bluuebunny/crossref_metadata_2025_split huggingface dataset:
Selective dopaminergic lesions of the ventral tegmental area impair preference for sucrose but not for male sexual pheromones in female mice
Authors: Martínez‐Hernández José , Lanuza Enrique , Martínez‐García Fernando 
Published: August 2006

AbstractThe role of the meso‐accumbens dopaminergic pathway in reward‐related behaviours is the subject of intense investigation. In this regard, here we analyse the effects of specific lesions of dopaminergic cells of the ventral tegmental area (VTA) of female mice on two goal‐directed behaviours, namely sucrose preference (intake of sucrose solution vs. water) and preference for male sexual pheromones (exploration of male‐soiled vs. clean bedding). The results indicate that partial lesions of the VTA that impair neither locomotion nor general exploratory behaviour reduce the preference for sucrose (over a 48‐h period) but do not alter the innate attraction that females display for male sexual pheromones (in 5‐min tests). This differential effect of the lesions can be interpreted as demonstrating the existence of separate neural mechanisms and circuits for signalling the reward of different natural reinforcers (e.g. sweet taste of sucrose and sexual pheromones). Alternatively, VTA lesions may result in an impaired attribution of incentive salience (which depends on the dopaminergic tegmento‐striatal system) of sucrose‐predicting cues, thus leading to a long‐term decrease in sucrose consumption. By contrast, the same lesions do not affect the unconditioned attraction to male‐derived pheromones, which may depend on amygdalo‐striatal pathways.
Differential down‐regulation of voltage‐gated calcium channel currents by glutamate and BDNF in embryonic cortical neurons
Authors: Bouron Alexandre , Boisseau Sylvie , De Waard Michel , Peris Leticia 
Published: August 2006

SummaryIn the embryonic brain, post‐mitotic cortical neurons migrate from their place of origin to their final location. Various external factors such as hormones, neurotransmitters or peptides regulate their migration. To date, however, only a few studies have investigated the effects of these external factors on the electrical properties of the newly formed embryonic cortical neurons. The aim of the present study was to determine whether glutamate and brain‐derived neurotrophic factor (BDNF), known to regulate neuronal cell migration, could modulate currents through voltage‐gated calcium channels (ICa) in cortical neurons isolated from embryonic day 13 (E13) mouse foetuses. Whole cell recordings of ICa showed that E13 cortical cells kept 1 day in vitro expressed functional low‐ and high‐voltage activated (LVA and HVA) Ca2+ channels of T‐, L‐ and N‐types. A 1‐day glutamate treatment non‐specifically inhibited LVA and HVA ICa whereas BDNF down‐regulated HVA with N‐type ICa being more depressed than L‐type ICa. The glutamate‐induced ICa inhibition was mimicked by NMDA. BDNF exerted its action by recruiting trkB receptors and SKF‐96365‐sensitive channels. BAPTA prevented the glutamate‐ and the BDNF‐dependent inhibition of Ica, indicating a Ca2+‐dependent mechanism of action. It is proposed that an influx of Ca2+ through NMDA receptors depresses the expression of LVA and HVA Ca2+ channels whereas a Ca2+ influx through SKF‐96365‐sensitive TRPC (transient receptor potential protein of C subtype) channels preferentially inhibits the expression of HVA Ca2+ channels. Glutamate and BDNF appear as potent modulators of the electrical properties of early post‐mitotic neurons. By down‐regulating ICa they could exert a neuroprotective action on embryonic cortical neurons.
Role of the synprint site in presynaptic targeting of the calcium channel CaV2.2 in hippocampal neurons
Authors: Szabo Zsolt , Obermair Gerald J. , Cooper Conan B. , Zamponi Gerald W. , Flucher Bernhard E. 
Published: August 2006

