bluuebunny/crossref_metadata_2025_split huggingface dataset:
Modifications of cognitive and motor tasks affect the occurrence of event‐related potentials in the human cortex
Authors: Rektor Ivan , Brázdil Milan , Nestrašil Igor , Bareš Martin , Daniel Pavel 
Published: September 2007

AbstractThis study concerns the question of how task modification affects the frequency occurrence of event‐related potentials (ERP) inside the active cortical areas. In 13 candidates for epilepsy surgery, 156 sites in the temporal (74), frontal (73), and parietal (9) cortices were recorded by means of depth and subdural electrodes. Four modifications of the somatosensory evoked P3‐like potentials were performed; (i) an oddball paradigm with silent counting of target stimuli (P3c); (ii) an oddball paradigm with a hand movement in response to target stimuli (P3m); (iii) an S1–S2 paradigm, ERP in the P300 time window after the S2 stimulus, with silent counting of target stimuli (S2c), and (iv) an S1–S2 paradigm with a hand movement in response to target stimuli (S2m). In comparing the oddball paradigms with the S1–S2 (contingent negative variation, CNV) paradigms, four regions emerge that are significantly linked with the oddball P3; the prefrontal cortex, the cingulate, the amygdalo‐hippocampal complex, and the lateral temporal cortex. A prominent role of the cingulate and the fronto‐orbital cortex in the cognitive processing of movement was supported when tasks with identical cognitive loads but different required responses were compared. Even relatively simple cognitive tasks activate many cortical regions. The investigated areas were activated in all tests; however, small regions in each field were active or inactive in relation to the nature of the task. The study indicates a variable and task‐dependent internal organization of a highly complex and widely distributed system of active cortical areas.
Recovery from spinal cord injury differs between rat strains in a major histocompatibility complex‐independent manner
Authors: Birdsall Abrams M. , Josephson Anna , Dominguez Cecilia , Öberg Johanna , Diez Margarita , Spenger Christian , Olson Lars , Piehl Fredrik , Lidman Olle 
Published: September 2007

AbstractInflammation is a common characteristic of spinal cord injury. The nature of this response, whether it is beneficial or detrimental, has been the subject of debate. It has been reported that susceptibility to autoimmunity is correlated with increased functional impairment following spinal cord injury. As the ability to mount an autoimmune response has most consistently been associated with certain haplotypes of the major histocompatibility complex (MHC), we analysed the possible effects of the MHC haplotype on functional impairment and recovery following spinal cord injury. A contusion injury was induced in experimental autoimmune encephalomyelitis‐susceptible and ‐resistant rats [Dark Agouti, Lewis and Piebald Viral Glaxo (PVG), respectively]. We found that locomotion recovered significantly better in Dark Agouti rats compared with PVG and Lewis rats but an F2 intercross (PVG × PVG‐RT1av1) excluded the possibility that this difference was MHC haplotype‐dependent. Thus, we conclude that recovery following spinal cord injury is subject to considerable genetic heterogeneity that is not coupled to the MHC haplotype region. Continued research of genetic variants regulating recovery following spinal cord injury is warranted.
Frontal and temporal functional connections of the living human brain
Authors: Lacruz M. E. , García Seoane J. J. , Valentin A. , Selway R. , Alarcón G. 
Published: September 2007

AbstractConnections between human temporal and frontal cortices were investigated by intracranial electroencephalographic responses to electrical stimulation with 1‐ms single pulses in 51 patients assessed for surgery for treatment of epilepsy. The areas studied were medial temporal, entorhinal, lateral temporal, medial frontal, lateral frontal and orbital frontal cortices. Findings were assumed to be representative of human brain as no differences were found between epileptogenic and non‐epileptogenic hemispheres. Connections between intralobar temporal and frontal regions were common (43–95%). Connections from temporal to ipsilateral frontal regions were relatively uncommon (seen in 0–25% of hemispheres). Connections from frontal to ipsilateral temporal cortices were more common, particularly from orbital to ipsilateral medial temporal regions (40%). Contralateral temporal connections were rare (< 9%) whereas contralateral frontal connections were frequent and faster, particularly from medial frontal to contralateral medial frontal (61%) and orbital frontal cortices (57%), and between both orbital cortices (67%). Orbital cortex receives profuse connections from the ipsilateral medial (78%) and lateral (88%) frontal cortices, and from the contralateral medial (57%) and orbital (67%) frontal cortices. The high incidence of intralobar temporal connections supports the presence of temporal reverberating circuits. Frontal cortex projects within the lobe and beyond, to ipsilateral and contralateral structures.
Brain imaging of analgesic and antihyperalgesic effects of cyclooxygenase inhibition in an experimental human pain model: a functional MRI study
Authors: Maihöfner Christian , Ringler Ralf , Herrndobler Franz , Koppert Wolfgang 
Published: September 2007

