bluuebunny/crossref_metadata_2025_split huggingface dataset:
In Situ Hybridization and Reverse Transcription‐Polymerase Chain Reaction Studies on the Expression of the GABAc Receptor ρ1‐ and ρ2‐subunit Genes in Avian and Rat Brain
Authors: Albrecht Barbara E. , Breitenbach Ute , Stühmer Thorsten , Harvey Robert J. , Darlison Mark G. 
Published: April 2006

AbstractThe pharmacological properties of homo‐oligomeric channels formed by the GABA type A receptor‐like ρl and ρ2 polypeptides are very reminiscent of those of the GABA type C receptors that have been extensively characterized in the retina. Similar receptors have been reported to occur in certain brain regions of a variety of vertebrate species. We have used in situ hybridization to investigate the expression patterns of the ρ1‐ and ρ ‐polypeptide genes in the brain of the 1‐day‐old chick (Gallus domesticus) and the adult rat (Rattus norvegicus). Our results show that in the chick both the ρ1‐ and ρ2‐subunit transcripts are present in the cerebellum, the optic tectum, the epithalamus and the nucleus pretectalis. However, the two messenger RNAs are often found in different populations of cells. Thus, only the ρ1‐subunit gene is expressed in the deep cerebellar nuclei, the dorsal thalamus, the ectostriatum and the tractus vestibulomesencephalicus, while only the ρ2‐subunit gene is transcribed in the nucleus habenularis lateralis and the nucleus isthmo‐opticus. In contrast, neither of the ρ‐polypeptide messenger RNAs can be detected by in situ hybridization in the rat central nervous system. Reverse transcription‐polymerase chain reaction amplification has been used to confirm the expression of the two ρ‐subunit genes in the chicken brain. Surprisingly, this highly sensitive technique also revealed transcription of these genes in the rat brain. We conclude that the ρl‐ and ρ2‐subunit genes are expressed at a much higher level in the avian brain than in the rat brain and that, at least in birds, subtypes of the GABC receptor exist.
The Recognition Memory Deficit Caused by Mediodorsal Thalamic Lesion in Non‐human Primates: A Comparison with Rhinal Cortex Lesion
Authors: Parker Amanda , Eacott M. J. , Gaffan David 
Published: April 2006

AbstractTwo earlier studies found that rhinal cortex ablations in the monkey (Macaca fascicularis) impaired delayed matching‐to‐sample (DMS) when the stimuli in the experiment came from a large population of possible stimuli, but not when the stimulus population was small, while uncinate fascicle section had no effect on DMS whatever the stimulus population size. The mediodorsal thalamus receives a large projection from the rhinal cortex, and has been implicated in recognition memory performance. We trained monkeys preoperatively in delayed matching‐to‐sample with large and small stimulus populations, exactly as in the earlier studies, then examined the effect of bilaterally ablating the medial portion of the mediodorsal thalamic nucleus. Mediodorsal lesion impaired postoperative delayed matching‐to‐sample performance with a large stimulus set, but had no effect on performance of DMS with a small stimulus population. In comparison with the earlier data from rhinal cortex lesions with the same methods, wherever a deficit was seen in the rhinal‐lesioned animals the mediodorsal thalamic nucleus‐lesioned animals showed a smaller deficit. We conclude that other efferents from the rhinal cortex, possibly those to the adjacent inferior temporal cortex, enable better performance in the mediodorsal thalamic nucleus‐lesioned animals than in the animals with rhinal cortex ablation.
Plasticity in the Stress‐Regulating Circuit: Decreased Input from the Bed Nucleus of the Stria Terminalis to the Hypothalamic Paraventricular Nucleus in Wistar Rats following Adrenalectomy
Authors: Mulders W. H. A. M. , Meek J. , Hafmans T. G. M. , Cools A. R. 
Published: April 2006

