bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tonotopic organization and parcellation of auditory cortex in the FM‐bat Carollia perspicillata
Authors: Esser Karl‐Heinz , Eiermann Arne 
Published: March 2003

AbstractIn the short‐tailed fruit bat (Carollia perspicillata), the auditory cortex was localized autoradiographically and studied electrophysiologically in detail by using metal microelectrodes and 10‐ms tone stimuli. Because, in the weakly‐anaesthetized preparation, neuronal responses to pure‐tones were even found throughout the non‐primary auditory cortex, characteristic frequencies and minimum thresholds of neuron clusters (multiunits) could be mapped consistently and used to define auditory cortical fields conventionally (i.e. as in studies of auditory cortex of non‐echolocating mammals). Thus, within the electrophysiologically demarcated auditory cortex, six auditory fields were defined by criteria, as for example a gradient of characteristic frequencies (primary auditory cortex, AI; anterior auditory field, AAF; secondary auditory cortex, AII), reversal of the gradient across the field border (AI, AAF), uniform representation of a restricted band of frequencies (i.e. > 60 kHz; high‐frequency fields I and II, HFI and HFII), and transition from low to high minimum thresholds or vice versa [dorsoposterior field (DP), AII, HFI, HFII]. As supportive evidence for the distinction of these auditory cortical fields, differences in neuronal response properties were also used. In comparison with other mammals (e.g. cat and mouse), both the relative position of the auditory fields (mainly AI, AAF, DP and AII) and the representational principles for sound parameters within these forebrain areas seem to reflect a ‘fundamental plan’ (discussion below) of mammalian auditory cortical organization. Two coherent dorsally displaced high‐frequency representations (HFI, HFII) covering ∼ 40% of the total auditory cortical surface seem particularly suited for the processing of the dominant biosonar second and third harmonic of this species, and hence can be regarded as an adaptation for echolocation.
Differential neuronal responsiveness in primate perirhinal cortex and hippocampal formation during performance of a conditional visual discrimination task
Authors: Xiang J. ‐Z. , Brown M. W. 
Published: March 2003

AbstractNeuronal responses in the hippocampal formation, including the entorhinal cortex, have been compared with those in the inferior temporal cortex, including the perirhinal cortex, during performance by monkeys of a visual conditional discrimination task. In the task, the arrangement of three geometric shapes determined the correctness of either a left or right behavioural response according to a conditional rule. Neurons that responded differently to different types of trial were common (50% of the visually responsive neurons) in the entorhinal cortex, perirhinal cortex and area TE of the inferior temporal cortex, but significantly less common in the hippocampus (13%). This differential incidence suggests a more important role for the rhinal cortices and area TE than for the hippocampus in this task. Based on the neuronal responses, arguments are advanced that the animals probably solved the task by a strategy that did not require spatial or hippocampal processing. Thus, of the differential responses, those that would allow the animals to solve the task by using a conditional rule and so avoid spatial processing were twice as common (37%) as those allowing solution to be by selection of a particular spatially directed response to each arrangement of shapes (19%). Moreover, the differential latencies of responses that allowed the task to be solved by a conditional rule were shorter (< ∼ 165 ms), and hence processing was faster, than those that provided information about particular individual types of trial (∼ 195 ms). Even so, hippocampal responsiveness in the conditional task was differentially enhanced when compared with that during a recognition memory task, and the neuronal responses potentially allow the animal to employ a second, alternative strategy that might be expected to depend on hippocampal processing.
CNS‐specific prostacyclin ligands as neuronal survival‐promoting factors in the brain
Authors: Satoh Takumi , Ishikawa Yasuyuki , Kataoka Yosky , Cui Yilong , Yanase Hisato , Kato Koichi , Watanabe Yumiko , Nakadate Kazuhiko , Matsumura Kiyoshi , Hatanaka Hiroshi , Kataoka Kiyoshi , Noyori Ryoji , Suzuki Masaaki , Watanabe Yasuyoshi 
Published: March 2003

