bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sexual dimorphisms in the effect of low‐level p25 expression on synaptic plasticity and memory
Authors: Ris L. , Angelo M. , Plattner F. , Capron B. , Errington M. L. , Bliss T. V. P. , Godaux E. , Giese K. P. 
Published: June 2005

Abstractp25, a degradation product of p35, has been reported to accumulate in the forebrain of patients with Alzheimer's disease. p25 as well as p35 are activators of cyclin‐dependent kinase 5 (Cdk5) although p25/Cdk5 and p35/Cdk5 complexes have distinct properties. Several mouse models with high levels of p25 expression exhibit signs of neurodegeneration. On the contrary, we have shown that low levels of p25 expression do not cause neurodegeneration and are even beneficial for particular types of learning and memory [Angelo et al., (2003) Eur J. Neurosci., 18, 423–431]. Here, we have studied the influence of low‐level p25 expression in hippocampal synaptic plasticity and in learning and memory for each sex separately in two different genetic backgrounds (129B6F1 and C57BL/6). Surprisingly, we found that low‐level p25 expression had different consequences in male and female mutants. In the two genetic backgrounds LTP induced by a strong stimulation of the Schaffer's collaterals (four trains, 1‐s duration, 5‐min interval) was severely impaired in male, but not in female, p25 mutants. Furthermore, in the two genetic backgrounds spatial learning in the Morris water maze was faster in female p25 mutants than in male transgenic mice. These results suggest that, in women, the production of p25 in Alzheimer's disease could be a compensation for some early learning and memory deficits.
Characterization of organotypic ventral mesencephalic cultures from embryonic mice and protection against MPP+ toxicity by GDNF
Authors: Jakobsen B. , Gramsbergen J. B. , Møller Dall A. , Rosenblad C. , Zimmer J. 
Published: June 2005

AbstractWe characterized organotypic ventral mesencephalic (VM) cultures derived from embryonic day 12 (E12) mice (CBL57/bL6) in terms of number of dopaminergic neurons, cell soma size and dopamine production in relation to time in vitro and tested the effects of 1‐methyl‐4‐phenylpyridinium (MPP+) and glial derived neurotrophic factor (GDNF) to validate this novel culture model. Dopamine production and dopaminergic neuron soma size increased dramatically with time in vitro, whereas the number of dopamine neurons declined by approximately 30% between week 1 and week 2, which was further reduced after week 4. GDNF treatment (100 ng/mL) increased dopaminergic neuron soma size (up to 43%) and DOPAC production (approximately three‐fold), but not the number of dopamine neurons in control cultures. One‐week‐old cultures were more vulnerable to MPP+, than three‐week‐old cultures. The EC50 for dopamine depletion after 2 days exposure and 15 days of recovery were 0.6 and 7 µm, respectively. Both pre‐treatment and post‐treatment with GDNF are important to obtain maximal protection against MPP+ toxicity. In one‐week‐old cultures (5 µm MPP+, 2 days) GDNF provided potent neuroprotection with dopamine contents reaching control levels and number of tyrosine hydroxylase (TH)+ cells up to 80% of control, but in three‐week‐old cultures (10 µm MPP+, 2 days) the protective potential of GDNF was markedly reduced. Long recovery periods after MPP+ exposure are required to distinguish between reversible or irreversible toxic and/or trophic effects.
Neuroanatomical correlates of voluntary inhibition of accommodation/vergence under monocular open‐loop viewing conditions
Authors: Richter H. O. , Andersson J. , Schneider H. , Långström B. 
Published: June 2005