AbstractThe bed nucleus of the stria terminalis is involved in the stress‐regulating circuit by funnelling limbic information to the hypothalamic paraventricular nucleus. Since adrenalectomy influences both limbic structures (by inducing cell death in the hippocampus) and the hypothalamic paraventricular nucleus (by increased corticotrophin‐releasing hormone synthesis), we investigated whether the bed nucleus of the stria terminalis is also influenced by adrenalectomy. For this purpose, we analysed and compared the projections from the bed nucleus of the stria terminalis to the hypothalamic paraventricular nucleus in normal and adrenalectomized rats by anterograde tracer injections in the bed nucleus of the stria terminalis. Quantitative analysis of the fibre pattern in the hypothalamic paraventricular nucleus of normal rats revealed a homogeneous distribution of fibres of the bed nucleus of the stria terminalis over the different subdivisions of the hypothalamic paraventricular nucleus. In adrenalectomized rats, the absolute fibre density was significantly lower in the whole hypothalamic paraventricular nucleus (1.17 ± 0.27 10−3μm/μm3 in adrenalectomized rats versus 2.59 ± 0.24 10−3μm/μm3 in normal rats; P < 0.01) and all its subdivisions. The largest decrease of fibre density was found in the corticotrophin‐releasing hormone‐rich part of the hypothalamic paraventricular nucleus (relative fibre density; adrenalectomized rats: 0.602 ± 0.106, versus 1.095 ± 0.019 in normal rats, P < 0.01). These results show a loss of input from the bed nucleus of the stria terminalis to the hypothalamic paraventricular nucleus, and particularly to the corticotrophin‐releasing hormone neurons, following adrenalectomy. The data suggest that this pathway within the stress‐regulating circuit is functionally affected by corticosteroids in adult rats and may imply that human disorders associated with corticosteroid imbalance are allied to a changed circuitry in the brain.
GDNF is a Trophic Factor for Adult Rat Corticospinal Neurons and Promotes their Long‐term Survival after Axotomy In vivo
Authors: Giehl Klaus M. , Schacht Claudia M. , Yan Qiao , Mestres Pedro 
Published: April 2006

AbstractGlial cell line‐derived neurotrophic factor (GDNF) is a trophic factor for several neuronal populations involved in motor control. The present study evaluates the trophic actions of GDNF on corticospinal neurons, an important central nervous system motor projection into the spinal cord. Death of spinal motoneurons and corticospinal neurons is observed in the neurodegenerative disease amyotrophic lateral sclerosis. Axotomy of adult rat corticospinal neurons at internal capsule levels induces half of them to die, and the surviving population displays severe atrophy. To examine the trophic effects of GDNF on corticospinal neurons, Fast Blue‐labelled corticospinal neurons were stereotaxically axotomized at internal capsule levels and GDNF was infused intracortically to lesioned corticospinal neurons at total doses of 2, 4, 10, 20, 40, 100 and 300 μg for 7 days. GDNF prevented axotomy‐induced death of corticospinal neurons at doses between 2 and 40 μg and abolished or attenuated their atrophy at all doses examined. In addition, treatment with 8 μg GDNF for the first 2 weeks after axotomy resulted in the long‐term survival of corticospinal neurons for 42 days. With regard to the development of treatment strategies for upper motoneuron degeneration in amyotrophic lateral sclerosis, application of GDNF via the cerebrospinal fluid may be more relevant than intracortical delivery as its diffusion within the brain parenchyma is limited. lntraventricular as well as intracisternal infusion of GDNF (300 μg over 7 days) completely prevented corticospinal neuron death. These results show that GDNF promotes the long‐term survival of corticospinal neurons and has a positive effect on their size in vivo Furthermore, the survival‐promoting effect of GDNF on corticospinal neurons after delivery via cerebrospinal fluid has important clinical implications for potential treatment of the upper motoneuron degeneration seen in amyotrophic lateral sclerosis.
Bcl‐2 Regulates the Levels of the Cysteine Proteases ICH and CPP32/Yama in Human Neuronal Precursor Cells
Authors: Korhonen Laura , Hamnér Susanne , Olsson Per‐Anders , Lindholm Dan 
Published: April 2006

