bluuebunny/crossref_metadata_2025_split huggingface dataset:
The serotonin inhibition of high‐voltage‐activated calcium currents is relieved by action potential‐like depolarizations in dissociated cholinergic nucleus basalis neurons of the guinea‐pig
Authors: Williams Sylvain , Serafin Mauro , Mühlethaler Michel , Bernheim Laurent 
Published: March 2003

AbstractThe aim of the present study was to investigate whether the voltage‐dependent inhibition of calcium currents by serotonin 5‐HT1A agonists can be alleviated (facilitated) by action potential‐like depolarizations. In dissociated cholinergic basal forebrain neurons using whole‐cell recordings, it is shown that a selective serotonin 5‐HT1A agonist (8‐OH‐DPAT) predominantly blocks N‐type HVA calcium current, although a minor reduction of P‐type current was also observed. The inhibition may principally occur through Gi‐Go subtypes of G‐proteins because it was prevented by N‐ethylmaleimide, a substance known to block specifically pertussis‐sensitive G‐proteins. The inhibitory effect of 8‐OH‐DPAT on calcium currents is voltage‐dependent because it was alleviated by long‐lasting depolarizing prepulses. Interestingly, the inhibition could also be reversed by prepulses made‐up of action potential‐like depolarizations that were given at a frequency of 200 Hz. This observation may have important implications during periods of high‐frequency rhythmic bursts, a firing pattern that is prevalent in cholinergic basal forebrain neurons.
Immunocytochemical localization of somatostatin receptor sst2A in the rat spinal cord and dorsal root ganglia
Authors: Schulz Stefan , Schreff Matthias , Schmidt Harald , Händel Manuela , Przewlocki Ryszard , Höllt Volker 
Published: March 2003

AbstractIntrathecal administration of octreotide, a stable somatostatin analogue, provides pain relief in patients, and locally applied somatostatin inhibits firing of nociceptive dorsal horn neurons. In the present study, we have raised polyclonal antibodies that specifically detect the somatostatin receptor sst2A and used these antisera for immunocytochemical localization of the receptor protein in the rat spinal cord and dorsal root ganglia. In the superficial layers of the dorsal horn, sst2A‐like immunoreactivity (Li) formed a dense network consisting of neuronal perikarya and dendrites which were often closely apposed by, but not co‐contained within, somatostatin‐14‐immunoreactive nerve fibres and terminals. sst2A‐Li was resistant to dorsal rhizotomy and did not colocalize with either substance P or calcitonin gene‐related peptide suggesting that sst2A‐Li was not located to primary afferents, but rather confined to second‐order spinal neurons. The position of sst2A‐Li perikarya and dendrites in the dorsal horn appeared to be similar to those containing μ‐opioid receptor‐Li; however, double labelling experiments revealed no instances of coexistence of these two receptors. sst2A‐Li was also observed in the dorsal root ganglia predominantly targeted to the somatic plasmalemma of medium size neurons distinct from those expressing somatostatin‐14 or δ‐opioid receptors. Thus, the present results not only provide a morphological substrate for spinal octreotide analgesia but also show that somatostatin and opioids are poised to modulate nociceptive transmission by distinct anatomical systems.
Differential time‐ and dose‐related effects of haemorrhage on tyrosine hydroxylase and neuropeptide Y mRNA expression in medullary catecholamine neurons
Authors: Chan Raymond K. W. , Sawchenko Paul E. 
Published: March 2003