AbstractProstacyclin (PGI2) is a critical regulator of the cardiovascular system, via dilatation of vascular smooth muscle and inhibition of platelet aggregation (Moncada, S. 1982, Br. J. Pharmacol., 76, 3). Our previous studies demonstrated that a novel subtype of PGI2 receptor, which is clearly distinct from a peripheral subtype in terms of ligand specificity, is expressed in the rostral region of the brain, e.g. cerebral cortex, hippocampus, thalamus and striatum, and that (15r)‐16‐m‐17,18,19,20‐tetranorisocarbacyclin (15r‐TIC) and 15‐deoxy‐16‐m‐17,18,19,20‐tetranorisocarbacyclin (15‐deoxy‐TIC) specifically bind to the central nervous system (CNS)‐specific PGI2 receptor. Here, we report that these CNS‐specific PGI2 receptor ligands, including PGI2 itself, prevented the neuronal death. They prevented apoptotic cell death of hippocampal neurons induced by high (50%) oxygen atmosphere, xanthine + xanthine oxidase, and serum deprivation. IC50s for neuronal death were ∼ 30 and 300 nm for 15‐deoxy‐TIC and 15r‐TIC, respectively, which well correlated with the binding potency for the CNS‐specific PGI2 receptor. 6‐Keto‐PGF1α (a stable metabolite of PGI2), peripheral nervous system‐specific PGI2 ligands and other prostaglandins (PGs) than PGI2 did not show such neuroprotective effects. In vivo, 15r‐TIC protected CA1 pyramidal neurons against ischaemic damage in gerbils. These results indicate that CNS‐specific PGI2 ligands have neuronal survival‐promoting activity both in vitro and in vivo, and may represent a new type of therapeutic drug for neurodegeneration.
Acute inflammatory responses to mechanical lesions in the CNS: differences between brain and spinal cord
Authors: Schnell Lisa , Fearn Sara , Klassen Henry , Schwab Martin E. , Perry V. Hugh 
Published: March 2003

AbstractLesion‐induced inflammatory responses in both brain and spinal cord have recently become a topic of active investigation. Using C57BL/6J mice, we compared the tissue reaction in these two central nervous system (CNS) compartments with mechanical lesions of similar size involving both grey and white matter. This evaluation included the quantitative assessment of neutrophils, lymphocytes and activated macrophages/microglia, as well as astrocyte activation, upregulation of vascular cell adhesion molecules (ICAM‐1, VCAM‐1, PECAM) and the extent of blood–brain barrier (BBB) breakdown. Time points analysed post‐lesioning included 1, 2, 4 and 7 days (as well as 10 and 14 days for the BBB). We found clear evidence that the acute inflammatory response to traumatic injury is significantly greater in the spinal cord than in the cerebral cortex. The numbers of both neutrophils and macrophages recruited to the lesion site were significantly higher in the spinal cord than in the brain, and the recruitment of these cells into the surrounding parenchyma was also more widespread in the cord. The area of BBB breakdown was substantially larger in the spinal cord and vascular damage persisted for a longer period. In the brain, as in spinal cord, the area to which neutrophils were recruited correlated well with the area of BBB breakdown. It will be of interest to determine the extent to which the infiltration of inflammatory cells contributes, either directly or indirectly, to the vascular permeability and secondary tissue damage or, conversely, to local tissue repair in the brain and the spinal cord.
Differential expression of the presynaptic cytomatrix protein bassoon among ribbon synapses in the mammalian retina
Authors: Brandstätter Johann Helmut , Fletcher Erica Lucy , Garner Craig Curtis , Gundelfinger Eckart Dieter , Wässle Heinz 
Published: March 2003

AbstractBassoon is a 420‐kDa presynaptic protein which is highly concentrated at the active zones of nerve terminals of conventional synapses, both excitatory glutamatergic and inhibitory GABAergic, in rat brain. It is thought to be involved in the organization of the cytomatrix at the site of neurotransmitter release. In the retina, there are two structurally and functionally distinct types of synapses: ribbon and conventional synapses. Antibodies against bassoon were applied to sections of rat and rabbit retina. Strong punctate immunofluorescence was found in the outer and inner plexiform layers. Using pre‐ and post‐embedding immunostaining and electron microscopy, bassoon was localized in the outer plexiform layer at ribbon synapses formed by rods and cones but was absent from basal synaptic contacts formed by cones. In the inner plexiform layer a different picture emerged. As in the brain, bassoon was found at conventional inhibitory GABAergic synapses, made by amacrine cells, but it was absent from the bipolar cell ribbon synapses. These data demonstrate differences in the molecular composition of the presynaptic apparatuses of outer and inner plexiform layer ribbon synapses. Thus, differential equipment with cytomatrix proteins may account for the functional differences observed between the two types of ribbon synapses in the retina.
State‐dependent blockade of haloperidol‐induced sensitization of catalepsy by MK‐801
Authors: Schmidt Werner J. , Tzschentke Thomas M. , Kretschmer Beate D. 
Published: March 2003