AbstractMembers of the Bcl‐2 family are major regulators of cell death and survival. Bcl‐2 has been shown to heterodimerize with the death‐inducing protein Bax, but the mechanism of action of Bcl‐2 is not fully understood. Here we show, using the human NT‐2 neuronal cell line, that overexpression of Bcl‐2 leads to dramatic down‐regulation of the cysteine proteases ICH and CPP32/Yama, which are directly involved in cell death. In addition, the nuclear enzyme poly(ADP‐ribose) polymerase was cleaved in control cells but not in cells overexpressing Bcl‐2 following induction of apoptosis. The mRNA levels of ICH and CPP32/Yama were differentially affected by Bcl‐2 overexpression, suggesting both transcriptional and post‐transcriptional effects of the protein. These results demonstrate novel mechanisms of action of Bcl‐2 in influencing the expression of death effectors such as the cysteine proteases. The relative levels of Bcl‐2 and of various cysteine proteases ultimately determine survival and death of different cells, including neurons.
Sustained Neurotransmitter Release: New Molecular Clues
Authors: Brodin Lennart , Löw Peter , Gad Helge , Gustafsson Jenny , Pieribone Vincent A. , Shupliakov Oleg 
Published: April 2006

AbstractChemical synapses convey impulses at high frequency by exocytosis of synaptic vesicles. To avoid failure of synaptic transmission, rapid replenishment of synaptic vesicles must occur. Recent molecular perturbation studies have confirmed that the recycling of synaptic vesicles involves clathrin‐mediated endocytosis. The rate of exocytosis would thus be limited by the capacity of the synaptic clathrin machinery unless vesicles could be drawn from existing pools. The mobilization of vesicles from the pool clustered at the release sites appears to provide a mechanism by which the rate of exocytosis can intermittently exceed the rate of recycling. Perturbation of synapsins causes disruption of vesicle clusters and impairment of synaptic transmission at high but not at low frequencies. Both clathrin‐mediated recycling and mobilization of vesicles from the reserve pool are thus important in the replenishment of synaptic vesicles. The efficacy of each mechanism appears to differ between synapses which operate with different patterns of activity.
Autoinhibition of Supraoptic Nucleus Vasopressin Neurons In Vivo: A Combined Retrodialysis/Electrophysiological Study in Rats
Authors: Ludwig Mike , Leng Gareth 
Published: April 2006

AbstractTo examine the role of endogenous vasopressin on the electrical activity of vasopressin neurons within the supraoptic nucleus of the rat brain in vivo, we have developed a novel technical approach for administering neuroactive drugs directly into the extracellular environment of the neuronal dendrites. A microdialysis probe was used for controlled local drug administration into the dendritic area of the nucleus during extracellular recording of single neurons in vivo. Vasopressin or selective V1 receptor antagonists were administered for between 10 and 30 min via a U‐shaped microdialysis probe placed flat on the surface of the supraoptic nucleus after transpharyngeal exposure of the nucleus in urethane‐anaesthetized rats. Microdialysis administration (retrodialysis) of vasopressin inhibited vasopressin neurons by reducing their firing rate, sometimes to total inactivity. Retrodialysis of V1‐receptor antagonists partially reversed the effect of vasopressin, and a subsequent vasopressin administration was not effective in reducing the activity of these neurons, suggesting a receptor‐mediated action of endogenous vasopressin. In addition, the duration of the periods of activity and the mean frequency during the active phase were increased in vasopressin neurons after retrodialysis of V1‐receptor antagonist, indicating a physiological role of endogenous vasopressin. Neither vasopressin nor the antagonists altered the activity of continuously firing oxytocin neurons. Thus, vasopressin released within the supraoptic nucleus may act via V1 receptors located specifically on vasopressin neurons to regulate their phasic activity by an auto‐inhibitory action. Since vasopressin release from the dendrites of vasopressin neurons is increased and prolonged after various forms of stimulation, it is proposed that this mechanism will act to limit excitation of vasopressin neurons, and hence secretion from the neurohypophysis. In addition, combined in vivo retrodialysis/ single cell recording allows controlled introduction of neuroactive substances into the extracellular fluid in the immediate vicinity of recorded neurons. This is shown to provide a novel approach to study neurotransmitter actions on supraoptic neurons in vivo.
Plateau Potentials in Cat Neocortical Association Cells In Viva Synaptic Control of Dendritic Excitability
Authors: Contreras D. , Dürmüller N. , Steriade M. 
Published: April 2006