AbstractHypotensive haemorrhage induces nuclear Fos expression and upregulates tyrosine hydroxylase (TH) mRNA in catecholamine‐containing cell groups of the rat medulla oblongata. To shed light on the significance of the coexistence of neuropeptide Y (NPY) in aminergic neurons, the impact of graded levels of haemorrhage on temporal changes in the expression of TH and NPY mRNAs was compared; concurrent staining for Fos permitted comparisons between cells that ostensibly were and were not targeted by the stimulus. A 15% haemorrhage provoked increased NPY expression in all medullary catecholamine cell groups except the A2; these changes were detected predominantly in Fos‐immunoreactive neurons (Fos‐ir) at later (2–4 h) time points. Upregulation of TH and NPY mRNAs in Fos‐ir neurons followed distinct time courses, with NPY responses peaking more rapidly, particularly in the C1 and C2 cell groups. Adrenergic cell groups displayed greater maximal increases in NPY expression than the A1 noradrenergic cell group while the converse was true of TH mRNA response. Increasing the severity of haemorrhage resulted in more pronounced increases in both mRNA responses in each aminergic region. These findings indicate that haemorrhage differentially affects TH and NPY expression in medullary catecholamine cell groups that participate in the maintenance of cardiovascular homeostasis. The differential nature of these responses suggests them not to be a simple consequence of metabolic alterations pursuant to increased synaptic activity. The prompt and robust NPY mRNA responses in adrenergic neurons suggests a mechanism by which peptide content of these cell groups' terminal projections is defended.
Retrograde amnesia for spatial information: a dissociation between intra and extramaze cues following hippocampus lesions in rats
Authors: Ramos Juan M. J. 
Published: March 2003

AbstractSeveral recent studies have shown a flat retrograde amnesia for spatial information following lesions to the hippocampus in rats and mice. However, the results of the present investigation demonstrate that in rats that presurgically learned a spatial reference memory task based on extramaze cues, a temporally graded retrograde amnesia is evident following lesions to the hippocampus (1, 16, 32 or 64 days after learning) if two conditions are met. First, that a wide range of retention intervals is used, and second, that independent groups of rats are tested, not a single group that learns different spatial discrimination tasks at different times (expt 1). The results of expt 2 show that the hippocampus does not serve as a consolidating mechanism when the spatial task learned presurgically is based on intramaze cues. Taken together, these results indicate that the hippocampus is critical for the storage and/or retrieval of spatial reference information that was learned up to 1 month before hippocampus damage; however, in the absence of the hippocampus, efficient retention can still occur provided that the spatial knowledge was learned in a simple associative manner.
Rapid increase in PKA activity during long‐term potentiation in the hippocampal afferent fibre system to the prefrontal cortex in vivo
Authors: Jay Thérèse M. , Gurden Hirac , Yamaguchi Tomoko 
Published: March 2003

AbstractThe purpose of the present study was to examine whether cAMP‐dependent protein kinase (PKA) was implicated in the process of long‐term potentiation (LTP) in the hippocampal afferent fibre system to the prefrontal cortex in vivo. Using a biochemical approach, we measured PKA activity at different times after induction of LTP. We show that there is an NMDA receptor‐dependent increase in PKA activity in the prefrontal cortex, only at five minutes after LTP induction. These data demonstrate a role of PKA in the induction and not the expression of cortical LTP and suggest that if PKA is involved in the late phase of LTP, it does not appear to be a persistent activation.
Transient features of the thalamic reticular nucleus in the human foetal brain
Authors: Ulfig Norbert , Nickel Jens , Bohl Jürgen 
Published: March 2003

AbstractThe architectonic organization and neuronal types of the human foetal reticular nucleus (RN) – with special reference to transient characteristics – have been investigated using antisera against calretinin, parvalbumin and neurofilament epitopes of somata and dendrites (SMI 311). The RN consists of four subdivisions (clearly distinguishable in the 6/7th gestational month): The main portion appears as a prominent structure on account of its extension and high packing density of neurons which coexpress calretinin and parvalbumin. These two calcium‐binding proteins are also expressed by the perireticular nucleus forming a conspicuous grey within the internal capsule. Perireticular cells form clusters which are in continuity with the main portion, globus pallidus, ganglionic eminence and pregeniculate nucleus. In double‐labellings, a medial subnucleus stands out distinctly as it only expresses calretinin. SMI 311‐immunopreparations show neurons revealing a high degree of diversification and elaborated dendritic trees. Several transient characteristics become obvious: the perireticular nucleus, not visible in the adult, represents a distinct entity in the human foetal brain. The main portion and the pregeniculate nucleus appearing as prominent greys are dramatically reduced in size later on. The percentage of RN‐neurons expressing calretinin, the diversity of neuronal types and elaborated dendritic trees are reduced. The transient features can be correlated with the RN's putative functional roles in development: early RN‐afferents to the dorsal thalamus may represent pioneer fibres providing guiding cues for outgrowing axons from or into the thalamus. Moreover, the RN may serve as an intermediate target for growing axons which are sorted and directed towards different final targets.
β‐Actin is confined to structures having high capacity of remodelling in developing and adult rat cerebellum
Authors: Micheva Kristina D. , Vallée Annie , Beaulieu Clermont , Herman Ira M. , Leclerc Nicole 
Published: March 2003