AbstractOne of the most distressing symptoms of many neuropathic pain syndromes is the enhanced pain sensation to tactile or thermal stimulation (hyperalgesia). In the present study we used functional magnetic resonance imaging (fMRI) and explored brain activation patterns during acute impact pain and mechanical hyperalgesia in the human ultraviolet (UV)‐B model. To investigate pharmacological modulation, we examined potential differential fMRI correlates of analgesic and antihyperalgesic effects of two intravenous cyclooxygenase inhibitors, i.e. parecoxib and acetylsalicylic acid (ASA). Fourteen healthy volunteers participated in this double‐blinded, randomized and placebo‐controlled crossover study. Tactile stimuli and mechanical impact hyperalgesia were tested at the site of a UV‐B irradiation and acute mechanical pain was tested at a site distant from the irradiated skin. These measurements were conducted before and 30 min after a 5‐min intravenous infusion of either saline (placebo), parecoxib 40 mg or ASA 1000 mg. Acute mechanical pain and mechanical hyperalgesia led to widespread activations of brain areas known to comprise the human pain matrix. Analgesic effects were found in primary (S1) and secondary (S2) somatosensory cortices, parietal association cortex (PA), insula, anterior parts of the cingulate cortex and prefrontal cortices. These brain areas were also modulated under antihyperalgesic conditions. However, we observed a greater drug‐induced modulation of mainly PA and inferior frontal cortex during mechanical hyperalgesia; during acute mechanical pain there was a greater modulation of mainly bilateral S2. Therefore, the results of the present study suggest that there is a difference in the brain areas modulated by analgesia and antihyperalgesia.
Noise‐improved signal detection in cat primary visual cortex via a well‐balanced stochastic resonance‐like procedure
Authors: Funke Klaus , Kerscher Nicolas J. , Wörgötter Florentin 
Published: September 2007

AbstractAdding noise to a weak signal can paradoxically improve signal detection, a process called ‘stochastic resonance’ (SR). In the visual system, noise might be introduced by the image jitter resulting from high‐frequency eye movements, like eye microtremor and microsaccades. To test whether this kind of noise might be beneficial or detrimental for cortical signal detection, we performed single‐unit recordings from area 17 of anaesthetized cats while jittering the visual stimulus in a frequency and amplitude range resembling the possible range of eye movements. We used weak, sub‐ and peri‐threshold visual stimuli, on top of which we superimposed noise with variable jitter amplitude. In accordance with the typical SR effect, we found that small noise levels actually increased the signal‐to‐noise ratio (SNR) of previously weak cortical visual responses, while originally strong responses were little affected or even reduced. Above a certain noise level, the SNR dropped a little, but not as a result of increased background activity − as would be proposed by SR theory − but because of a lowered response to signal and noise. Therefore, it seems that the ascending visual pathway optimally utilizes signal detection improvement by a SR‐like process, while at the same time preventing spurious noise‐induced activity and keeping the SNR sufficiently high.
Brain edema and breakdown of the blood–brain barrier during methamphetamine intoxication: critical role of brain hyperthermia
Authors: Kiyatkin Eugene A. , Brown P. Leon , Sharma Hari S. 
Published: September 2007

AbstractTo clarify the role of brain temperature in permeability of the blood–brain barrier (BBB), rats were injected with methamphetamine (METH 9 mg/kg) at normal (23 °C) and warm (29 °C) environmental conditions and internal temperatures were monitored both centrally (nucleus accumbens, NAcc) and peripherally (skin and nonlocomotor muscle). Once NAcc temperatures peaked or reached 41.5 °C (a level suggesting possible lethality), animals were administered Evans blue dye (protein tracer that does not normally cross the BBB), rapidly anaesthetized, perfused and had their brains removed. All METH‐treated animals showed brain and body hyperthermia associated with relative skin hypothermia, suggesting metabolic activation coupled with peripheral vasoconstriction. While METH‐induced NAcc temperature elevation varied from 37.60 to 42.46 °C (or 1.2–5.1 °C above baseline), it was stronger at 29 °C (+4.13 °C) than 23 °C (+2.31 °C). Relative to control, METH‐treated animals had significantly higher brain levels of water, Na+, K+ and Cl–, suggesting brain edema, and intense immunostaining for albumin, indicating breakdown of the BBB. METH‐treated animals also showed strong immunoreactivity for glial fibrillary acidic protein (GFAP), possibly suggesting acute abnormality or damage of astrocytes. METH‐induced changes in brain water, albumin and GFAP correlated linearly with NAcc temperature (r = 0.93, 0.98 and 0.98, respectively), suggesting a key role of brain hyperthermia in BBB permeability, development of brain edema and subsequent functional and structural neural abnormalities. Therefore, along with a direct destructive action on neural cells and functions, brain hyperthermia, via breakdown of the BBB, may be crucial for both decompensation of brain functions and cell injury following acute METH intoxication, possibly contributing to neurodegeneration resulting from chronic drug use.
Antagonism of group III metabotropic glutamate receptors results in impairment of LTD but not LTP in the hippocampal CA1 region, and prevents long‐term spatial memory
Authors: Altinbilek Bengi , Manahan‐Vaughan Denise 
Published: September 2007