AbstractThe dendrites of neocortical pyramidal cells are bombarded by myriads of synaptic inputs and express active conductances generating prominent plateau potentials. We have examined in vivo the possibility that spontaneous synaptic inputs trigger or terminate plateau potentials after blockage of K+ currents. Under barbiturate anaesthesia, pairs of cortical cells were intracellularly recorded with sharp electrodes from the cat's association cortex (areas 5–7). In one pyramidal cell, K+ channels were blocked with intracellular Cs+, while in the simultaneously impaled pyramidal cell the K+ conductances were left intact to act as a control; this second cell allowed recognition of spontaneous spindle‐related synaptic activity. Depolarizing current pulses elicited single, all‐or‐none plateau potentials (60–70 mV, 0.1–0.4 s). Plateau potentials slowly repolarized towards a break point of fast repolarization around ‐20 mV. Thalamic‐evoked inhibitory postsynaptic potentials consistently shut off the plateaus. Synchronized spontaneous activity, as occurring during thalamic‐generated spindle oscillations, either triggered or blocked the plateaus. These results suggest that spontaneously occurring synaptic activation during synchronized oscillatory states, such as those that occur during sleep spindles in vivu, may exert a strong control over the dendritic excitability in neocortical pyramidal cells.
Olivocerebellar Axon Regeneration and Target Reinnervation Following Dissociated Schwann Cell Grafts in Surgically Injured Cerebella of Adult Rats
Authors: Bravin Monica , Savio Tiziana , Strata Piergiorgio , Rossi Ferdinando 
Published: April 2006

AbstractThe ability of Schwann cells to induce the regeneration of severed olivocerebellar and Purkinje cell axons across an injury up to their deafferented targets was tested by transplanting freshly dissociated cells from newborn rat sciatic nerves into surgically lesioned adult cerebella. The grafted glial cells consistently filled the lesion gap and migrated into the host parenchyma. Transected olivocerebellar axons vigorously regenerated into the graft, where their growth pattern and direction followed the arrangement of Schwann cell bundles. Although some of these axons terminated within the transplant, many of them rejoined the cerebellar parenchyma beyond the lesion. Here, their fate depended on the territory encountered. No growth occurred in the white matter. Numerous fibres penetrated into the granular layer and formed terminal branches that remained confined within this layer. A few of them, however, regenerated up to the molecular layer and formed climbing fibres on Purkinje cell dendrites. By contrast, the growth of transected Purkinje cell axons into the grafts was very poor. These results underscore the different intrinsic responsiveness of Purkinje cell and olivocerebellar axons to the growth‐promoting action of Schwann cells, and show that the development and outcome of the regenerative phenomena is strongly conditioned by the spatial organization and specific features of the environmental cues encountered by the outgrowing axons along the course they follow. However, Schwann cells effectively bridge the lesion gap, induce the regeneration of olivocerebellar axons, and direct their growth up to the deafferented host cortex, where some of them succeed in reinnervating their natural targets.
NOS Expression in Nigral Cells after Excitotoxic and Non‐excitotoxic Lesion of the Pedunculopontine Tegmental Nucleus
Authors: González‐Hernández Tomás , Abdala Patricio , Rodríguez Manuel 
Published: April 2006

