bluuebunny/crossref_metadata_2025_split huggingface dataset:
Postnatal maturation of GABAA and GABAC receptor function in the mammalian superior colliculus
Authors: Boller Mathias , Schmidt Matthias 
Published: March 2003

AbstractIn the stratum griseum superficiale (SGS) of the mammalian superior colliculus, GABAC receptors seem to control the excitability of projection neurons by selective inactivation of local GABAergic interneurons. As the onset of visual responses to SC begins well after birth in the rat, it is possible to study developmental changes in GABAergic mechanisms that are linked to the onset of visual information processing. In order to analyse postnatal changes in inhibitory mechanisms that involve GABA receptor function, we used extracellular field potential (FP) recordings and single cell patch‐clamp techniques in slices from postnatal day 4 (P4) to P32 and examined the effects of GABA and muscimol on electrically evoked SGS cell activity. While GABAA receptor activation affected FP amplitudes throughout postnatal development, GABAC receptor activation did not significantly change FP amplitudes until the third postnatal week. Results from patch‐clamping single cells, however, clearly demonstrate that GABAC receptors are already functional at P4 – similar to GABAA receptors. Throughout postnatal development, activation of GABAC receptors leads to a strong inhibition of inhibitory postsynaptic activity, indicating that GABAC receptors are expressed by inhibitory interneurons. Furthermore, the proportion of neurons that show decreased excitatory postsynaptic activity during GABAC receptor activation correlates with the proportion of GABAergic interneurons in SGS. Our patch‐clamp results indicate that the functional expression of GABAC receptors by GABAergic interneurons does not change significantly during postnatal development. However, our measurements of FP amplitudes indicate that the maturation of the efferent connections of these GABAergic neurons within SGS during the third postnatal week strongly changes GABAC receptor function.
Visual stimulation‐induced phosphorylation of neurofilament‐L in the visual cortex of dark‐reared rats
Authors: Hashimoto Ryota , Nakamura Yu , Imamura Kazuyuki , Nakadate Kazuhiko , Kashiwagi Yujiro , Matsumoto Naohiko , Takeda Masatoshi 
Published: March 2003

AbstractIn dark‐reared animals, visual exposure is expected to induce drastic changes in both the physiology and anatomy of the cortical neurons, including the rearrangement of their cytoskeletal structures. Phosphorylation of neurofilament‐L (NF‐L) is probably associated with relatively short‐term structural plasticity in vivo, because the assembly and disassembly of the filaments are regulated by phosphorylation of the head domain of NF‐L. Thus, by using a series of site‐ and phosphorylation state‐specific antibodies against NF‐L, we examined how visual activation induces the phosphorylation of NF‐L in the rat brain. We found no specific immunoreactivity for phosphorylated NF‐L in the brain of naive rats, whereas one‐hour ambient light exposure after dark rearing for ten weeks from birth induced marked phosphorylation of NF‐L selectively. Also, the NF‐L phosphorylation was found to be localized in the primary and secondary visual cortical areas. These findings suggest that the selective phosphorylation of NF‐L plays an important role in the structural plasticity related to the visual experience.
Dual effects of NMDA receptor activation on polysialylated neural cell adhesion molecule expression during brainstem postnatal development
Authors: Bouzioukh Farima , Tell Fabien , Rougon Geneviève , Jean André 
Published: March 2003

AbstractHere we show a dual role of N‐methyl‐d‐aspartate receptor (NMDAR) activation in controlling polysialylated neural cell adhesion molecule (PSA‐NCAM) dynamic expression in the dorsal vagal complex (DVC), a gateway for many primary afferent fibres. In this structure the overall expression of PSA‐NCAM decreases during the first 2 weeks after birth to persist only at synapses in the adult. Electrical stimulation of the vagal afferents causes a rapid increase of PSA‐NCAM expression both in vivo and in acute slices before postnatal day (P) 14 whereas a similar stimulation induces a decrease after P15. Inhibition of NMDAR activity in vitro completely prevented these changes. These regulations depend on calmodulin activation and cGMP production at all stages. By contrast, blockade of neuronal nitric oxide synthase (nNOS) prevented these changes only after P10 in agreement with its late expression in the DVC. The pivotal role of NMDAR is also supported by the observation that chronic blockade induces a dramatic decrease in PSA‐NCAM expression.
Circadian activity rhythm in methamphetamine‐treated Clock mutant mice
Authors: Masubuchi Satoru , Honma Sato , Abe Hiroshi , Nakamura Wataru , Honma Ken‐ichi 
Published: March 2003

