by other stimuli. In newly isolated neurons no Fos‐IR is detected in response to stimulation by serum alone and a response to depolarization or cyclic AMP is obtained only if neurons are stimulated within a short period after ganglion excision. In established cultures none of these stimuli, nor the trauma of cutting neurites or spiking cell bodies with a microinjection needle induce Fos‐IR unless NGF is present or had been removed for <8–16 h. The lack of response is not due to a general decrease in the rate of protein or RNA synthesis. These findings show that in regenerating sympathetic neurons NGF induces c‐Fos and suggest that NGF may activate a master trigger that is required for c‐Fos expression to be induced by other stimuli.
Mechanisms of AMPA Neurotoxicity in Rat Brain Slices
Authors: Garthwaite Giti , Garthwaite John 
Published: April 2006

AbstractThe mechanisms underlying the neurodegenerative effects of the glutamate receptor agonist, AMPA (α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate), were studied using brain slice preparations of young rat (8–9 days old) cerebellum and hippocampus. Rapid AMPA toxicity (exerted on some cerebellar interneurons) was inhibited by including the appropriate receptor blocker, CNQX (6‐cyano‐7‐nitroquinoxaline‐2,3‐dione, 10 μM), in the exposing solution. The degeneration of other neurons, including Purkinje cells and hippocampal pyramidal neurons, persisted. It could, however, be largely prevented if CNQX was included for 1.5 h during the post‐incubation period, suggesting that an enduring ‘rebound’ AMPA receptor activation was responsible for this delayed type of degeneration, not the exposure itself. In cerebellar slices, independent evidence for the occurrence, postexposure, of persisting AMPA receptor stimulation was obtained electrophysiologically. Omission of Ca2+ during the exposure period (and for 10 min beforehand) markedly reduced rapid AMPA toxicity but was ineffective in protecting most of the Purkinje cells. However, if the slices were previously starved of Ca2+ for 1 h, then most of these neurons survived, even if the ion was reinstated during the recovery period. Slow AMPA toxicity, which takes place during long (2 h) exposures, could be inhibited either by CNQX or by omission of Ca2+ (30 min preincubation). The results indicate that the rapid oedematous necrosis induced by AMPA, like that caused by N‐methyl‐d‐aspartate and kainate, is likely to involve excessive influx of Ca2+. In contrast, the induction of the delayed mechanism, as well as its ‘expression’ during the postincubation period, probably depends on intracellular Ca2+, rather than Ca2+ influx.
Calcitonin Gene‐related Peptide (CGRP)‐like Immunoreactivity and CGRP mRNA in Rat Spinal Cord Motoneurons after Different Types of Lesions
Authors: Piehl Fredrik , Arvidsson Ulf , Johnson Hans , Cullheim Staffan , Villar Marcelo , Dagerlind Åke , Terenius Lars , Hökfelt Tomas , Ulfhake Brun 
Published: April 2006

AbstractBy use of the indirect immunofluorescence (IF) technique, radioimmunoassay (RIA) and in situ hybridization (ISH) histochemistry, the staining pattern, content and expression of calcitonin gene‐related peptide (CGRP) in lumbar motoneurons of normal rats and rats subjected to sciatic nerve transection (SNT), ventral root transection (VRT), low thoracic spinal cord transection (SCT) alone or in combination with a subsequent SNT, as well as rats subjected to chemical lesioning of 5‐hydroxytryptamine (5‐HT) neurons by 5,7‐dihydroxytryptamine (5,7‐DHT), were studied. We here confirm that a large number of the lumbar motoneurons normally contain CGRP‐like immunoreactivity (LI) and CGRP mRNA. SNT induced a transient increase in CGRP‐LI, with a peak at days 2–5 after lesion, and normalized levels again after ∼2–3 weeks. Comparable results were obtained with IF and RIA. This increase is probably a consequence of increased CGRP synthesis, since a parallel up‐regulation of CGRP mRNA levels was seen. A normalization of CGRP mRNA did not occur during the period studied, despite an apparent normalization of peptide levels after 2 weeks, and this may in turn be due to an increased turnover and/or release of CGRP. The up‐regulation of CGRP is probably caused by the axon injury itself, since a similar cellular reaction with respect to CGRP was observed in motoneurons subjected to VRT. However, SNT, which also lesions dorsal root afferents and causes a decline in CGRP‐LI in the dorsal horn, induced an increase in CGRP‐LI in motoneurons on the contralateral side also. Thus, it may be that severance of dorsal root afferents and/or changes in reflex activity may also influence the production of CGRP in motoneurons. SCT, which severs all descending synaptic input to the motor nucleus and causes a paralysis of muscles innervated by motoneurons below the lesion, resulted in a marked decline in both content of CGRP‐LI (IF and RIA) and expression of CGRP mRNA. However, treatment with 5,7‐DHT, which lesions 5‐HT neurons, including those giving rise to the bulbospinal serotoninergic pathway, did not cause any dramatic changes in motor behaviour but induced an increase in both motoneuron content of CGRP‐LI and expression of CGRP mRNA. In rats first subjected to SCT, which depresses CGRP, followed 2 weeks later by SNT, we found a marked increase in both content of CGRP‐LI (IF and RIA) and expression of mRNA coding for CGRP. In summary our results show that the cellular production of the CGRP peptide, normally expressed in motoneurons, is influenced in a complex way by motoneuron injury as well as changes in the afferent input. There also appear to be important differences in the expression of CGRP in small (gamma) and large (alpha) motoneurons as well as between motoneurons of different nuclei, in normal as well as axotomized rats.
Bypassing the Saccadic Pulse Generator: Possible Control of Head Movement Trajectory by Rat Superior Colliculus
Authors: King Sheila M. , Dean Paul , Redgrave Peter 
Published: April 2006