AbstractRecently it has emerged that hippocampal long‐term depression (LTD) may play an important role in the acquisition and storage of spatial memories. This form of synaptic plasticity is tightly regulated by metabotropic glutamate receptors (mGluRs) that negatively couple to adenylyl cyclase. Activation of group III mGluRs is necessary for persistent hippocampal LTD, but is not required for depotentiation or long‐term potentiation (LTP) in the dentate gyrus in vivo. In the CA1 region antagonism of group III mGluRs prevents LTD in vivo. Effects on LTP in vivo are as yet unknown. We investigated the effects of group III mGluR antagonism on LTP and LTD at Schaffer collateral‐CA1 synapses, and on spatial learning in the eight‐arm radial maze. Daily application of the group III mGluR antagonist (R,S)‐α‐cyclopropyl‐4‐phosphonophenylglycine (CPPG) resulted in impairment of long‐term (reference) memory, with effects becoming apparent 4 days after training and drug treatment began. Short‐term (working) memory was unaffected throughout the 10‐day study. Application of CPPG prevented LTD, but not LTP, in the CA1 region. These data suggest that activation of group III mGluRs is required for the establishment of spatial long‐term memory. Their exclusive role in mediating hippocampal LTD provides correlational evidence for a role for LTD in the type of spatial learning studied.
Hydroxy‐α‐sanshool activates TRPV1 and TRPA1 in sensory neurons
Authors: Koo Jae Yeon , Jang Yongwoo , Cho Hawon , Lee Chang‐Hun , Jang Kyoung Hwa , Chang Yong Ha , Shin Jongheon , Oh Uhtaek 
Published: September 2007

AbstractSanshools are major active ingredients of Zanthoxylum piperitum and are used as food additives in East Asia. Sanshools cause irritant, tingling and sometimes paresthetic sensations on the tongue. However, the molecular mechanism underlying the pungent or tingling sensation induced by sanshools is not known. Because many transient receptor potential (TRP) channels are responsible for the sensations induced by various spices and food additives, we expressed 17 TRP channels in human embryonic kidney (HEK) cells and investigated their activation by hydroxy‐α‐sanshool (HαSS) or hydroxy‐β‐sanshool (HβSS) isolated from Zanthoxylum piperitum. It was found that HαSS, but not HβSS, depolarized sensory neurons with concomitant firing of action potentials and evoked inward currents. Among 17 TRP channels expressed in HEK cells, HαSS caused Ca2+ influx in cells transfected with TRPV1 or TRPA1, and evoked robust inward currents in cells transfected with TRPV1 or TRPA1. In primary cultured sensory neurons, HαSS induced inward currents and Ca2+ influx in a capsazepine‐dependent manner. Moreover, HαSS‐induced currents and Ca2+ influx were greatly diminished in TRPV1–/– mice. HαSS evoked licking behavior when injected into a single hind paw of wild‐type mice, but this was much reduced in TRPV1‐deficient mice. These results indicate that TRPV1 and TRPA1 are molecular targets of HαSS in sensory neurons. We conclude that the activations of TRPV1 and TRPA1 by HαSS explain its unique pungent, tingling sensation.
Divergent co‐transmitter actions underlie motor pattern activation by a modulatory projection neuron
Authors: Stein Wolfgang , DeLong Nicholas D. , Wood Debra E. , Nusbaum Michael P. 
Published: September 2007