AbstractSequences in the cytoplasmic II–III loop of CaV2 voltage‐gated calcium channels, termed the synaptic protein interaction (synprint) site, are considered important for the functional incorporation of presynaptic calcium channels into the synaptic vesicle fusion apparatus. Two novel CaV2.2 splice variants lack large parts of the cytoplasmic II‐III loop (Δ1 R756‐L1139, Δ2 K737‐A1001) including the synprint protein–protein interaction domain. Here we expressed green fluorescent protein (GFP)‐α1B subunit fusion constructs of CaV2.2 splice variants in mouse hippocampal neurons to study their distribution in distinct neuronal compartments and to address the question of whether and how the synprint site functions in the presynaptic targeting of N‐type calcium channels. Similar to full‐length GFP‐α1B but divergent from the somatodendritic α1C‐HA (CaV1.2) channel type, the splice variants GFP‐α1B‐Δ1 and GFP‐α1B‐Δ2 were targeted into the axons. Nevertheless, their ability to form bona fide presynaptic clusters was almost abolished for GFP‐α1B‐Δ1 and significantly reduced for GFP‐α1B‐Δ2. Thus, the synprint site is important for normal synaptic targeting of CaV2.2 but not essential. Conversely, insertion of the synprint site into the II–III loop of α1C‐HA did not restore axonal targeting or synaptic clustering. Together these results indicate that protein–protein interactions with the synprint site must cooperate with other targeting mechanisms in the incorporation of CaV2.2 into presynaptic specializations of hippocampal neurons but are neither necessary nor sufficient for axonal targeting. The unique targeting properties of the splice variants lacking the synprint site are suggestive of specific functions of these calcium channels apart from activating fast synaptic transmission.
5‐HT4 receptor activation induces long‐lasting EPSP‐spike potentiation in CA1 pyramidal neurons
Authors: Mlinar Boris , Mascalchi Simona , Mannaioni Guido , Morini Raffaella , Corradetti Renato 
Published: August 2006

AbstractRecent studies implicated involvement of the 5‐hydroxytryptamine4(5‐HT4) receptor in cognitive and emotional processes. The highest 5‐HT4 receptor densities in the brain are found in the limbic system including the hippocampus. Here we used the selective 5‐HT4 receptor full agonist,N‐pentyl‐N′‐aminoguanidine carbazimidamide (SDZ‐216454) to characterize effects of 5‐HT4 receptor activation in whole‐cell and field recordings in the area CA1 in hippocampal slices prepared from 3 to 4‐ and 6 to 9‐week‐old rats, respectively. Extracellular recordings showed that transient 5‐HT4 receptor activation by 10–20 min application of SDZ‐216454 induces field excitatory postsynaptic potential (fEPSP)‐population spike potentiation (ESP5‐HT4), which persisted for as long as we held the recordings (> 2 h). ESP5‐HT4displayed characteristics different from EPSP‐spike potentiation that accompanies long‐term potentiation; it developed without an associated increase in synaptic transmission, was independent on afferent input, activity of postsynaptic neurons andN‐methyl‐d‐aspartate receptor activation; and was expressed in the presence of GABA receptor antagonists. ESP5‐HT4was also induced by transient application of the natural neurotransmitter, 5‐HT. The increase in the evoked population spike (PS) induced by SDZ‐216454 was not prevented by blockers of hyperpolarization‐activated cation current (Ih), Cs+and ZD‐7288, but was mimicked and occluded by 150 µmBa2+. Whole‐cell voltage‐clamp recordings from pyramidal neurons demonstrated that SDZ‐216454 application increases membrane resistance with a concomitant decrease in a Ba2+‐sensitive inwardly rectifying K+current and the Ba2+‐insensitive K+current underlying slow afterhyperpolarization (IsAHP). We conclude that 5‐HT4 receptor activation may cause a long‐lasting excitability increase in CA1 pyramidal neurons by inhibition of a Ba2+‐sensitive inwardly rectifying K+current.
Distinct expression of Cbln family mRNAs in developing and adult mouse brains
Authors: Miura Eriko , Iijima Takatoshi , Yuzaki Michisuke , Watanabe Masahiko 
Published: August 2006

