bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spinal cord injury‐induced lesional expression of the repulsive guidance molecule (RGM)
Authors: Schwab Jan M. , Conrad Sabine , Monnier Philippe P. , Julien Sylvie , Mueller Bernhard K. , Schluesener Hermann J. 
Published: January 2009

AbstractThe repulsive guidance molecule (RGM) is involved in the formation of the central nervous system (CNS) during development by modulating guidance of growing axons. However, a role of RGM in CNS injury remains to be established. We studied the expression of RGM in the spinal cord of rats with spinal cord injury (SCI). After SCI, RGM+ cells accumulated in lesions and peri‐lesional areas. During the first days after SCI, RGM expression was confined to neurons, ballooned neurite fibers/retraction bulbs, smooth muscle/endothelial cells, and to leucocytes infiltrating the lesion. Lesional RGM expression was frequently confined to hypertrophic β‐APP+ and RhoA+ neurites/retraction bulbs. With maturation of the lesion, we observed RGM expression by components of the developing scar tissue (cicatrix), such as fibroblastoid cells, reactive astrocytes and in addition a pronounced extracellular RGM deposition resembling neo‐laminae. Frequent RGM+, RhoA+ coexpression by lesional retraction bulbs represent first preliminary evidence of RGM to exert growth inhibitory effects by the second messenger system RhoA. To date, RGM is one of the most potent axonal growth inhibitors identified and present in axonal growth impediments (i) oligodendrocytes; (ii) the plexus choroideus and (iii) components of the developing scar.
Migration of cells from primary transplants of allo‐ and xenografted foetal striatal tissue in the adult rat brain
Authors: Hurelbrink Carrie B. , Barker Roger A. 
Published: January 2009

AbstractPrimary neural cells derived from human xenografts migrate extensively following transplantation into the adult rat CNS. However, it is unknown whether cells from allografts have the same capability to migrate within the adult rat brain. Moreover, it is unclear whether human‐derived cells migrate to this extent as an inherent property of being in a xenograft environment, or whether it is due to the large size of the developed human brain compared with the adult rat brain. In order to address these issues we have designed an experimental paradigm to investigate the potential for cells derived from grafts of primary rat, mouse and human foetal striatal tissue to migrate following intrastriatal transplantation in an adult rat model of Huntington's disease (HD). Green fluorescent protein (GFP)‐expressing rat and mouse donors and an antibody specific to human nuclear antigen enabled identification of graft‐derived cells within the host brain, and double‐labelling with GFP and neuronal nuclear antigen or immunostaining with human‐specific tau identified graft‐derived neurons. Twelve weeks post‐transplantation, cells had migrated throughout the host in all groups; however, human cells and neurons had migrated significantly more than rat or mouse cells. These results demonstrate that neural cells derived from allografts are capable of migrating in the adult rat CNS and that the extent of migration is most likely determined by the size of the mature donor adult brain. This has important implications for the use of allo‐ and xenogeneic tissue as a source for transplantation in treating diffuse neurodegenerative disorders such as HD.
Regulation of miRNA expression during neural cell specification
Authors: Smirnova Lena , Gräfe Anja , Seiler Andrea , Schumacher Stefan , Nitsch Robert , Wulczyn F. Gregory 
Published: January 2009

AbstractMicroRNA (miRNA) are a newly recognized class of small, noncoding RNA molecules that participate in the developmental control of gene expression. We have studied the regulation of a set of highly expressed neural miRNA during mouse brain development. Temporal control is a characteristic of miRNA regulation in C. elegans and Drosophila, and is also prominent in the embryonic brain. We observed significant differences in the onset and magnitude of induction for individual miRNAs. Comparing expression in cultures of embryonic neurons and astrocytes we found marked lineage specificity for each of the miRNA in our study. Two of the most highly expressed miRNA in adult brain were preferentially expressed in neurons (mir‐124, mir‐128). In contrast, mir‐23, a miRNA previously implicated in neural specification, was restricted to astrocytes. mir‐26 and mir‐29 were more strongly expressed in astrocytes than neurons, others were more evenly distributed (mir‐9, mir‐125). Lineage specificity was further explored using reporter constructs for two miRNA of particular interest (mir‐125 and mir‐128). miRNA‐mediated suppression of both reporters was observed after transfection of the reporters into neurons but not astrocytes. miRNA were strongly induced during neural differentiation of embryonic stem cells, suggesting the validity of the stem cell model for studying miRNA regulation in neural development.
Neurons expressing relaxin 3/INSL 7 in the nucleus incertus respond to stress
Authors: Tanaka Masaki , Iijima Norio , Miyamoto Yasumasa , Fukusumi Shoji , Itoh Yasuaki , Ozawa Hitoshi , Ibata Yasuhiko 
Published: January 2009