AbstractThe purpose of this work is to identify human neural circuits involved in inhibition of accommodation/vergence by contrasting the cortical functions subservient to negative voluntary accommodation/vergence (NVA) with those evoked by active fixation in darkness (FIX). Five subjects with normal corrected acuity were studied using positron emission tomography and the HO bolus technique. The dominant right eye viewed a laser speckle pattern (633 nm) whose direction and velocity of motion were determined by the refractive state of the eye. The speckle pattern was presented at a distance of 1.8 m (0.55 D). The non‐dominant eye was patched. Subjects performed two tasks counterbalanced for order effects: (i) attempted fixation on the remembered target in darkness with the dominant eye open and ‘fixating’; and (ii) voluntary reduction of the laser speckle flow during each alternate 20‐s epoch when a convex +2.0 D lens was placed in front of the right eye causing the speckle pattern to move downwards at 3 °/s. Comparison of the condition of NVA with the condition of FIX indicated widespread occipital activation. Decreases in absolute regional cerebral blood flow occurred in the superior parietal cortex (BA 5), frontal cortex (BA 8 and 10) and within the postcentral/precentral gyrus (BA 1/2/3/4) bilaterally where deactivation clusters eclipsed the presumed neck and shoulder areas. Negative accommodation/vergence appears to be driven by a reduction of parasympathetic tone, and has the effect of shutting down brain regions known to be involved in regulating visual search as well as a centrally controlled eye–head–neck–shoulder motor programme responsible for posturing gaze.
Loss of forebrain cholinergic neurons and impairment in spatial learning and memory in LHX7‐deficient mice
Authors: Fragkouli Apostolia , Hearn Catherine , Errington Mick , Cooke Sam , Grigoriou Maria , Bliss Tim , Stylianopoulou Fotini , Pachnis Vassilis 
Published: June 2005

AbstractThe identification of the genetic determinants specifying neuronal networks in the mammalian brain is crucial for the understanding of the molecular and cellular mechanisms that ultimately control cognitive functions. Here we have generated a targeted allele of the LIM‐homeodomain‐encoding gene Lhx7 by replacing exons 3–5 with a LacZ reporter. In heterozygous animals, which are healthy, fertile and have no apparent cellular deficit in the forebrain, b‐galactosidase activity reproduces the pattern of expression of the wild‐type Lhx7 locus. However, homozygous mutant mice show severe deficits in forebrain cholinergic neurons (FCNs), while other classes of forebrain neurons appear unaffected. Using the LacZ reporter as a marker, we show that in LHX7‐deficient mice FCN progenitors survive but fail to generate cholinergic interneurons in the striatum and cholinergic projection neurons in the basal forebrain. Analysis of behaviour in a series of spatial and non‐spatial learning and memory tasks revealed that FCN ablation in Lhx7 mutants is associated with severe deficits in spatial but only mild impairment of non‐spatial learning and memory. In addition, we found no deficit in long‐term potentiation in mutant animals, suggesting that FCNs modulate hippocampal function independently of its capacity to store information. Overall our experiments demonstrate that Lhx7 expression is required for the specification or differentiation of cholinergic forebrain neurons involved in the processing of spatial information.
Lesions to the subthalamic nucleus decrease impulsive choice but impair autoshaping in rats: the importance of the basal ganglia in Pavlovian conditioning and impulse control
Authors: Winstanley Catharine A. , Baunez Christelle , Theobald David E. H. , Robbins Trevor W. 
Published: June 2005

AbstractAlthough the subthalamic nucleus (STN) is involved in regulating motor function, and inactivation of this structure relieves the motor symptoms in Parkinsonian patients, recent data indicate that corticosubthalamic connections are involved in both the regulation of attention and the ability to withhold from responding. Considerable evidence suggests that the neural circuitry underlying such behavioural disinhibition or impulsive action can be at least partially dissociated from that implicated in impulsive decision‐making and it has been suggested that the tendency to choose impulsively is related to the ability to form and use Pavlovian associations. To explore these hypotheses further, STN‐lesioned rats were tested on the delay‐discounting model of impulsive choice, where impulsivity is defined as the selection of a small immediate over a larger delayed reward, as well as in a rodent autoshaping paradigm. In contrast to previous reports of increased impulsive action, STN lesions decreased impulsive choice but dramatically impaired the acquisition of the autoshaping response. When the STN was lesioned after the establishment of autoshaping behaviour, lesioned subjects were more sensitive to the omission of reward, indicative of a reduction in the use of Pavlovian associations to control autoshaping performance. These results emphasize the importance of the STN in permitting conditioned stimulus–unconditioned stimulus associations to regulate goal‐seeking, a function which may relate to the alterations in impulsive choice observed in the delay‐discounting task. These data bear a striking similarity to those observed after lesions of the orbitofrontal cortex and are suggestive of an important role for corticosubthalamic connections in complex cognitive behaviour.
A kind of auditory ‘primitive intelligence’ already present at birth
Authors: Carral Vanessa , Huotilainen Minna , Ruusuvirta Timo , Fellman Vineta , Näätänen Risto , Escera Carles 
Published: June 2005