AbstractThe substantia nigra (SN) receives afferents from cholinergic neurons of the pedunculopontine tegmental nucleus (PPTg), a neuronal population that shows high levels of nitric oxide synthase (NOS), the enzyme responsible for the synthesis of nitric oxide. We have investigated the effects of the injection in PPTg of two neurotoxins, kainic acid (an excitotoxic neurotoxin), and ethylcholine mustard azirinium ion (AF64A, a non‐excitotoxic neurotoxin), upon the SN cells of the rat, by using choline acetyltransferase (ChAT) immunohistochemistry as a marker of cholinergic neurons, and nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry and NOS immunohistochemistry as markers of nitric oxide‐producing neurons. Our results show that in normal rats, the SN contains two populations of NOS‐positive neurons: large cholinergic neurons of PPTg that invade the caudal region of the SN, and small elongated neurons lying in the SN pars compacta. After ipsilateral PPTg lesion, another population of nigral cells, constituted by medium sized neurons, became NADPHd/NOS‐positive. This was much more evident in AF64A‐injected rats, in which many medium sized neurons showed enzymatic activity and normal morphological features, at least during the 90 days after injection. Kainic acid‐injected rats, in contrast, showed nigral cell degeneration, an effect not found in AF64A material, and only a few NOS‐positive neurons. NADPHd/NOS activity was never present in degenerating neurons. These findings suggest that induction of NOS activity is not involved in nigral cell degeneration, and that nitric oxide could have a protective rather than a neurotoxic role. The possible role of nitric oxide in the pathogenesis of Parkinson's disease is discussed.
The ExDression Pattern of the Orphan Nuclear Receptor RORβ in the Developing and Adult Rat Nervous System Suggests a Role in the Processing of Sensory Information and in Circadian Rhythm
Authors: Schaeren‐Wierners Nicole , André Elisabeth , Kapfhammer Josef P. , Becker‐André Michael 
Published: April 2006

AbstractRORβ is an orphan nuclear receptor related to retinoid and thyroid hormone receptors and is exclusively expressed in the central nervous system (CNS). Here we present an in situ hybridization analysis of the distribution of RORβ mRNA in the developing and adult rat CNS. The receptor localizes to areas involved in the processing of sensory information. In the cerebral cortex, RORβ mRNA was exclusively detected in non‐pyramidal neurons of layer IV and, less so, layer V. The highest expression was found in primary sensory cortices. In the thalamus highest RORβ expression was found in the sensory relay nuclei projecting to the respective cortical areas. In contrast, sensory projection neurons in the periphery, for example retinal ganglion cells and neurons of the sensory ganglia showed only little RORβ expression. RORβ is also expressed in areas involved in the generation and maintenance of circadian rhythms ‐ the suprachiasmatic nucleus, the pineal gland and the retina. In the latter two tissues, RORβ mRNA abundance oscillates with circadian rhythmicity peaking during the hours of darkness. RORβ rnRNA could not be detected in striatum, hippocampus, cerebellum, the motor nuclei of the cranial nerves or the ventral part of the spinal cord. During development, RORβ is expressed in many areas as early as embryonic day (E) 15, anticipating the distribution pattern in the adult. Our data suggest that RORβ regulates genes whose products play essential roles in the context of sensory input integration as well as in the context of circadian timing system.
Choline is a Selective Agonist of α7 Nicotinic Acetylcholine Receptors in the Rat Brain Neurons
Authors: Alkondon Manickavasagom , Pereira Edna F. R. , Cartes Wellington S. , Maelicke Alfred , Albuquerque Edson X. 
Published: April 2006

AbstractIn the present study, we demonstrate that choline, a precursor of acetylcholine (ACh) and a product of acetylcholine hydrolysis by acetylcholinesterase (AChE), acts as an efficient and relatively selective agonist of α7–containing nicotinic acetylcholine receptors (nAChR) in neurons cultured from the rat hippocampus, olfactory bulb and thalamus as well as in PC12 cells. Choline was able to activate postsynaptic and presynaptic α7 nAChRs, with the latter action resulting in the release of other neurotransmitters. Although choline was approximately one order of magnitude less potent than ACh (EC50 of 1.6 mM for choline and 0.13 mM for ACh), it acted as a full agonist at α7 nAChRs. In contrast, choline did not activate α4β2 agonist‐bearing nAChRs on hippocampal neurons, and acted as a partial agonist at α3β4‐containing nAChRs on PC12 cells. The ethyl alcohol moiety of choline is required for the selective action on α7 nAChR. Exposure of cultured hippocampal neurons for 10 min to choline (10–100 μM) resulted in desensitization of the native α7 nAChRs. Moreover, chronic exposure (10 days) of the cultured hippocampal neurons to a desensitizing concentration of choline (∼30 μM) decreased their responsiveness to ACh. The selective action of choline on native α7 nAChRs suggests that this naturally occurring compound may act in vivo as an endogenous ligand for these receptors. Putative physiological actions of choline include retrograde messenger activity during the development of the mammalian central nervous system and during periods of elevated synaptic activity that leads to long‐term potentiation.