AbstractIt is well established that the Clock gene is essential for expressing circadian activity rhythms in mammals under constant darkness. The Clock gene product is a positive component of a molecular feedback loop which is assumed to generate the circadian rhythm. On the other hand, chronic treatment of methamphetamine (MAP) induces locomotor activity rhythm in a circadian domain, which is independent of the suprachiasmatic nucleus (SCN) and is driven by a pacemaker outside the SCN. However, it is not known whether the pacemaker outside the SCN possesses a similar molecular mechanism to that in the SCN. Here we show that MAP restores locomotor activity rhythm in arrhythmic homozygous Clock mutant (Clock/Clock) mice under constant darkness. This result indicates that the Clock mutation does not affect the MAP‐induced locomotor rhythm.
Presynaptic group I and II metabotropic glutamate receptors oppositely modulate striatal acetylcholine release
Authors: Marti M. , Paganini F. , Stocchi S. , Bianchi C. , Beani L. , Morari M. 
Published: March 2003

AbstractThe effect of metabotropic glutamate receptor agonists and antagonists on KCl (20 mm)‐induced endogenous acetylcholine release from rat striatal synaptosomes was investigated. The group I agonist (S)‐3,5‐dihydroxyphenylglycine (DHPG), 1–1000 nm, potentiated in a concentration‐dependent way the KCl‐induced acetylcholine release, reaching maximal efficacy at 100 nm (+93 ± 14%). The effect of DHPG (10 nm) was counteracted by coapplication of (7‐hydroximino)cyclopropan‐b‐chromen‐1a‐carboxylate (CPCCOEt), 10 µm, a metabotropic glutamate receptor type one selective antagonist, and 2‐methyl‐6‐(phenylethynyl)pyridine (MPEP), 10 µm, a metabotropic glutamate receptor type five selective antagonist, but not by application of either antagonist alone. The group II agonist (2S, 1′R, 2′R, 3′R)‐2‐(2,3‐dicarboxycyclopropyl)glycine (DCG‐IV), 1–1000 nm, inhibited in a concentration‐dependent way the KCl‐induced acetylcholine release displaying maximal efficacy at 300 nm (−32 ± 2%). The effect of DCG‐IV 300 nm was counteracted by the group II selective antagonist (2S)‐α‐ethylglutamic acid (EGLU), 300 µm. The group III agonist l‐amino‐4‐phosphonobutyric acid (L‐AP4) failed to alter the KCl‐induced acetycholine release up to 300 µm. We conclude that metabotropic glutamate receptors belonging to group I and II are located on the axon terminals of striatal cholinergic interneurons, their activation resulting in facilitation and inhibition, respectively, of acetylcholine release.
Brain‐derived neurotrophic factor induces long‐lasting potentiation of synaptic transmission in visual cortex in vivo in young rats, but not in the adult
Authors: Jiang Bin , Akaneya Yukio , Ohshima Minoru , Ichisaka Satoshi , Hata Yoshio , Tsumoto Tadaharu 
Published: March 2003