AbstractRelaxin 3/INSL 7 has recently been identified as a new member of the insulin/relaxin superfamily. Although it was reported to be dominantly expressed in the brain, its detailed distribution and function in the central nervous system are still obscure. In the present study we demonstrated that in the rat relaxin 3 was mainly expressed in neurons of the nucleus incertus (NI) of the median dorsal tegmental pons. Other relaxin 3‐expressing neurons were scattered in the pontine raphe nucleus, the periaqueductal gray and dorsal area to the substantia nigra in the midbrain reticular formation. Relaxin 3‐immunoreactive fibers projected particularly densely in the septum, hippocampus, lateral hypothalamus and intergeniculate leaflet of the thalamus. Ultrastructural examination revealed that relaxin 3 was localized in the dense‐cored vesicles in the perikarya and was also observed in the synaptic terminals of axons. As almost all relaxin 3‐containing neurons express corticotropin‐releasing factor (CRF) type 1 receptor in the NI, we examined the response of relaxin 3 neurons to intracerebroventricular administration of CRF; 65% of relaxin 3 neurons expressed c‐Fos 2 h after intracerebroventricular administration of 1 µg CRF. We then confirmed that c‐Fos was induced in 60% of relaxin 3 neurons in the NI and the expression of relaxin 3 mRNA increased significantly in the NI after water‐restraint stress. Collectively, these results suggest that relaxin 3 produced in the NI is released from nerve endings and is involved in the regulation of the stress response.
Involvement of NMDA and AMPA/KA receptors in the nucleus accumbens core in instrumental learning guided by reward‐predictive cues
Authors: Giertler Christian , Bohn Ines , Hauber Wolfgang 
Published: January 2009

AbstractThe use of reward‐predictive cues to guide behavior critically involves the nucleus accumbens. However, little is known regarding the role of ionotropic glutamate receptors in the core subregion of the nucleus accumbens (AcbC) in instrumental learning guided by reward‐predictive cues. Here we examined the effects of an intra‐AcbC blockade of NMDA and AMPA/KA receptors on the acquisition of an instrumental response in a reaction time (RT) task in rats. In this task, discriminative cues signaled in advance the upcoming reward magnitude (5 or 1 food pellet) associated with a lever release. During early acquisition (days 1–6) rats received daily bilateral injections of either the NMDA receptor antagonist AP5 (5.0 µg per side, n = 14), the AMPA/KA receptor antagonist CNQX (2.5 µg per side, n = 14) or vehicle (0.5 µL per side, n = 19). No treatment was given during late acquisition (days 7–12). The main result was that rats which received intra‐AcbC injections of AP5 or CNQX during early acquisition exhibited a general RT increase of responses to high and low reward. However, treatment with AP5 and CNQX did not interfere with discriminative guidance of RTs by cue‐associated reward magnitudes, i.e. during acquisition RTs of responses to expected high reward became significantly faster than RTs of responses to expected low reward. Our findings suggest that NMDA and AMPA/KA receptors in the AcbC play a critical role in invigorating responding during instrumental learning, but seem less important in guiding responding according to reward‐predictive cues.
Adult gaze influences infant attention and object processing: implications for cognitive neuroscience
Authors: Reid Vincent M. , Striano Tricia 
Published: January 2009

AbstractInfants follow others' gaze toward external objects from early in ontogeny, but whether they use others' gaze in processing information about objects remains unknown. In Experiment 1, 4‐month‐old infants viewed a video presentation of an adult gazing toward one of two objects. When presented with the same objects alone a second time, infants looked reliably less at the object to which the adult had directly gazed (cued object). This suggests that the uncued object was perceived as more novel than the object previously cued by the adult's gaze. In Experiment 2, adult gaze was not directed towards any object. In this control experiment, infants looked at both objects equally in the test phase. These findings show that adult eye gaze biases infant visual attention and information processing. Implications of the paradigm for cognitive neuroscience are presented and the results are discussed in terms of neural structures and change over ontogeny.
Autonomic arousal in an appetitive context in primates: a behavioural and neural analysis
Authors: Braesicke Katrin , Parkinson John A. , Reekie Yvonna , Man Mei‐See , Hopewell Lucy , Pears Andrew , Crofts Harriet , Schnell Christian R. , Roberts Angela C. 
Published: January 2009