Abstract‘Primitive intelligence’ in audition refers to the capacity of the auditory system to adaptatively model the acoustic regularity and react neurophysiologically to violations of such regularity, thus supporting the ability to predict future auditory events. In the present study, event‐related brain potentials to pairs of tones were recorded in 11 human newborns to determine the infants' ability to extract an abstract acoustic rule, the direction of a frequency change. Most of the pairs (standard,P = 0.875) were of ascending frequency (i.e. the second tone higher than the first), while the remaining pairs (deviant,P = 0.125) were of descending frequency (the second tone being lower). Their frequencies varied among seven levels to prevent discrimination between standard and deviant pairs on the basis of absolute frequencies. We found that event‐related brain potentials to deviant pairs differed in amplitude from those to standard pairs at 50–450 ms from the onset of the second tone of a pair, indicating the infants' ability to represent the abstract rule. This finding suggests the early ontogenetic origin of ‘primitive intelligence’ in audition that eventually may form a prerequisite for later language acquisition.
GABAB and CB1 cannabinoid receptor expression identifies two types of septal cholinergic neurons
Authors: Nyíri Gábor , Szabadits Eszter , Cserép Csaba , Mackie Ken , Shigemoto Ryuichi , Freund Tamás F. 
Published: June 2005

AbstractSeptohippocampal cholinergic neurons play key roles in learning and memory processes, and in the generation of hippocampal theta rhythm. The range of receptors for endogenous modulators expressed on these neurons is unclear. Here we describe GABAB 1a/b receptor (GABABR) and type 1 cannabinoid receptor (CB1R) expression in rat septal cholinergic [i.e. choline acetyltransferase (ChAT)‐positive] cells. Using double immunofluorescent staining, we found that almost two‐thirds of the cholinergic cells in the rat medial septum were GABABR positive, and that these cells had significantly larger somata than did GABABR‐negative cholinergic neurons. We detected CB1R labelling in somata after axonal protein transport was blocked by colchicine. In these animals about one‐third of the cholinergic cells were CB1R positive. These cells again had larger somata than CB1R‐negative cholinergic neurons. The analyses confirmed that the size of GABABR‐positive and CB1R‐positive cholinergic cells were alike, and all CB1R‐positive cholinergic cells were GABABR positive as well. CB1R‐positive cells were invariably ChAT positive. All retrogradely labelled septohippocampal cholinergic cells were positive for GABABR and at least half of them also for CB1R. These data shed light on the existence of at least two cholinergic cell types in the medial septum: one expresses GABABR and CB1R, has large somata and projects to the hippocampus, whereas the other is negative for GABABR and CB1R and has smaller somata. The results also suggest that cholinergic transmission in the hippocampus is fine‐tuned by endocannabinoid signalling.
The dopamine‐synthesizing cells in the swimming larva of the tunicate Ciona intestinalis are located only in the hypothalamus‐related domain of the sensory vesicle
Authors: Moret Frédéric , Christiaen Lionel , Deyts Carole , Blin Maryline , Joly Jean‐Stéphane , Vernier Philippe 
Published: June 2005

AbstractDopamine is a major neuromodulator synthesized by numerous cell populations in the vertebrate forebrain and midbrain. Owing to the simple organization of its larval nervous system, ascidian tunicates provide a useful model to investigate the anatomy, neurogenesis and differentiation of the dopaminergic neural network underlying the stereotypical swimming behaviour of its chordate‐type larva. This study provides a high‐resolution cellular analysis of tyrosine hydroxylase (TH)‐positive and dopamine‐positive cells in Ciona intestinalis embryos and larvae. Dopamine cells are present only in the sensory vesicle of the Ciona larval brain, which may be an ancestral chordate feature. The dopamine‐positive cells of the ascidian sensory vesicle are located in the expression domain of homologues of vertebrate hypothalamic markers. We show here that the larval coronet cells also arise from this domain. As a similar association between coronet cells and the hypothalamus was reported in bony and cartilaginous fishes, we propose that part of the ascidian ventral sensory vesicle is the remnant of a proto‐hypothalamus that may have been present in the chordate ancestor. As dopaminergic cells are specified in the hypothalamus in all vertebrates, we suggest that the mechanisms of dopamine cell specification are conserved in the hypothalamus of Ciona and vertebrates. To test this hypothesis, we have identified new candidate regulators of dopaminergic specification in Ciona based on their expression patterns, which can now be compared with those in vertebrates.
Photoperiod regulates multiple gene expression in the suprachiasmatic nuclei and pars tuberalis of the Siberian hamster (Phodopus sungorus)
Authors: Johnston Jonathan D. , Ebling Francis J. P. , Hazlerigg David G. 
Published: June 2005