AbstractNMDA receptor antagonists have been shown to block several forms of neural and behavioural plasticity. The prototypical and most widely‐used noncompetitive NMDA receptor antagonist is dizocilpine (MK‐801). Here we have examined the effect of MK‐801 on the context‐dependent augmentation (‘sensitization’) of catalepsy in rats which develops with repeated administration of haloperidol. It was found that over a 7‐day treatment period animals receiving haloperidol (0.25 or 0.5 mg/kg) plus MK‐801 (0.16 mg/kg) showed a context‐dependent day‐to‐day increase in catalepsy similar to animals that received haloperidol alone. However, when all animals were treated with haloperidol alone on day 8 of the experiment, animals that had received haloperidol plus MK‐801 before displayed a much smaller cataleptic response, similar to that observed in the haloperidol group on the first treatment day, i.e. the previously‐established enhancement of catalepsy was no longer expressed. These results may be explained in terms of state‐dependency effects induced by MK‐801. Implications of these findings for the clinical use of NMDA receptor antagonists in the treatment of Parkinson's disease are discussed.
Expression of c‐fos, NGFI‐A and secretogranin II mRNA in brain regions during initiation of cocaine self‐administration in mice
Authors: Kuzmin Alexander , Johansson Björn 
Published: March 2003

AbstractIntravenous cocaine self‐administration in mice was studied to find correlates of the acquisition of cocaine‐oriented operant behaviour in the expression of nerve growth factor‐induced clone A (NGFI‐A), c‐fos and secretogranin II mRNAs. Yoked control animals, receiving cocaine passively, served as controls for the neurochemical effect of non‐contingent cocaine infusion. Animals controlling their cocaine infusions did more nose‐pokes during a 30‐min trial than yoked controls and animals receiving only saline, indicating a reinforcing effect of cocaine. Compared with saline, an increase in c‐fos mRNA in lateral and basolateral amygdala was found in active cocaine‐receiving animals, and a decrease in yoked controls receiving cocaine. There is previous evidence for an involvement of the amygdala, particularly its basolateral part, in cocaine's effects on motivation. In caudate putamen, both contingent and non‐contingent cocaine increased c‐fos mRNA. Non‐contingent cocaine infusions increased NGFI‐A mRNA expression in the core of nucleus accumbens, medial caudate putamen and frontal cortex, whereas self‐administration eliminated these effects. In the core of the nucleus accumbens and piriform cortex there was increased, and in medial amygdala decreased secretogranin II mRNA in yoked controls compared with saline controls. In contrast, in basomedial and central nuclei of amygdala, increased secretogranin II mRNA was found in self‐administering mice. Previous studies measuring gene expression after cocaine administration obviously did not give the complete picture of changes in gene expression in the drug‐taking organism. As differences in c‐fos and secretogranin II mRNA between active mice and yoked controls were robust, measuring these mRNAs may identify neurons selectively involved in acquisition of cocaine‐taking behaviour.
Inferior olivary‐induced expression of Fos‐like immunoreactivity in the cerebellar nuclei of wild‐type and Lurcher mice
Authors: Oldenbeuving Annemarie W. , Eisenman Leonard M. , De Zeeuw Chris I. , Ruigrok Tom J. H. 
Published: March 2003

AbstractEarlier behavioural studies have shown that the expression of the immediate‐early gene c‐fos, as visualized by the immunohistochemical detection of Fos, in the inferior olive (IO) correlated closely with expression in related areas of the cerebellar nuclei. It has been speculated that the expression of c‐fos within the cerebellar nuclei may be induced by enhanced spiking activity of the immunopositive neurons in the inferior olive. Two potential mechanisms may play a role in this process: a direct induction by way of the collaterals of the olivary climbing fibres to the cerebellar nuclei, or indirectly, by climbing fibre activity‐induced depression of mossy fibre‐parallel fibre‐induced simple spike frequency of the Purkinje cells resulting in a subsequent disinhibition of the related parts of the cerebellar nuclei. In an attempt to distinguish between these possible mechanisms, we analysed Fos immunoreactivity in the olivocerebellar system of wild‐type mice and in the mutant mouse Lurcher which lacks Purkinje cells. The tremorgenic agent harmaline, which is known to induce enhanced and rhythmic firing of olivary neurons was given intraperitoneally to anaesthetized mice of both genotypes. Harmaline application coincides with the induction of Fos‐immunoreactive neurons in most areas of the IO in both wild‐type and Lurcher mice. Both types of mice also showed enhanced expression in the larger neurons of the cerebellar nuclei. However, in the smaller, GABAergic nucleo‐olivary neurons, increased c‐fos expression was only observed in the wild‐type mice. We conclude that: (i) increased olivary activity indeed may result in increased c‐Fos expression in related areas of the cerebellar nuclei; (ii) because the indirect mode of induction is not operative in Lurcher mice, the olivary collateral innervation of the cerebellar nuclei is sufficient for c‐fos induction in the larger nucleobulbar neurons in Lurcher and potentially also in wild‐type mice; however (iii) for the nucleo‐olivary cells an intact cerebellar cortical input is necessary to evoke increased expression of c‐fos following harmaline application.
Differential projections from the anterior and posterior divisions of the accessory olfactory bulb to the medial amygdala in the opossum, Monodelphis domestica
Authors: Martínez‐Marcos Alino , Halpern Mimi 
Published: March 2003