AbstractBrain‐derived neurotrophic factor (BDNF) rapidly enhances excitatory synaptic transmission in cortical slices. To date, however, a question of how long such an action persists remains unanswered as it is hard to record synaptic responses longer than several hours in slice preparations. To address this question and to investigate possible age‐dependency of the action, we analysed effects of a brief application of BDNF and nerve growth factor (NGF) on field potentials of visual cortex in rats of postnatal days 13–17 and 19–24 and in the adulthood for 10–24 h. Evoked potentials to stimulation of the lateral geniculate nucleus were recorded simultaneously from two cortical sites into which the neurotrophin and control solution were injected. An application of BDNF induced a slowly developing increase in the field potential amplitude in young rats. The amplitude attained a plateau level 3–4 h after the infusion; 139 ± 26% (mean ± SD) and 132 ± 21% of the baseline in the rats at P13‐17 and P19‐24, respectively. This potentiation remained stable from 4 to 8 h, then gradually decreased to the baseline 15–16 h after the infusion. NGF applied in the same way did not induce potentiation. An inhibitor of BDNF receptors blocked the potentiation when it was applied immediately after the BDNF application, but was not effective about 2 h later. In the adults, BDNF did not potentiate field potentials. These results indicate that BDNF induces synaptic potentiation lasting for several hours only in the developing cortex through processes downstream of receptor activation.
Bax and caspases are inhibited by endogenous nitric oxide in dorsal root ganglion neurons in vitro
Authors: Thippeswamy T. , McKay J. S. , Morris R. 
Published: March 2003

AbstractAxotomised dorsal root ganglia (DRG) neurons show an increased expression of neuronal nitric oxide synthase (nNOS) compared with neurons from the intact ganglia. Increased nNOS expression resulted in synthesis of nitric oxide (NO) and the subsequent activation of cGMP in satellite glia cells surrounding the DRG neuron soma. In dissociated DRG we have demonstrated that the increase in nNOS expression is regulated by nerve growth factor and that the subsequent inhibition of NO production or cGMP synthesis precipitates apoptosis of neurons expressing nNOS and some non‐nNOS neurons. Hence, NO or the NO–cGMP cascade appears to have a neuroprotective action in trophic factor‐deprived DRG neurons. In the present study, using immunocytochemistry, we have investigated some of the factors associated with apoptosis that are activated when nNOS activity is blocked with NOS inhibitor in DRG neurons in vitro. Marked elevation of bax was observed within a few hours of NOS inhibition in nNOS containing neurons, whereas pretreatment of cultures with l‐arginine completely abolished this effect in almost all nNOS neurons and 8‐bromo‐cGMP in some neurons. The apoptosis precipitated by NOS inhibition was also partially prevented by a number of caspase inhibitors; of those a caspase‐9 blocker was the most effective. These observations further support the neuroprotective role of NO/NO‐cGMP in stressed DRG neurons in an autocrine fashion that involves the suppression of bax, caspase‐3 and ‐9 activation.
Changes in reward‐induced brain activation in opiate addicts
Authors: Martin‐Soelch C. , Chevalley A.‐F. , Künig G. , Missimer J. , Magyar S. , Mino A. , Schultz W. , Leenders K. L. 
Published: March 2003

AbstractMany studies indicate a role of the cerebral dopaminergic reward system in addiction. Motivated by these findings, we examined in opiate addicts whether brain regions involved in the reward circuitry also react to human prototypical rewards. We measured regional cerebral blood flow (rCBF) with H215O positron emission tomography (PET) during a visuo‐spatial recognition task with delayed response in control subjects and in opiate addicts participating in a methadone program. Three conditions were defined by the types of feedback: nonsense feedback; nonmonetary reinforcement; or monetary reward, received by the subjects for a correct response. We found in the control subjects rCBF increases in regions associated with the meso‐striatal and meso‐corticolimbic circuits in response to both monetary reward and nonmonetary reinforcement. In opiate addicts, these regions were activated only in response to monetary reward. Furthermore, nonmonetary reinforcement elicited rCBF increases in limbic regions of the opiate addicts that were not activated in the control subjects. Because psychoactive drugs serve as rewards and directly affect regions of the dopaminergic system like the striatum, we conclude that the differences in rCBF increases between controls and addicts can be attributed to an adaptive consequence of the addiction process.
Ethanol reduces excitability in a subgroup of primary sensory neurons by activation of BKCa channels
Authors: Gruß Marco , Henrich Michael , König Peter , Hempelmann Gunter , Vogel Werner , Scholz Andreas 
Published: March 2003