AbstractPhotoperiod regulates the seasonal physiology of many mammals living in temperate latitudes. Photoperiodic information is decoded by the master circadian clock in the suprachiasmatic nuclei (SCN) of the hypothalamus and then transduced via pineal melatonin secretion. This neurochemical signal is interpreted by tissues expressing melatonin receptors (e.g. the pituitary pars tuberalis, PT) to drive physiological changes. In this study we analysed the photoperiodic regulation of the circadian clockwork in the SCN and PT of the Siberian hamster. Female hamsters were exposed to either long or short photoperiod for 8 weeks and sampled at 2‐h intervals across the 24‐h cycle. In the SCN, rhythmic expression of the clock genes Per1, Per2, Cry1, Rev‐erbα, and the clock‐controlled genes arginine vasopressin (AVP) and d‐element binding protein (DBP) was modulated by photoperiod. All of these E‐box‐containing genes tracked dawn, with earlier peak mRNA expression in long, compared to short, photoperiod. This response occurred irrespective of the presence of additional regulatory cis‐elements, suggesting photoperiodic regulation of SCN gene expression through a common E‐box‐related mechanism. In long photoperiod, expression of Cry1 and Per1 in the PT tracked the onset and offset of melatonin secretion, respectively. However, whereas Cry1 tracked melatonin onset in short period, Per1 expression was not detectably rhythmic. We therefore propose that, in the SCN, photoperiodic regulation of clock gene expression primarily occurs via E‐boxes, whereas melatonin‐driven signal transduction drives the phasing of a subset of clock genes in the PT, independently of the E‐box.
Occipital (V6) and parietal (V6A) areas in the anterior wall of the parieto‐occipital sulcus of the macaque: a cytoarchitectonic study
Authors: Luppino Giuseppe , Hamed Suliann Ben , Gamberini Michela , Matelli Massimo , Galletti Claudio 
Published: June 2005

AbstractThe anterior wall of the parieto‐occipital sulcus (POs) of the macaque monkey, classically considered as part of Brodmann's area 19, contains two functionally distinct areas: a ventral, purely visual area, V6, and a dorsal area, V6A, containing visual neurons and neurons related to the control of arm movements. The aim of this study was to establish whether areas V6 and V6A, so far identified only on a functional basis, have a cytoarchitectonic counterpart. The cytoarchitectonic analysis of 13 hemispheres from ten macaque brains, cut along different planes of section, showed that the anterior wall of the POs contains three distinct areas. One is located in the ventralmost part of the wall, another in the dorsalmost part of the wall, and the third occupies an intermediate position. The ventralmost region displays architectonic features typical of the occipital cytoarchitectonic domain, whereas the two dorsal areas display architectonic features typical of the posterior parietal cortex. Analysis of myeloarchitecture and of the distribution of SMI‐32 immunoreactivity confirmed the cytoarchitectonic parcellation. Correlation of cytoarchitectonic maps with functional and hodological data strongly suggests that the ventral region corresponds to area V6, whereas the other two regions correspond to different subsectors of V6A, here named V6Av and V6Ad, respectively. The present data are in line with electrophysiological and hodological data, which suggest that area V6 is a classic extrastriate area, whereas V6A is an area of the posterior parietal cortex. They also suggest that V6A includes two separate cortical subdivisions, a view supported by preliminary functional and hodological data that needs further confirmation.
Functional properties of neuronal nicotinic acetylcholine receptors in the chick retina during development
Authors: Lecchi Marzia , McIntosh J. Michael , Bertrand Sonia , Safran Avinoam B. , Bertrand Daniel 
Published: June 2005