AbstractThe vomeronasal sensory epithelium of mammals contains apical and basal cell populations expressing different G proteins and putative pheromone receptors, which project, respectively, to the anterior and posterior divisions of the accessory olfactory bulb (AOB). In order to analyse whether these segregated pathways are preserved in the connections between the AOB and the amygdala, conjugated dextran‐amines were iontophoretically injected into the anterior and posterior divisions of the AOB. We found that efferent projections from both divisions essentially overlap throughout the vomeronasal recipient amygdala. In the medial amygdaloid complex, both divisions project to lamina 1A of layer 1 of the anterodorsal, anteroventral, posterodorsal and posteroventral nuclei. The posterior division alone, however, projects to lamina 1B and layers 2 and 3 of the anterodorsal, anteroventral and posteroventral nuclei. These results constitute a link between molecular, anatomical and functional approaches on the study of the vomeronasal system. Molecular and functional studies support that the two segregated pathways between the vomeronasal organ and the AOB are functionally different. Similarly, the anatomical approaches to the further connections of this system indicate that the medial amygdala possesses ventral and dorsal divisions that are hodologically and functionally different. The present results demonstrate a differential projection from the posterior AOB to the ventral division of the medial amygdala. These findings indicate that the segregated pathways of the vomeronasal system continue to the level of the amygdala, and they provide some clues about the functional implications.
FAK+ and PYK2/CAKβ, two related tyrosine kinases highly expressed in the central nervous system: similarities and differences in the expression pattern
Authors: Menegon Andrea , Burgaya Ferran , Baudot Pierre , Dunlap David D. , Girault Jean‐Antoine , Valtorta Flavia 
Published: March 2003

AbstractFocal adhesion kinase (FAK) and proline‐rich tyrosine kinase 2/cell adhesion kinase β (PYK2/CAKβ) are related, non‐receptor, cytoplasmic tyrosine kinases, highly expressed in the central nervous system (CNS). In addition, FAK+ is a splice isoform of FAK containing a 3‐amino acid insertion in the carboxy‐terminal region. In rat hippocampal slices, FAK+ and PYK2/CAKβ are differentially regulated by neurotransmitters and depolarization. We have studied the regional and cellular distribution of these kinases in adult rat brain and during development. Whereas PYK2/CAKβ expression increased with postnatal age and was maximal in the adult, FAK+ levels were stable. PYK2/CAKβ mRNAs, detected by in situ hybridization, were expressed at low levels in the embryonic brain, and became very abundant in the adult forebrain. Immunocytochemistry of the adult brain showed a widespread neuronal distribution of FAK+ and PYK2/CAKβ immunoreactivities (ir). PYK2/CAKβ appeared to be particularly abundant in the hippocampus. In hippocampal neurons in culture at early stages of development, FAK+ and PYK2/CAKβ were enriched in the perikarya and growth cones. FAK+ extended to the periphery of the growth cones tips, whereas PYK2/CAKβ appeared to be excluded from the lamellipodia. During the establishment of polarity, a proximal‐distal gradient of increasing PYK2/CAKβ‐ir could be observed in the growing axon. In most older neurons, FAK+‐ir was confined to the cell bodies, whereas PYK2/CAKβ‐ir was also present in the processes. In vitro and in vivo, a subpopulation of neurons displayed neurites with intense FAK+‐ir. Thus, FAK+ and PYK2/CAKβ are differentially regulated during development yet they are both abundantly expressed in the adult brain, with distinctive but overlapping distributions.
Retinoic Acid Modulates Gap Junctional Permeability Between Horizontal Cells Of The Mammalian Retina
Authors: Weiler Reto , He Shigang , Vaney David I. 
Published: March 2003