AbstractNeurons undergo complex morphological changes during differentiation and in cases of plasticity. A major determinant of cell morphology is the actin cytoskeleton, which in neurons is comprised of two actin isoforms, non‐muscle γ‐ and β‐actin. To better understand their respective roles during differentiation and plasticity, their cellular and subcellular localization was examined in developing and adult cerebellar cortex. It was observed that γ‐actin is expressed at a constant level throughout development, while the level of β‐actin expression rapidly decreases with age. At the light microscopic level, γ‐actin staining is ubiquitous and the only developmental change observed is a relative reduction of its concentration in cell bodies and white matter. In contrast, β‐actin staining almost completely disappears from the cytoplasm of cell bodies, primary dendrites and axons. In young cerebellar cultures, γ‐actin is found in the cell body, neurites and growth cones, while β‐actin is mainly found in growth cones, as previously reported in other primary neuronal culture systems [Kaech et al. (1997), J. Neuroscience, 17, 9565–9572; Bassell et al. (1998), J. Neuroscience, 18, 251–265]. Electron microscopy of post‐embedding immunogold‐labelled tissue confirms the widespread distribution of γ‐actin, and also reveals an increased concentration of γ‐actin in dendritic spines in the adult. During development, β‐actin accumulation is observed in actively growing structures, e.g. growth cones, filopodia, cell bodies and axonal tracts. In the adult cerebellar cortex, β‐actin is preferentially found in dendritic spines, structures which are known to retain their capacity for morphological modifications in the adult brain. This differential subcellular localization and developmental regulation of the two actin isoforms point to their different roles in neurons.
Acute phencyclidine neurotoxicity in rat forebrain: induction of haem oxygenase‐1 and attenuation by the antioxidant dimethylthiourea
Authors: Rajdev Sunita , Fix Andrew S. , Sharp Frank R. 
Published: March 2003

AbstractPhencyclidine and otherN‐methyl‐d‐aspartate receptor antagonists are toxic to pyramidal neurons in the posterior cingulate/retrosplenial cortex of rat brain. Previous studies have shown induction of heat shock protein 70 in affected neurons. In this study, expression of haem oxygenase‐1, a heat shock protein induced by oxidative stress, was examined in rat forebrain after administration of a single intraperitoneal dose of phencyclidine (50 mg/kg). Northern and Western blot analyses of brain tissue extracts from phencyclidine‐treated rats revealed a marked induction of haem oxygenase‐1 mRNA and protein, respectively. Immunohistochemistry studies revealed that phencyclidine increased haem oxygenase‐1 immunoreactivity primarily in posterior cingulate/retrosplenial, piriform and entorhinal cortices, striatum and hippocampus. Haem oxygenase‐1 protein was induced in non‐neuronal cells, mainly astrocytes. Some microglia expressing haem oxygenase‐1 protein were also found in the posterior cingulate/retrosplenial cortex. Haem oxygenase‐1 immunoreactive astrocytes and microglia were present in close proximity to the heat shock protein 70‐positive neurons in the posterior cingulate/retrosplenial cortex following phencyclidine. Pretreatment of rats with 1,3‐dimethylthiourea, an antioxidant, significantly reduced haem oxygenase‐1 protein induction by phencyclidine. Thus, induction of haem oxygenase‐1 in glia by phencyclidine appears to be mediated mostly by oxidative stress. Experiments with the amino cupric silver stain for neuronal degeneration revealed phencyclidine‐induced neurotoxicity in the posterior cingulate/retrosplenial cortex. The number of affected neurons was significantly reduced after 1,3‐dimethylthiourea pretreatment. This suggests that the neurotoxicity ofN‐methyl‐d‐aspartate antagonists is due in part to the oxidative stress and may be amenable to therapeutic interventions.
Functional relationship between age‐related immunodeficiency and learning deterioration
Authors: Zhang Yongxiang , Moriguchi Toru , Saito Hiroshi , Nishiyama Nobuyoshi 
Published: March 2003