AbstractAcetylcholine (ACh) has been recognized for a long time as a major neurotransmitter in the retina, however, little is known about the contribution of acetylcholine receptors in synaptic processing. Moreover, even less information is available concerning their role during development. To address this question further, we examined the physiological and pharmacological properties of neuronal nicotinic acetylcholine receptors (nAChRs) in retinal ganglion cells from embryonic (E) 12–18‐day‐old Leghorn chicks. Patch‐clamp recordings in whole‐cell configuration revealed that at E12 approximately 21% of the ganglion cells responded to acetylcholine pulses with inward currents. The number of responsive cells progressively increased to 57% at E15 to reach up to 15 positive cells out of 15 cells tested at E18. Acetylcholine‐evoked responses could be subdivided, according to their time course, into fast and slowly desensitizing. Taking advantage of the selectivity of the frog toxin epibatidine (Epi), that preferentially activates heteromeric neuronal nicotinic acetylcholine receptors, we compared the currents evoked by this toxin vs. the effects of acetylcholine. A further characterization of the receptor diversity during development was to assess their sensitivity to the α‐conotoxin MII (α‐CTX‐MII), which has been shown to preferentially block α6‐ and α3β2‐containing receptors. These data demonstrate that ganglion cells of the chick retina express multiple receptor subtypes that progressively develop as a function of retina maturation.
Reduced infarct volume and differential effects on glial cell activation after hyperbaric oxygen treatment in rat permanent focal cerebral ischaemia
Authors: Günther Albrecht , Küppers‐Tiedt Lea , Schneider Philipp‐Moritz , Kunert Ivonne , Berrouschot Jörg , Schneider Dietmar , Roßner Steffen 
Published: June 2005

AbstractPermanent middle cerebral artery occlusion (MCAO) causes neurodegeneration and a robust activation of glial cells primarily in sensorimotor brain regions of rats. It has been shown that hyperbaric oxygen (HBO) increases oxygen supply to ischaemic areas and reduces neuronal cell loss. The effects of HBO treatment on microgliosis and astrogliosis in permanent cerebral ischaemia have not been addressed so far, but might be critical for neurodegeneration and neuroprotection, respectively. Therefore, we used spontaneously hypertensive rats with permanent MCAO to investigate the time window to start HBO and to compare the effects of different HBO treatment frequencies on infarct volume and on differences with regard to microgliosis and astrogliosis. Seven days after MCAO the infarct volume was calculated from Nissl‐stained brain sections by image analysis. HBO significantly decreased the infarct volume when used as early as 15, 90 or 180 min post‐MCAO by 24%, 16% and 13%, respectively, in the single‐treatment group. Repetitive HBO treatment (first HBO session 90 min after MCAO) was not effective. Microglial cells and astrocytes were detected by cytochemical fluorescent labelling and confocal laser scanning microscopy. In the single‐treatment group we observed significantly higher astrocyte immunoreactivity but decreased microglial density in the peri‐infarct region. These effects of HBO treatment on glial cells were not present in rats where HBO did not reduce the infarct volume (360 min after MCAO). Our data indicate that HBO‐induced suppression of microgliosis and aggravated response of astrocytes might contribute to the reported beneficial effects of early HBO treatment in cerebral ischaemia.
Knowing good from bad: differential activation of human cortical areas by positive and negative outcomes
Authors: Nieuwenhuis Sander , Slagter Heleen A. , Von Geusau Niels J. Alting , Heslenfeld Dirk J. , Holroyd Clay B. 
Published: June 2005

AbstractPrevious research has identified a component of the event‐related brain potential (ERP), the feedback‐related negativity, that is elicited by feedback stimuli associated with unfavourable outcomes. In the present research we used event‐related functional magnetic resonance imaging (fMRI) and electroencephalographic (EEG) recordings to test the common hypothesis that this component is generated in the caudal anterior cingulate cortex. The EEG results indicated that our paradigm, a time estimation task with trial‐to‐trial performance feedback, elicited a large feedback‐related negativity (FRN). Nevertheless, the fMRI results did not reveal any area in the caudal anterior cingulate cortex that was differentially activated by positive and negative performance feedback, casting doubt on the notion that the FRN is generated in this brain region. In contrast, we found a number of brain areas outside the posterior medial frontal cortex that were activated more strongly by positive feedback than by negative feedback. These included areas in the rostral anterior cingulate cortex, posterior cingulate cortex, right superior frontal gyrus, and striatum. An anatomically constrained source model assuming equivalent dipole generators in the rostral anterior cingulate, posterior cingulate, and right superior frontal gyrus produced a simulated scalp distribution that corresponded closely to the observed scalp distribution of the FRN. These results support a new hypothesis regarding the neural generators of the FRN, and have important implications for the use of this component as an electrophysiological index of performance monitoring and reward processing.