AbstractCentral to many emotional responses is the accompanying peripheral somatic and autonomic arousal, feedback from which has been hypothesized to enhance emotional memory and to contribute to appraisal processes and decision making, and dysfunction of which may contribute to antisocial behaviour. Whilst peripheral arousal may accompany both positive and negative emotional contexts, its relationship with the former is poorly understood, as are the neural mechanisms underlying such a relationship. The purpose of the present study was to determine the autonomic correlates of anticipation, as well as consumption, of high incentive food, in the freely moving common marmoset and to investigate the contribution of the amygdala to such effects. Blood pressure (BP) and heart rate (HR) were measured remotely by a telemetric device implanted into the descending aorta and behavioural responses were monitored whilst marmosets viewed preferred or non‐preferred foods and were then allowed access to eat those foods. A marked rise in blood pressure in unrestrained marmosets was observed in response both to the sight of highly preferred foods (anticipatory period) as well as during the actual consumption of those foods (consummatory period). Excitotoxic lesions of the amygdala abolished the autonomic arousal in the anticipatory period, but spared both the behavioural arousal in the anticipatory period and the autonomic arousal in the consummatory period. Together these data serve as an important step towards understanding the role of autonomic arousal in emotion and its neural underpinnings.
Regulation of corticosteroid receptors in the rat brain: the role of serotonin and stress
Authors: Robertson D. A. F. , Beattie J. E. , Reid I. C. , Balfour D. J. K. 
Published: January 2009

AbstractIt has been suggested that physiological resistance to repeated stress is associated with increased 5‐hydroxytryptamine (5‐HT) release in the dorsal hippocampus and that dysregulation of this neuroadaptation may be implicated in the psychopathology of depression. This study used 5,7‐dihydroxytryptamine lesions to investigate the role of 5‐HT projections to the hippocampus in physiological responses to repeated stress and putative changes in corticosteroid receptor immunoreactivity in the brain. Repeated exposure to elevated open platform stress (1 h/day) caused regionally selective changes in glucocorticoid and mineralocorticoid receptor immunoreactivity in the dorsal hippocampus that were not observed in ventral hippocampus, frontal cortex, hypothalamus or parietal cortex. Glucocorticoid receptor immunoreactivity in the dorsal hippocampus was decreased after 5 days but increased after 20 days of stress. Mineralocorticoid receptor immunoreactivity was increased after 5 or 10 days of stress. The increases in glucocorticoid and mineralocorticoid receptor immunoreactivity, evoked by repeated stress, were abolished by lesions of the principal 5‐HT projections to the hippocampus. The lesions abolished the increased defecation observed in stressed animals, but had no effects on the plasma corticosterone response to the stressor or the habituation of this response observed following repeated stress. The experiments have revealed a dissociation in the regulation of corticosteroid receptor expression in the dorsal and ventral hippocampus by repeated stress and 5‐HT. The data suggest that adaptation to inescapable stress is associated with regionally selective changes in corticosteroid receptor expression in dorsal hippocampus that are largely 5‐HT‐dependent, although these changes do not mediate habituation of the pituitary adrenocortical response to the stressor.
Two populations of glutamatergic axons in the rat dorsal raphe nucleus defined by the vesicular glutamate transporters 1 and 2
Authors: Commons Kathryn G. , Beck Sheryl G. , Bey Vincent W. 
Published: January 2009