AbstractCbln1 belongs to the C1q and tumour necrosis factor superfamily, and plays crucial roles as a cerebellar granule cell‐derived transneuronal regulator for synapse integrity and plasticity in Purkinje cells. Although Cbln2–Cbln4 are also expressed in the brain and could form heteromeric complexes with Cbln1, their precise expressions remain unclear. Here, we investigated gene expression of the Cbln family in developing and adult C57BL mouse brains by reverse transcriptase‐polymerase chain reaction (RT‐PCR), Northern blot, and high‐resolution in situ hybridization (ISH) analyses. In the adult brain, spatial patterns of mRNA expression were highly differential depending on Cbln subtypes. Notably, particularly high levels of Cbln mRNAs were expressed in some nuclei and neurons, whereas their postsynaptic targets often lacked or were low for any Cbln mRNAs, as seen for cerebellar granule cells/Purkinje cells, entorhinal cortex/hippocampus, intralaminar group of thalamic nuclei/caudate‐putamen, and dorsal nucleus of the lateral lemniscus/central nucleus of the inferior colliculus. In the developing brain, Cbln1, 2, and 4 mRNAs appeared as early as embryonic day 10–13, and exhibited transient up‐regulation during the late embryonic and neonatal periods. For example, Cbln2 mRNA was expressed in the cortical plate of the developing neocortex, displaying a high rostromedial to low caudolateral gradient. In contrast, Cbln3 mRNA was selective to cerebellar granule cells throughout development, and its onset was as late as postnatal day 7–10. These results will provide a molecular‐anatomical basis for future studies that characterize roles played by the Cbln family.
Impaired behavioural and molecular adaptations to dopamine denervation and repeated L‐DOPA treatment in Nur77‐knockout mice
Authors: St‐Hilaire Michel , Bourhis Emmanuelle , Lévesque Daniel , Rouillard Claude 
Published: August 2006

AbstractWe have previously shown that dopamine (DA) denervation and repeated L‐DOPA treatment modulate the pattern of Nur77 mRNA expression in the striatum. However, the exact role of this nuclear receptor in L‐DOPA‐induced molecular and behavioural adaptations observed in animal models of Parkinson's disease is still unknown. In the present study, we investigated the effects of Nur77 gene deletion on the development of behavioural sensitization and on changes in the regulation of neuropeptides and DA D3 receptor expression following DA denervation and repeated L‐DOPA treatment in Nur77+/+ and Nur77–/– hemiparkinsonian mice. One week postsurgery, hemiparkinsonian mice were treated with L‐DOPA (10 mg/kg) plus benserazide (3 mg/kg) once a day for 7 days. Despite similar extents of nigrostriatal denervation, L‐DOPA‐induced rotational response was exacerbated in Nur77–/– mice compared to Nur77+/+ ones. However, the rate of increase of the rotational behaviour after repeated L‐DOPA injections was similar in the two mouse strains. Lesioning the nigrostriatal pathway increased enkephalin (ENK) and neurotensin (NT) mRNA levels in both mouse strains. However, the up‐regulation of these neuropeptides was significantly reduced in Nur77–/– mice. There was no difference in the modulation of D3 receptor density and dynorphin (DYN) mRNA expression between the two mouse strains. The present results suggest that Nur77 is involved in setting the threshold level for L‐DOPA‐induced rotational behaviour, rather than controlling the development of behavioural sensitization. This specific behavioural change is associated with a selective regulation of neuropeptide expression specifically in the indirect striatal output pathway.
Lactosamine modulates the rate of migration of GnRH neurons during mouse development
Authors: Bless Elizabeth , Raitcheva Denitza , Henion Timothy R. , Tobet Stuart , Schwarting Gerald A. 
Published: August 2006

AbstractGonadotropin‐releasing hormone (GnRH) neurons are derived from progenitor cells in the olfactory placodes and migrate from the vomeronasal organ (VNO) across the cribriform plate into the forebrain. At embryonic day (E)12 in the mouse most of these neurons are still in the nasal compartment but by E15 most GnRH neurons have migrated into the forebrain. Glycoconjugates with carbohydrate chains containing terminal lactosamine are expressed by neurons in the main olfactory epithelium and in the VNO. One of the key enzymes required to regulate the synthesis and expression of lactosamine, β1,3‐N‐acetylglucosaminyltransferase‐1 (β3GnT1), is strongly expressed by neurons in the olfactory epithelium and VNO, and on neurons migrating out of the VNO along the GnRH migratory pathway. Immunocytochemical analysis of lactosamine and GnRH in embryonic mice reveals that the percentage of lactosamine+–GnRH+ double‐labeled neurons decreases from > 80% at E13, when migration is near its peak, to ∼ 30% at E18.5, when most neurons have stopped migrating. In β3GnT1–/– mice, there is a partial loss of lactosamine expression on GnRH neurons. Additionally, a greater number of GnRH neurons were retained in the nasal compartment of null mice at E15 while fewer GnRH neurons were detected later in embryonic development in the ventral forebrain. These results suggest that the loss of lactosamine on a subset of GnRH neurons impeded the rate of migration from the nose to the brain.
Effects of expectation on amygdala‐kindled convulsions and interictal behaviour in rats: confirmation of a Pavlovian mechanism
Authors: Barnes Steven J. , Pinel John P. J. , Wee Ellisa , Archambault Jason , Ailon Tamir 
Published: August 2006