AbstractIn the retina, all‐trans retinoic acid (at‐RA) could function as a light signal because its production increases with the level of illumination. Given the well‐established effects of retinoic acid on cell coupling in other tissues, it is possible that the changing levels of at‐RA modulate the gap junctional permeability between retinal neurons. This study examines the effects of retinoic acid on horizontal cell coupling, which is known to be modulated by the ambient light level. Single horizontal cells were injected under visual control with either Neurobiotin (mouse retina) or Lucifer yellow (rabbit retina) and the extent of tracer coupling or dye coupling was used to monitor the gap junctional permeability. In the mouse retina, the injection of Neurobiotin revealed a network of ≈ 150–250 tracer‐coupled horizontal cells. The tracer coupling was completely abolished by incubating the retina in 150 μm at‐RA for 35 min. In the rabbit retina, the injection of Lucifer yellow into A‐type horizontal cells revealed networks of ≈ 15–30 dye‐coupled horizontal cells. Incubation in 150 μm at‐RA reduced the dye coupling within 12 min and complete uncoupling was achieved after 35 min. The uncoupling effects of at‐RA in the mouse and rabbit retinas were concentration‐ and time‐dependent and they were reversible after washout. The coupling was not affected by either the 9‐cis form of retinoic acid or by at‐RA that had been isomerized by intensive light. The uncoupling effect of at‐RA persisted following treatment with a D1 receptor antagonist and thus was dopamine‐independent. This study has established that at‐RA is able to modulate the gap junctional permeability between horizontal cells in the mammalian retina, where its light‐dependent release has already been demonstrated.
5‐HT1A and 5‐HT1B receptors control the firing of serotoninergic neurons in the dorsal raphe nucleus of the mouse: studies in 5‐HT1B knock‐out mice
Authors: Evrard A. , Laporte A. M. , Chastanet M. , Hen R. , Hamon M. , Adrien J. 
Published: March 2003

AbstractThe characteristics of the spontaneous firing of serotoninergic neurons in the dorsal raphe nucleus and its control by serotonin (5‐hydroxytryptamine, 5‐HT) receptors were investigated in wild‐type and 5‐HT1B knock‐out (5‐HT1B–/–) mice of the 129/Sv strain, anaesthetized with chloral hydrate. In both groups of mice, 5‐HT neurons exhibited a regular activity with an identical firing rate of 0.5–4.5 spikes/s. Intravenous administration of the 5‐HT reuptake inhibitor citalopram or the 5‐HT1A agonist 8‐hydroxy‐2‐(di‐n‐propylamino)tetralin (8‐OH‐DPAT) induced a dose‐dependent inhibition of 5‐HT neuronal firing which could be reversed by the selective 5‐HT1A antagonist N‐[2‐[4‐(2‐methoxyphenyl)‐1‐piperazinyl]ethyl]‐N‐(2‐pyridinyl)cyclohexane carboxamide (WAY 100635). Both strains were equally sensitive to 8‐OH‐DPAT (ED50 ∼ 6.3 μg/kg i.v.), but the mutants were less sensitive than wild‐type animals to citalopram (ED50 = 0.49 ± 0.02 and 0.28 ± 0.01 mg/kg i.v., respectively, P < 0.05). This difference could be reduced by pre‐treatment of wild‐type mice with the 5‐HT1B/1D antagonist 2′‐methyl‐4′‐(5‐methyl‐[1,2,4]oxadiazol‐3‐yl)‐biphenyl‐4‐carboxylic acid [4‐methoxy‐3‐(4‐methyl‐piperazine‐1‐yl)‐phenyl]amide (GR 127935), and might be accounted for by the lack of 5‐HT1B receptors and a higher density of 5‐HT reuptake sites (specifically labelled by [3H]citalopram) in 5‐HT1B–/– mice. In wild‐type but not 5‐HT1B–/– mice, the 5‐HT1B agonists 3‐(1,2,5,6‐tetrahydro‐4‐pyridyl)‐5‐propoxypyrrolo[3,2‐b]pyridine (CP 94253, 3 mg/kg i.v.) and 5‐methoxy‐3‐(1,2,3,6‐tetrahydropyridin‐4‐yl)‐1H‐indole (RU 24969, 0.6 mg/kg i.v.) increased the firing rate of 5‐HT neurons (+22.4 ± 2.8% and +13.7 ± 6.0%, respectively, P < 0.05), and this effect could be prevented by the 5‐HT1B antagonist GR 127935 (1 mg/kg i.v.). Altogether, these data indicate that in the mouse, the firing of 5‐HT neurons in the dorsal raphe nucleus is under both an inhibitory control through 5‐HT1A receptors and an excitatory influence through 5‐HT1B receptors.