AbstractDisordered immune responses are supposed to alter the function of the central nervous system through the neuroendocrine immunomodulation network. In this paper, we studied the influence of the immune function on learning performances from the angle of pharmacology using aged garlic extract (AGE), an immunomodulator. Splenocyte proliferation, induced by concanavalin A or lipopolysaccharide, and the antibody production response were declined in senescence accelerated mouse‐prone 8 (SAMP8) aged 12 months compared with age‐matched SAMR1 (SAM‐resistant 1). Chronic oral administration of AGE‐containing food (2%, w/w) significantly enhanced the immune responses of both SAMP8 and SAMR1. Male ddY mice were thymectomized 4 weeks after birth and fed AGE‐containing food after the operation until the experiments were finished. Learning performances, brain monoamine content and choline acetyltransferase (ChAT) activity, as well as the immune response were evaluated 10 months after the operation. Thymectomy resulted in not only immunodeficiency, but also deteriorated learning ability. AGE treatment prevented the reduction of the antibody production response induced by thymectomy and improved the thymectomy‐induced deterioration of learning behaviours in passive avoidance performance and in a spatial memory task. The contents of hypothalamic noradrenaline, 3,4‐dihydroxyphenylacetic acid and homovanillic acid, and the hypothalamic ChAT activity were increased in thymectomized mice compared to those of sham‐operated control, while AGE treatment restored them to the control levels. These results suggest that the improvement of immune function is closely related to the amelioration of age‐associated deterioration of learning and memory.
Development of the histaminergic neurons and expression of histidine decarboxylase mRNA in the zebrafish brain in the absence of all peripheral histaminergic systems
Authors: Eriksson Krister S. , Peitsaro Nina , Karlstedt Kaj , Kaslin Jan , Panula Pertti 
Published: March 2003

AbstractThe histamine‐storing neural system in adult and developing zebrafish (Danio rerio) was studied with immunocytochemical and chromatographical methods. Furthermore, the gene for histidine decarboxylase was partially cloned and its expression mapped with in situ hybridization. The histamine‐storing neurons were only seen in the caudal hypothalamus, around the posterior recess of the diencephalic ventricle. Almost all parts of the brain, except the cerebellum, contained at least some histamine‐immunoreactive fibres. The ascending projections had the rostral part of the dorsal telencephalon as a major target. Descending projections terminated in the torus semicircularis, central grey and inferior olive. A prominent innervation of the optic tectum, which has not been reported in other fish, was seen. The in situ hybridization gave a strong signal in cells with the same anatomical position as the histamine‐immunoreactive neurons. The first histamine‐immunoreactive neurons appeared in the ventral hypothalamus at about 85 h post‐fertilization, and at 90 h, immunoreactive fibres terminated in the dorsal telencephalon. The embryonic histamine production described in mammals was lacking in this species. Both immunocytochemical and chromatographical studies indicated that histamine is absent in all other parts of the zebrafish body, and no specific hybridization was seen in any other part of the fish than the hypothalamus. The zebrafish could therefore be a very useful model for pharmacological in vivo studies of the histaminergic system of the brain, since the powerful peripheral actions of histamine should be lacking in this species.
Different regions of the periaqueductal grey are involved differently in the expression and conditioned inhibition of fear‐potentiated startle
Authors: Fendt Markus 
Published: March 2003

AbstractThe fear‐potentiated startle paradigm is a useful model for investigating the neural systems underlying the mediation and modulation of fear and anxiety. A series of previous studies showed that the periaqueductal grey is involved in the expression and inhibition of fear‐potentiated startle, but it was uncertain whether the different columns of the periaqueductal grey play different roles. In the present study, picrotoxin, a GABAA (γ‐aminobutyric acid) chloride‐channel blocker, was injected into the dorsal, lateral and ventrolateral columns of the periaqueductal grey in order to examine the effects of neural disinhibition on expression and conditioned inhibition of fear‐potentiated startle. Picrotoxin injections into the lateral periaqueductal grey increase potentiation of the startle response by conditioned fear, injections into the ventrolateral periaqueductal grey block fear‐potentiated startle. Picrotoxin injections into the dorsal periaqueductal grey decreased conditioned inhibition but did not affect expression of fear‐potentiated startle. The baseline startle amplitude was not influenced by picrotoxin injections into the different columns of the periaqueductal grey. Picrotoxin injections into neighbouring brain areas did not have any effect on baseline startle amplitude nor did they have an effect on expression or conditioned inhibition of fear‐potentiated startle. Based on the present results, the possible pathways underlying the expression and conditioned inhibition of fear‐potentiated startle in rats are discussed.
Synaptic inhibition in the isolated respiratory network of neonatal rats
Authors: Brockhaus Johannes , Ballanyi Klaus 
Published: March 2003