AbstractMost glutamatergic neurons in the brain express one of two vesicular glutamate transporters, vGlut1 or vGlut2. Cortical glutamatergic neurons highly express vGlut1, whereas vGlut2 predominates in subcortical areas. In this study immunohistochemical detection of vGlut1 or vGlut2 was used in combination with tryptophan hydroxylase (TPH) to characterize glutamatergic innervation of the dorsal raphe nucleus (DRN) of the rat. Immunofluorescence labeling of both vGlut1 and vGlut2 was punctate and homogenously distributed throughout the DRN. Puncta labeled for vGlut2 appeared more numerous then those labeled for vGlut1. Ultrastructural analysis revealed axon terminals containing vGlut1 and vGlut2 formed asymmetric‐type synapses 80% and 95% of the time, respectively. Postsynaptic targets of vGlut1‐ and vGlut2‐containing axons differed in morphology. vGlut1‐labeled axon terminals synapsed predominantly on small‐caliber (distal) dendrites (42%, 46/110) or dendritic spines (46%, 50/110). In contrast, vGlut2‐containing axons synapsed on larger caliber (proximal) dendritic shafts (> 0.5 µm diameter; 48%, 78/161). A fraction of both vGlut1‐ or vGlut2‐labeled axons synapsed onto TPH‐containing dendrites (14% and 34%, respectively). These observations reveal that different populations of glutamate‐containing axons innervate selective dendritic domains of serotonergic and non‐serotonergic neurons, suggesting they play different functional roles in modulating excitation within the DRN.
Molecular and functional characterization of an Ih‐channel from lobster olfactory receptor neurons
Authors: Gisselmann Günter , Marx Thomas , Bobkov Yuriy , Wetzel Christian H. , Neuhaus Eva M. , Ache Barry W. , Hatt Hanns 
Published: January 2009

AbstractWe isolated a cDNA named PAIH encoding a member of the Ih‐channel family expressed in olfactory receptor neurons (ORNs) of the spiny lobster Panulirus argus. Functional expression of recombinant PAIH in HEK293 cells generated a slowly activating, noninactivating inward current under whole‐cell voltage‐clamp to hyperpolarizing voltage steps, the amplitude and activation rate of which increase with increasing hyperpolarization. The channel is weakly selective for K+. Intracellular cAMP or cGMP shifts activation of the current to less negative potentials in a concentration‐dependent manner. Finally, the channel is blocked by the Ih‐channel blocker ZD7288. An Ih‐channel sharing the properties of the recombinant channel occurs in cultured lobster ORNs. PAIH immunoreactivity localizes the protein to the transduction compartment of the ORNs in situ, and selectively applying the blocker to the transduction compartment reduces spontaneous activity in the ORN. Collectively, these results implicate for the first time a functional role for an Ih‐channel in olfactory signal transduction.
Enhancement of learning behaviour by a potent nitric oxide‐guanylate cyclase activator YC‐1
Authors: Chien Wei‐Lin , Liang Keng‐Chen , Teng Che‐Ming , Kuo Sheng‐Chu , Lee Fang‐Yu , Fu Wen‐Mei 
Published: January 2009

AbstractMemory is one of the most fundamental mental processes, and various approaches have been used to understand the mechanisms underlying this process. Nitric oxide (NO), cGMP and protein kinase G (PKG) are involved in the modulation of synaptic plasticity in various brain regions. YC‐1, which is a benzylindazole derivative, greatly potentiated the response of soluble guanylate cyclase to NO (up to several hundreds fold). We have previously shown that YC‐1 markedly enhances long‐term potentiation in hippocampal and amygdala slices via NO‐cGMP‐PKG‐dependent pathway. We here further investigated whether YC‐1 promotes learning behaviour in Morris water maze and avoidance tests. It was found that YC‐1 shortened the escape latency in the task of water maze, increased and decreased the retention scores in passive and active avoidance task, respectively. Administration of YC‐1 30 min after foot‐shock stimulation did not significantly affect retention scores in response to passive avoidance test. Administration of scopolamine, a muscarinic antagonist, markedly impaired the memory acquisition. Pretreatment of YC‐1 inhibited the scopolamine‐induced learning deficit. The enhancement of learning behaviour by YC‐1 was antagonized by intracerebroventricular injection of NOS inhibitor L‐NAME and PKG inhibitors of KT5823 and Rp‐8‐Br‐PET‐cGMPS, indicating that NO‐cGMP‐PKG pathway is also involved in the learning enhancement action of YC‐1. YC‐1 is thus a good drug candidate for the improvement of learning and memory.
The neuroprotective effect of progesterone after traumatic brain injury in male mice is independent of both the inflammatory response and growth factor expression
Authors: Jones Nigel C. , Constantin Despina , Prior Malcolm J. W. , Morris Peter G. , Marsden Charles A. , Murphy Sean 
Published: January 2009