AbstractCo‐transmission is a common means of neuronal communication, but its consequences for neuronal signaling within a defined neuronal circuit remain unknown in most systems. We are addressing this issue in the crab stomatogastric nervous system by characterizing how the identified modulatory commissural neuron (MCN)1 uses its co‐transmitters to activate the gastric mill (chewing) rhythm in the stomatogastric ganglion (STG). MCN1 contains γ‐aminobutyric acid (GABA) plus the peptides proctolin and Cancer borealis tachykinin‐related peptide Ia (CabTRP Ia), which it co‐releases during the retractor phase of the gastric mill rhythm to influence both retractor and protractor neurons. By focally applying each MCN1 co‐transmitter and pharmacologically manipulating each co‐transmitter action during MCN1 stimulation, we found that MCN1 has divergent co‐transmitter actions on the gastric mill central pattern generator (CPG), which includes the neurons lateral gastric (LG) and interneuron 1 (Int1), plus the STG terminals of MCN1 (MCN1STG). MCN1 used only CabTRP Ia to influence LG, while it used only GABA to influence Int1 and the contralateral MCN1STG. These MCN1 actions caused a slow excitation of LG, a fast excitation of Int1 and a fast inhibition of MCN1STG. MCN1‐released proctolin had no direct influence on the gastric mill CPG, although it likely indirectly regulates this CPG via its influence on the pyloric rhythm. MCN1 appeared to have no ionotropic actions on the gastric mill follower motor neurons, but it did use proctolin and/or CabTRP Ia to excite them. Thus, a modulatory projection neuron can elicit rhythmic motor activity by using distinct co‐transmitters, with different time courses of action, to simultaneously influence different CPG neurons.
GABAergic projections from the hippocampus to the retrosplenial cortex in the rat
Authors: Miyashita Toshio , Rockland Kathleen S. 
Published: September 2007

AbstractThe retrosplenial cortex (RS) in rats has been implicated in a wide range of behaviors, including spatial navigation and memory. Relevant to this, the RS is closely interconnected with the hippocampus by multiple direct and indirect routes. Here, by injecting the retrograde tracer cholera toxin subunit B conjugated with Alexa488 (CTB‐Alexa488) in the granular retrosplenial cortex (GRS), we demonstrate a moderately dense non‐pyramidal projection from CA1. Neurons are in several layers, but mainly (about 65%) at the border of the stratum radiatum (SR) and stratum lacunosum moleculare (SLM). In particular, by double‐labeling with GAD67 or γ‐aminobutyric acid (GABA), we establish that these neurons are GABAergic. Further immunocytochemical screening for calcium‐binding proteins, somatostatin (SS) or cholecystokinin (CCK) failed to identify additional neurochemical subgroups; but a small subset (about 14%) is positive for the m2 muscarinic acetylcholine receptor (M2R). Terminations target layer 1 of the GRS, as shown by biotinylated dextran amine (BDA) injections into CA1 and confirmed by a very superficial injection of CTB‐Alexa488 in GRS. The superficial injection shows that there is a sparse GABAergic projection from the subiculum to layer 1 of the GRS, in addition to the dense excitatory connections to layer 3. The role of these dual inhibitory–excitatory pathways − within the subiculum, and in parallel from CA1 and the subiculum − remains to be determined, but may be related to synchronized oscillatory activity in the hippocampal complex and GRS, or to the generation of rhythmic activity within the GRS.
PKC activation sets an upper limit to the functional plasticity of GABAergic transmission induced by endogenous neurosteroids
Authors: Vergnano Angela Maria , Schlichter Rémy , Poisbeau Pierrick 
Published: September 2007

AbstractThe activity of GABAergic inhibitory interneurones located in lamina II of the spinal cord is of fundamental importance for the processing of peripheral nociceptive messages. We have recently shown that 3α‐hydroxy ring A‐reduced pregnane neurosteroids [3α5α‐neurosteroids (3α5αNS)], potent allosteric modulators of GABAAreceptors (GABAARs), are synthesized in the spinal cord and limit thermal hyperalgesia during inflammatory pain. Because changes in the expression of calcium‐dependent protein kinases [protein kinase C (PKC)] are observed during pathological pain in the spinal cord, we examined the possible interactions between PKC and 3α5αNS at synaptic GABAARs. Using patch‐clamp recordings of lamina II interneurones in the spinal cord of 15–20‐day‐old rats, we showed that synaptic inhibition mediated by GABAARs and its modulation by 3α5αNS in lamina II of the spinal cord largely depend on activation of PKC. Our experimental results suggested that activation of PKC locks synaptic GABAARs in a functional state precluding further positive allosteric modulation by endogenous and exogenous 3α5αNS. This effect was fully prevented by coadministration of chelerythrin, an inhibitor of PKC. Furthermore, application of chelerythrin alone rendered synaptic GABAARs hypersensitive to endogenously produced or exogenously applied 3α5αNS. These findings confirmed that there was a significant production of endogenous 3α5αNS in lamina II of the spinal cord but also indicated that PKC‐dependent phosphorylation processes were tonically activated to control GABAAR‐mediated inhibition under resting conditions. We therefore can conclude that PKC activation sets an upper limit to the functional plasticity of GABAergic transmission induced by endogenous neurosteroids.
Variations in glial cell line‐derived neurotrophic factor release from biodegradable nerve conduits modify the rate of functional motor recovery after rat primary nerve repairs
Authors: Piquilloud Gaël , Christen Thierry , Pfister Lukas A. , Gander Bruno , Papaloïzos Michaël Y. 
Published: September 2007