AbstractGramicidin‐perforated patch‐clamp recording revealed phasic Cl–‐mediated hyperpolarizations in respiratory neurons of the brainstem–spinal cord preparation from newborn rats. The in vitro respiratory rhythm persisted after block of γ‐aminobutyric acid (GABA), i.e. GABAA, receptor‐mediated inhibitory postsynaptic potentials (IPSPs) with bicuculline and/or glycinergic IPSPs with strychnine. In one class of expiratory neurons, bicuculline unmasked inspiration‐related excitatory postsynaptic potentials (EPSPs), leading to spike discharge. Bicuculline also blocked hyperpolarizations and respiratory arrest due to bath‐applied muscimol, whereas strychnine antagonized similar responses to glycine. The reversal potential of respiration‐related IPSPs and responses to GABA, muscimol or glycine was not affected by CO2/HCO3–‐free solutions, but shifted from about −65 mV to values more positive than −20 mV upon dialysis of the cells with 144 instead of 4 mm Cl–. Impairment of GABA uptake with nipecotic acid or glycine uptake with sarcosine evoked a bicuculline‐ or strychnine‐sensitive decrease of respiratory frequency which could lead to respiratory arrest. Also, the GABAB receptor agonist baclofen led to reversible suppression of respiratory rhythm. This in vitro apnoea was accompanied by a K+ channel‐mediated hyperpolarization (reversal potential −88 mV) of tonic cells, whereas membrane potential of neighbouring respiratory neurons remained almost unaffected. Both baclofen‐induced hyperpolarization and respiratory depression were antagonised by 2‐OH‐saclofen, which did not affect respiration‐related IPSPs per se. The results show that synaptic inhibition is not essential for rhythmogenesis in the isolated neonatal respiratory network, although (endogenous) GABA and glycine have a strong modulatory action. Hyperpolarizing IPSPs mediated by GABAA and glycine receptors provide a characteristic pattern of membrane potential oscillations in respiratory neurons, whereas GABAB receptors rather appear to be a feature of non‐respiratory neurons, possibly providing excitatory drive to the network.
Proliferation, migration and differentiation of neuronal progenitor cells in the adult mouse subventricular zone surgically separated from its olfactory bulb
Authors: Jankovski A. , Garcia C. , Soriano E. , Sotelo C. 
Published: March 2003

AbstractThe subventricular zone of the adult mammalian forebrain contains progenitor cells that, by migrating along a restricted pathway called the ‘rostral migratory stream’ (RMS), add new neurons to the olfactory bulb throughout life. To determine the influence of the olfactory bulb on the development of these progenitor cells, we performed lesions that interrupt this pathway and separate the olfactory bulb from the rest of the forebrain. By labelling cells born at several survival times after the lesions with the thymidine analogue bromodeoxyuridine (BrdU), we found that disconnection from the bulb influences the rate of BrdU incorporation by the progenitor cells. The number of labelled cells in lesioned mice was almost half that found in control mice. In the disconnected migratory pathway, the number of neurons expressing calretinin was increased indicating that neuronal differentiation was enhanced: newly born neurons occurred within and around the RMS, most of them expressed calretinin and left the pathway starting about 2 weeks after the lesion. Thereafter, these neurons preserving their phenotype, spread for long distances, and accumulated ectopically in dorsal regions of the anterior olfactory nucleus and the frontal cortex. Finally, transplantation of adult subventricular cells into the lesioned pathway showed that the lesion neither prevents neuronal migration nor alters its direction. Thus, although the olfactory bulb appears to regulate the pace of the developmental processes, its disconnection does not prevent the proliferation, migration and phenotypic acquisition of newly generated bulbar interneurons that, since they cannot reach their terminal domains, populate some precise regions of the lesioned adult forebrain.