AbstractSaccades produced by electrical stimulation of the superior colliculus in primates are influenced primarily by the location of the stimulating electrode, with the suprathreshold intensity or frequency of the stimulating pulse train having little effect. Any given collicular site produces a characteristic movement of relatively fixed amplitude and velocity. In accordance with this finding, in models of the saccadic eye movement system the superior colliculus specifies the change of eye position: the velocity of movement components are determined by ‘pulse generators’ located between the superior colliculus and the oculomotor neurons. Previous findings in rodents, however, have suggested that eye and head movements induced by stimulation at some collicular sites may be critically dependent on stimulation parameters, implying that in these animals the superior colliculus has access to a non‐saccadic control system. To investigate this possibility, rats with electrodes implanted into the lateral intermediate layers were stimulated with pulse trains of varying frequency and duration, and the resultant head movements analysed from video tape. At seven of the nine sites studied, amplitude of the horizontal component of the head movement was linearly related to stimulating frequency for fixed‐duration trains, in some cases over a ten‐fold range. Subsequent variation of train duration showed that amplitude was affected not by frequency as such, but by the number of pulses in the train; frequency was related to the mean velocity of the movement. By appropriate setting of these parameters, independent control of head movement amplitude and velocity could be achieved. These results suggest that the rodent superior colliculus may be able to control head movement without recourse to a pulse generator, and thus influence the trajectory of the movement directly. If so, it may prove to be a useful preparation for testing theories of trajectory formation.
Chromatic Discrimination in a Cortically Colour Blind Observer
Authors: Heywood C. A. , Cowey A. , Newcombe F. 
Published: April 2006

AbstractWe tested the ability of a subject with cerebral achromatopsia to discriminate between colours and to detect chromatic borders. He was unable to identify colours or to arrange them in an orderly series or choose the odd colour out of an array or even to pick out a colour embedded in an array of greys. Nevertheless, he could select the odd colour when the colours were contiguous, even when they were isoluminant, and could discriminate an ordered from a disordered chromatic series as long as the colours in each row abutted one other. His verbal replies showed that he did so by detecting an edge between two stimuli that were, to him, perceptually identical. Introducing a narrow isoluminant grey stripe between adjacent colours abolished or greatly impaired this ability. As long as isoluminant colours were contiguous the patient could identify the orientation of the chromatic borders. Photopic spectral sensitivity showed evidence both for activity of three cone channels and for chromatic opponent processing, indicating that postreceptoral chromatic processing is occurring despite the absence of any conscious awareness of colour. The results indicate that both parvocellular colour opponent and magnocellular broad‐band channels are active and that the cortical brain damage has selectively disrupted the appreciation of colour but not the ability to detect even isoluminant chromatic borders, which would be invisible to a retinal achromat. The subject's performance on non‐colour tasks involving the discrimination of shape, texture, greyness and position was excellent. His disorder is therefore not like that of macaque monkeys in which cortical area V4 has been removed, and which are much more severely impaired at discriminating shape than colour.
Genotypic m3‐Muscarinic Receptors Preferentially Inhibit M‐currents in DNA‐transfected NG108‐15 Neuroblastoma × Glioma Hybrid Cells
Authors: Robbins J. , Caulfield M. P. , Higashida H. , Brown D. A. 
Published: April 2006