AbstractAccelerating axonal regeneration to shorten the delay of reinnervation and improve functional recovery after a peripheral nerve lesion is a clinical demand and an experimental challenge. We developed a resorbable nerve conduit (NC) for controlled release of glial cell line‐derived neurotrophic factor (GDNF) with the aim of assessing motor functional recovery according to the release kinetics of this factor in a short gap model. Different types of resorbable NCs were manufactured from a collagen tube and multiple coating layers of poly(lactide‐coglycolide), varying in poly(lactide‐coglycolide) type and coating thickness to afford three distinct release kinetics of the neurotrophic factor. GDNF release was quantified in vitro. End‐to‐end suture and GDNF‐free NC served as controls. Thirty‐five Wistar rats underwent surgery. Motor recovery was followed from 1 to 12 weeks after surgery by video gait analysis. Morphometrical data were obtained at mid‐tube level and distal to the NC. NCs were completely resorbed within 3 months with minimal inflammation. GDNF induced a threefold overgrowth of fibers at mid‐tube level. However, the number of fibers was similar in the distal segment of all groups. The speed of recovery was inversely proportional to the number of fibers at the NC level but the level of recovery was similar for all groups at 3 months. The resorbable conduits proved their ability to modulate axonal regrowth through controlled release of GDNF. In relation to the dose delivered, GDNF strikingly multiplied the number of myelinated fibers within the NC but this increase was not positively correlated with the return of motor function in this model.
Differential expression of members of the RCAN family of calcineurin regulators suggests selective functions for these proteins in the brain
Authors: Porta Sílvia , Martí Eulàlia , De La Luna Susana , Arbonés Maria L. 
Published: September 2007

AbstractRCANs, also called Down Syndrome Critical Region‐1 (DSCR1)‐like proteins, Modulatory Calcineurin Interacting Proteins (MCIPs) or calcipressins, are regulators of calcineurin, a Ca2+‐dependent protein phosphatase involved in several neuronal functions. Despite the potential importance of the RCAN proteins in brain physiology, very little is known about their relative abundance and distribution patterns in the central nervous system. In this study we report the expression and distribution of RCAN mRNA transcripts and proteins in the mouse brain. RT‐PCR and Western blot analysis showed that all Rcan mRNAs (Rcan1‐1, Rcan1‐2, Rcan2‐1, Rcan2‐3 and Rcan3) and their corresponding protein products (RCAN1‐L, RCAN1‐S, RCAN2‐L, RCAN2‐S and RCAN3) are present in every adult mouse brain region examined. All protein isoforms are also expressed in these same brain regions at early postnatal stages. Within regions, RCAN1‐L, RCAN1‐S, RCAN2‐L and RCAN3 are differentially expressed depending on the region and developmental stage, whereas RCAN2‐S is distributed homogeneously. Detailed immunohistochemical analysis revealed significant differences in the cellular and subcellular distributions of RCAN proteins. In the adult, RCAN1 was mainly expressed in the neuropil throughout the brain. Although at lower levels, RCAN3 was also detected throughout the neuropil. In contrast, RCAN2 was highly expressed in scattered neurons, in both the nucleus and the cytoplasm. Interestingly, RCAN2 is the only member of the RCAN family that was detected in glial cells. Finally, the expression patterns of RCANs at early postnatal stages differed from those of the adult, in different brain areas, in both their distributions and relative abundance, suggesting that the expression of these proteins could be regulated during neuronal differentiation. The nonoverlapping expression patterns of the RCAN proteins shown here highlight the existence of different physiological scenarios and therefore suggest different RCAN functional activities in the brain, depending on the cellular context and developmental stage.