AbstractWe found evidence that the effects of exposure to the stimulation environment on the convulsions and interictal behaviour of basolateral amygdala (BA)‐kindled rats are the result of Pavlovian conditioning. In Experiment 1, the rats first received 45 BA stimuli in one environment (CS+) and 45 sham stimuli in another environment (CS–). During this first phase of the experiment, the CS+ and CS– began to exert differential effects on interictal behaviour and convulsions. Then, during the second phase, rats received 45 stimuli and 45 sham stimuli, either as before in their original CS+ and CS– (nonreversal rats) or with their original CS+ and CS– interchanged (reversal rats). During the second phase, the CS+ and CS– continued to exert the same pattern of differential effects on the interictal behaviour and convulsions of the nonreversal rats, whereas the reversal rats began to display the reverse pattern. In Experiment 2, rats received 60 sham stimuli in one environment (CS1). Then, half of the rats received 30 stimuli in a second environment (CS2) and 30 sham stimuli in CS1 (no‐pre‐exposure rats), whereas the other half (pre‐exposure rats) received 30 stimuli and 30 sham stimuli in CS1. Pre‐exposure to the stimulation environment attenuated the kindled convulsions. These findings confirm that the conditioned effects of kindling are mediated by a Pavlovian mechanism.
Electroconvulsive seizure increases adult hippocampal angiogenesis in rats
Authors: Newton Samuel S. , Girgenti Matthew J. , Collier Emily F. , Duman Ronald S. 
Published: August 2006

AbstractElectroconvulsive seizure has a proven therapeutic application in the treatment of severe depression and treatment‐resistant depression. Despite the efficacy of electroconvulsive seizure as a non‐chemical antidepressant treatment, the mechanism of action is unclear. Elevation in hippocampal trophic factor expression and concomitant cellular proliferation are thought to play a role in its action. We examined whether the reported induction of angiogenic factors and endothelial cell proliferation leads to an increase in vascular density. Two hippocampal regions, the dentate gyrus and the stratum lacunosum moleculare (SLM), were examined employing a combination of vascular density quantification, angiogenic gene expression analysis and immunohistochemistry. A 6% increase in vascular density was observed in the dentate gyrus but this did not achieve statistical significance. The SLM of the hippocampus exhibited a robust 20–30% increase in vascular density and was accompanied by an increase in expression of inhibitor of differentiation‐3. There was also an induction of the angiogenesis markers αVβ3 integrin and Del1. Increases in the vascular density of the SLM could be in response to enhanced metabolic activity in this region. This is supported by the induction of glutamine synthetase and the glutamate transporter GLT1.
Cross‐modal plasticity of the motor cortex while listening to a rehearsed musical piece
Authors: D'Ausilio A. , Altenmüller E. , Olivetti Belardinelli M. , Lotze M. 
Published: August 2006

AbstractLearning a musical piece requires the development of a strong linkage between sensory and motor representations. Audition plays a central role and a tight cortical auditory–motor corepresentation is a characteristic feature of music processing. Recent works have indicated the establishment of a functional connection between auditory and motor cortices during the learning of a novel piece, although no causal relation has yet been demonstrated. Here transcranial magnetic stimulation of the cortical motor representation involved in musical performance was used to test excitability changes in piano players during auditory presentation of a rehearsed and a non‐rehearsed piece. Results showed an increased motor excitability for the rehearsed but not for the non‐rehearsed piece. Moreover, we observed an increase of excitability over time as intracortical facilitation was already present after 30 min of training whereas cortico‐spinal facilitation increased after a longer training period (5 days).
Healthy‐side dominance of middle‐ and long‐latency neuromagnetic fields in idiopathic sudden sensorineural hearing loss
Authors: Li L. P. H. , Shiao A. S. , Chen L. F. , Niddam D. M. , Chang S. Y. , Lien C. F. , Lee S. K. , Hsieh J. C. 
Published: August 2006