AbstractThe ability of different genotypic muscarinic acetylcholine receptors (mAChR) to inhibit the neural K+‐current, IM, was assessed in clones of NG108‐15 mouse neuroblastoma × rat glioma cells transfected with DNA for the genomic mAChRs ml –4 using tight‐seal, whole‐cell patch clamp recording. No significant inhibition of IM was seen in native (non‐transfected) cells, or in m2 or m4 DNA‐transfected cells at concentrations of acetylcholine up to 1 mM or muscarine up to 100 μM. Both acetylcholine and muscarine produced complete inhibition of IM in m3 DNA‐transfected cells, but only partial (50–60%) inhibition in m1 DNA‐transfected cells at maximally effective concentrations. This difference could not be explained by differences in mAChR number, as measured by radioligand binding and was not eliminated by adding GTP to the pipette. It is concluded that genotypic m3 receptors couple most effectively to IM and that this may explain previously reported instances of pirenzepine‐resistant IM‐inhibition.
Long‐term Depression of Glutamate Currents in Cultured Cerebellar Purkinje Neurons Does Not Require Nitric Oxide Signalling
Authors: Linden David J. , Connor John A. 
Published: April 2006

AbstractCerebellar long‐term depression (LTD) is produced when conjunctive stimulation of parallel fibre (PF) and climbing fibre (CF) inputs to a Purkinje neuron (PN) results in a prolonged decrease in the strength of the PF‐PN synapse. In cultured PNs, LTD may be induced by substituting depolarization of the PN and iontophoretic glutamate pulses for CF and PF stimulation, respectively, allowing an unambiguous analysis of post‐synaptic processes (Linden et al., Neuron, 7, 81–89, 1991). Recent studies have suggested that release of the newly described second messenger, nitric oxide, in the cerebellar molecular layer, is necessary for LTD produced in the slice preparation by PF/CF conjunctive stimulation (Shibuki and Okada, Nature, 349, 326–328, 1991) or PF/depolarization conjunctive stimulation (Crepel and Jaillard, NeuroReport, 1, 133–136, 1990). We report that LTD of glutamate currents produced without synaptic stimulation in cultured PNs is unaffected by reagents that stimulate (sodium nitroprusside) or inhibit (haemoglobin, NG‐nitro‐l‐arginine) nitric oxide signalling.
Synaptic Activation of GABAA Receptors Causes a Depolarizing Potential Under Physiological Conditions in Rat Hippocampal Pyramidal Cells
Authors: Avoli Massimo 
Published: April 2006

AbstractIntracellular recordings with K‐acetate‐filled microelectrodes were performed in slices of the adult rat hippocampus maintained in vitro at 35–36°C to analyse the potentials associated with the orthodromic inhibitory sequence generated by CA1 pyramidal cells. In 43 of 72 cells, stimuli that were delivered in the stratum radiatum induced (i) an initial excitatory postsynaptic potential (EPSP), (ii) an early, hyperpolarizing inhibitory postsynaptic potential (IPSP) (peak latency from the stimulus artefact 20 ms), (iii) an intermediate depolarizing component (peak latency = 60–120 ms; duration = 60‐150 ms, and (iv) a late, long‐lasting hyperpolarizing IPSP (peak latency = 120–160 ms, duration >400 ms). In the remaining cells the orthodromic inhibitory response lacked the intermediate depolarization. The depolarizing component was selectively blocked by local applications of bicuculline or picrotoxin on the apical dendrites of pyramidal cells. This pharmacological procedure induced an increase in the amplitude of the EPSP that was capable of triggering 2–3 action potentials, but no reduction of the recurrent IPSP which is caused by GABAA receptors located close to the soma. The amplitude and duration of the depolarizing component was enhanced by lowering the temperature in the tissue chamber to 29–31°C or by application of the GABA uptake blocker nipecotic acid, further indicating that the depolarizing component represented an active phenomenon mediated through GABA. Application of the CI‐ pump blocker furosemide reduced and eventually blocked the early IPSP and the depolarizing component. These data demonstrate that under physiological conditions rat hippocampal pyramidal cells generate a depolarization that is presumably caused by an outwardly directed CI‐ movement due to the activation of GABAA receptors located on the apical dendrites. This novel mechanism might modulate hippocampal excitability in both physiological and pathophysiological conditions.
The Critical Period for Experience‐dependent Plasticity in a System of Binocular Visual Connections in Xenopus laevis: Its Temporal Profile and Relation to Normal Developmental Requirements
Authors: Keating M. J. , Grant S. 
Published: April 2006