AbstractPrevious studies suggest that progesterone may possess neuroprotective properties after traumatic insult but, with the exception of reduced formation of cerebral oedema, limited experimental evidence has been presented to support this claim. In the present study we focused on the effect of progesterone treatment on structural and functional deficits in an experimental model of traumatic brain injury. Female mice exhibited significantly (P = 0.0445) reduced lesion volumes compared with males after aseptic cryogenic cerebral injury (ACI), suggesting that female sex steroids provide protection against this injury. In male mice, progesterone treatment after injury (three intraperitoneal doses of 8 mg/kg) reduced lesion volume (P = 0.0429) and improved performance in a spatial cognitive task (Morris water maze; P = 0.0014). However, progesterone had no demonstrable effect on the formation of oedema as measured using T2‐weighted magnetic resonance imaging, nor did it affect brain water content. The pro‐inflammatory cytokines TNF‐α and IL‐1β, and growth factors BDNF and G‐CSF, were all strongly transcriptionally activated after ACI. However, progesterone administration did not affect expression of these genes. This study provides strong evidence that progesterone possesses neuroprotective properties in a mouse model of traumatic brain injury, but suggests that the steroid achieves this effect through mechanism(s) independent of the inflammatory response or growth factor up‐regulation.
Vasopressin facilitates glycinergic and GABAergic synaptic transmission in developing hypoglossal motoneurons
Authors: Reymond‐Marron I. , Raggenbass M. , Zaninetti M. 
Published: January 2009

AbstractThe hypoglossal nucleus of young rats contains vasopressin binding sites and vasopressin can directly excite hypoglossal motoneurons. In addition, indirect evidence suggests that vasopressin can enhance the synaptic input to motoneurons. We have characterized this latter effect by using brainstem slices and whole‐cell recordings. We found that, in the presence of blockers of fast glutamatergic transmission, vasopressin strongly facilitated inhibitory synaptic activity. On average, vasopressin caused a six‐fold increase in the frequency and a 1.5‐fold increase in the amplitude of GABAergic postsynaptic currents. The effect of vasopressin on glycinergic postsynaptic currents was similar in magnitude. Vasopressin did not affect the frequency of GABAergic or glycinergic miniature postsynaptic currents, indicating that the peptide‐induced facilitation of inhibitory transmission was mediated by receptors located on the somatodendritic region rather than on axon terminals of presynaptic neurons. The pharmacological profile of these receptors was determined by using d[Cha4]AVP and dVDAVP, selective agonists of V1b and V2 vasopressin receptors, respectively, and Phaa‐D‐Tyr‐(Et)‐Phe‐Gln‐Pro‐Arg‐Arg‐NH2, a selective antagonist of V1a vasopressin receptors. The two agonists had no effect on the frequency of inhibitory postsynaptic currents. By contrast, the antagonist suppressed the vasopressin‐induced facilitation of these currents, indicating that the receptors involved were exclusively of the V1a type. Thus, vasopressin exerts a dual action on hypoglossal motoneurons: a direct excitatory action and an indirect action mediated by GABAergic and glycinergic synapses. By virtue of this dual effect, vasopressin could alter the input–output properties of these motoneurons. Alternatively, it could play a role in generating or modulating specific motor patterns.
Translation of an integral membrane protein in distal dendrites of hippocampal neurons
Authors: Grigston Jeffrey C. , VanDongen Hendrika M. A. , McNamara II James O. , VanDongen Antonius M. J. 
Published: January 2009

AbstractMaintenance of synaptic plasticity requires protein translation. Because changes in synaptic strength are regulated at the level of individual synapses, a mechanism is required for newly translated proteins to specifically and persistently modify only a subset of synapses. Evidence suggests this may be accomplished through local translation of proteins at or near synapses in response to plasticity‐inducing patterns of activity. A number of proteins important for synaptic function are integral membrane proteins, which require a specialized group of organelles, proteins and enzymatic activities for proper synthesis. Dendrites appear to contain machinery necessary for the proper production of these proteins, and mRNAs for integral membrane proteins have been found localized to dendrites. Experiments are described that investigate the local translation of membrane proteins in the dendrites of cultured rat hippocampal neurons, using fluorescence recovery after photobleaching. Neurons were transfected with cDNAs encoding a fluorescently labeled transmembrane protein, TGN‐38. Under conditions where the transport of this reporter construct was inhibited, the appearance of newly synthesized protein was observed via fluorescent microscopy. The dendritic translation of this protein required activation of glutamate receptors. The results demonstrate a functional capacity for activity‐dependent synthesis of integral membrane proteins for distal dendrites in hippocampal neurons.