AbstractAny lesion along the neural axis may induce a subsequent functional reorganization at the level above. The present study used magnetoencephalography to investigate auditory‐evoked magnetic fields [a component of the middle‐latency auditory evoked fields peaking at ~50 ms (P50m) and a component of the long‐latency auditory evoked fields peaking at ~100 ms (N100m)] on stimulation of both healthy and affected ears in patients with acute unilateral idiopathic sudden sensorineural hearing loss (ISSNHL) of moderate degree in order to elucidate the functional plasticity of the auditory system. Sixteen right‐handed, previously untreated adult patients with acute unilateral left (n = 8) or right (n = 8) ISSNHL of moderate degree were studied. Sixteen right‐handed healthy volunteers with normal hearing served as control. Auditory neuromagnetic responses, measured by a whole‐head 306‐channel neuromagnetometer, were detected by monaural tone stimulation applied to affected and healthy ears, respectively, in different sessions. Intragroup and intergroup interhemispheric differences of peak dipole strengths and latencies of P50m and N100m, respectively, to monaural tones were evaluated. Healthy‐side amplitude dominance of both P50m and N100m was found in ISSNHL, i.e. contralateral dominance was preserved on affected‐ear stimulation but ipsilateral dominance was seen on healthy‐ear stimulation. The phenomena could be attributed to the combined contralateral attenuation and ipsilateral enhancement of P50m and N100m activity in response to healthy‐ear stimulation. Our findings confirmed that functional modulation can occur within the first few tens of milliseconds of evoked response at the auditory cortex in ISSNHL. The mechanisms of healthy‐side dominance might be ascribed to a functional retune of auditory pathways, i.e. conjoined contralateral inhibition and ipsilateral excitation of the auditory pathway in response to healthy‐ear stimulation. The effect could be registered in cortical responses.
Associative Pavlovian conditioning leads to an increase in spinophilin‐immunoreactive dendritic spines in the lateral amygdala
Authors: Radley Jason J. , Johnson Luke R. , Janssen William G. M. , Martino Jeremiah , Lamprecht Raphael , Hof Patrick R. , LeDoux Joseph E. , Morrison John H. 
Published: August 2006

AbstractChanges in dendritic spine number and shape are believed to reflect structural plasticity consequent to learning. Previous studies have strongly suggested that the dorsal subnucleus of the lateral amygdala is an important site of physiological plasticity in Pavlovian fear conditioning. In the present study, we examined the effect of auditory fear conditioning on dendritic spine numbers in the dorsal subnucleus of the lateral amygdala using an immunolabelling procedure to visualize the spine‐associated protein spinophilin. Associatively conditioned rats that received paired tone and shock presentations had 35% more total spinophilin‐immunoreactive spines than animals that had unpaired stimulation, consistent with the idea that changes in the number of dendritic spines occur during learning and account in part for memory.
Laminin and growth factor receptor activation stimulates differential growth responses in subpopulations of adult DRG neurons
Authors: Tucker Budd A. , Rahimtula Masuma , Mearow Karen M. 
Published: August 2006

AbstractNeurons in the adult rat dorsal root ganglion (DRG) can be classified into at least three separate subpopulations based on morphologic and phenotypic differences. In this study we have focused on the growth response of these specific subpopulations in vitro with respect to laminin (LN) and growth factor receptor activation. Using a cell selection approach we show that LN‐induced neurite growth occurs in the absence of added trophic factors only in heavy‐chain neurofilament‐positive and calcitonin gene‐related peptide‐positive DRG neurons [nerve growth factor (NGF)‐responsive population]. In contrast, LN alone is not sufficient to stimulate significant neurite growth from lectin Griffonia simplicifolia IB4‐positive neurons (IB4+ve), although it is still required to elicit a growth response from these cells in the presence of glial‐derived neurotrophic factor (GDNF, e.g. neurite growth occurred only when cells were plated on LN in the presence of GDNF). By using chemical inhibitors we demonstrate that only the phosphatidylinositol 3 kinase (PI 3‐K)/Akt pathway is required for neurite growth from the NGF‐responsive cell population. However, both the PI 3‐K/Akt and MEK/mitogen‐activated protein kinase signaling pathways are required for neurite growth from the IB4+ve cell population. Thus, we have identified specific signaling events and environmental requirements associated with neurite growth for different subpopulations of adult DRG neurons, pointing to potential therapeutic targets while identifying an inability for any one treatment alone to repair peripheral nerve damage.