AbstractA commissural system of ‘intertectal’ connections in Xenopus mediates the registration of binocular visual maps at the midbrain optic tectum. Following surgical eye rotation in larval animals, the system can completely alter its pattern of connectivity to restore binocular visual registration at the tectum. This experimentally induced plasticity is known to require visual experience and thought to be subject to an age‐related restriction: eye rotation in adult animals is reported to provoke no subsequent intertectal alteration. In this paper we describe the detailed age‐dependence of this plasticity. One eye was rotated in 238 animals of various developmental stages between mid‐larval and adult life. At each age, different animals received rotations of different sizes, ranging from 20 to 180°. The pattern of intertectal connectivity was mapped electrophysiologically 1–2 years postoperatively. A ‘critical’ period was defined around the time of metamorphosis: the vast majority of animals receiving a rotation in larval life (up to ‐2 weeks before metamorphic climax) showed altered intertectal connections, whereas none of the animals operated upon at 3 months or more postmetamorphosis displayed the plasticity. At intervening ages, altered intertectal connections were found only in response to progressively smaller eye rotations. The profile of this critical period was further shown to mirror temporal features of the changes in eye position that occur in Xenopus as natural consequences of head growth, and which themselves impose a normal developmental requirement for intertectal plasticity. We conclude that the capacity of the Xenopus intertectal system for plasticity in response to abnormal experience undergoes a progressive age‐dependent decline, and that the profile of this decline is delimited by normal requirements.
Contrasting Effects of Raclopride and SCH 23390 on the Cellular Content of Preproenkephalin A mRNA in Rat Striatum: A Quantitative Non‐radioactive In Situ Hybridization Study
Authors: Augood Sarah J. , Faull Richard L. M. , Emson Piers C. 
Published: April 2006

AbstractThe effects of acute i. p. administration of selective dopamine (DA) receptor antagonists on the expression of preproenkephalin A (PPE A) mRNA was investigated in the adult rat striatum. Animals were injected with either (a) a selective D1 receptor antagonist SCH 23390 (0.25 mg/kg), (b) a selective D2 receptor antagonist raclopride (5 mg/kg), or (c) SCH 23388 (0.25 mg/kg), the (S)‐enantiomer of SCH 23390. Control naive animals did not receive an injection. At specific time points following drug administration (1, 3 or 9 h), rats were killed and striatal tissue processed for in situ hybridization with an alkaline phosphatase‐labelled oligonucleotide probe complementary to a portion of the rat PPE A cDNA. Treatment of rats with SCH 23388 did not affect the content of PPE A mRNA expressed by striatal cells at any time point. However, 1 h after SCH 23390 administration, a significant decrease in striatal PPE A mRNA was detected, reflected by a decrease in the cellular content of mRNA. No significant changes in PPE A mRNA were detected in raclopride‐treated sections at this time point. In contrast, both 3 and 9 h after an injection of raclopride a significant increase in the cellular content of PPE A mRNA was detected in the striatum. No change in the cellular content of mRNA was detected in SCH 23390‐treated rats at these two latter time points. Throughout the striatum ‐46% of neurons were found to express PPE A mRNA, with the highest percentage of cells (55%) being detected in the mid‐caudal striatum. No significant differences in striatal DA content were detected with any drug treatment using HPLC electrochemical detection methods. These results demonstrate that acute administration of the DA D1 and D2 receptor antagonists has contrasting effects on the cellular content of PPE A mRNA in the adult rat striatum. These effects may reflect changes in the rate of mRNA transcription which may be mediated by cAMP.
Putative Single Quantum and Single Fibre Excitatory Postsynaptic Currents Show Similar Amplitude Range and Variability in Rat Hippocampal Slices
Authors: Raastad Morten , Storm Johan F. , Andersen Per 
Published: April 2006

AbstractTransmission at excitatory synapses in the mammalian brain is thought to depend on the release of transmitter quanta through exocytosis of presynaptic vesicles (Katz, 1969). The number of vesicles released by a single presynaptic action potential is important for understanding the impact of a single synapse, and the variability in transmission from one impulse to the next. In addition, the number of vesicles released may be an important factor for synaptic regulation and plasticity, such as facilitation, post‐tetanic potentiation and long‐term potentiation (LTP). Three recent studies suggest that an increase in the number of transmitter quanta underlies hippocampal LTP (Malinow and Tsien, 1990; Bekkers and Stevens 1990; Malinow, 1991), whereas other reports suggest a postsynaptic mechanism (Kauer et al 1988; Muller et al, 1988; Foster and McNaughton, 1989). We have used the whole‐cell recording technique to compare putative quantal and single fibre responses at excitatory synapses in rat hippocampal slices, and find (i) a surprisingly large variability in single fibre excitatory postsynaptic currents (sfEPSCs); (ii) an equally large variability of putative quantal (pq) EPSCs elicited by hyperosmolar media or ruthenium red; (iii) the observed amplitude ranges for the sfEPSCs and the pqEPSCs overlap almost completely; and (iv) in neither case can the variability be attributed to a scatter in electrotonic distance from the soma of the engaged synapses. Thus, the data are compatible with the hypothesis that a presynaptic action potential usually releases only a single quantum. Other possibilities are also discussed.