AbstractEthanol effects on the central nervous system have been well investigated and described in recent years; modulations, by ethanol, of several ligand‐gated and voltage‐gated ion channels have been found. In this paper, we describe a shortening of action potential duration (APD) by ethanol in ≈ 40% of small diameter neurons in rat dorsal root ganglia (DRG). In these neurons, designated as group A neurons, we observed an ethanol‐induced increase in whole‐cell outward‐current. As iberiotoxin, a specific blocker of large‐conductance calcium‐activated K+ channels (BKCa channels), blocks the effects of ethanol, we investigated the interaction between these channels and ethanol in outside‐out patches. Open probability of BKCa channels was increased 2–6 × depending on the concentration (40–80 mm≈ 2–4‰ v/v) of ethanol. Functional consequences were a prolongation of the refractory period, which was reversible after addition of iberiotoxin, and reduced firing frequency during ethanol application. In contrast, another type of neuron (group B) showed a prolonged APD during application of ethanol which was irreversible in most cases. In 90% of cases, neurons of group A showed a positive staining for isolectin B4 (I‐B4), a marker for nociceptive neurons. We suggest that the activation of BKCa channels induced by clinically relevant concentrations of ethanol, the resulting modulations of APD and refractory period of DRG neurons, might contribute to clinically well‐known ethanol‐induced analgesia and paresthesia.
Unilateral striatal dopamine depletion: time‐dependent effects on cortical function and behavioural correlates
Authors: Steiner Heinz , Kitai Stephen T. 
Published: March 2003

AbstractPreviously, we showed that unilateral blockade of D1 dopamine receptors in the striatum inhibits immediate‐early gene expression bilaterally throughout large parts of the cortex, including sensory‐evoked expression in the barrel cortex. To further investigate this dopamine regulation of cortical function, we examined the effects of dopamine depletion on cortical gene regulation and behavioural correlates. Two days after unilateral infusion of 6‐hydroxydopamine into the midbrain, rats displayed a (to some degree) bilateral reduction in cortical zif 268 expression that was more pronounced on the lesioned side. This decrease was found across motor, somatosensory, insular and piriform, but not cingulate, cortex, similar to the effects of blockade of striatal D1 receptors. Furthermore, whisker stimulation‐evoked c‐fos and zif 268 expression in the barrel cortex ipsilateral to the lesion was also attenuated by acute dopamine depletion. These cortical deficits were accompanied by a breakdown of spontaneous behaviours in an open‐field test. In contrast, 21 days after dopamine depletion, both basal and sensory‐evoked gene expression in the cortex were near‐normal. This cortical recovery was paralleled by recovery in locomotion and in sensory‐guided behaviour (scanning) related to the hemisphere contralateral to the lesion, but not in scanning by the dopamine‐depleted hemisphere. Our results suggest that striatal dopamine exerts a widespread facilitatory influence on cortical function that is necessary, but not sufficient, for normal behaviour. Moreover, the mechanisms mediating this cortical facilitation appear to be subject to substantial neuroplasticity after dopamine perturbation.
Cortico‐cortical connectivity of the human mid‐dorsolateral frontal cortex and its modulation by repetitive transcranial magnetic stimulation
Authors: Paus Tomáš , Castro‐Alamancos Manuel A. , Petrides Michael 
Published: March 2003

AbstractModulation of cortico‐cortical connectivity in specific neural circuits might underlie some of the behavioural effects observed following repetitive transcranial magnetic stimulation (rTMS) of the human frontal cortex. This possibility was tested by applying rTMS to the left mid‐dorsolateral frontal cortex (MDL‐FC) and subsequently measuring functional connectivity of this region with positron emission tomography (PET) and TMS. The results showed a strong rTMS‐related modulation of brain activity in the fronto‐cingulate circuit. These results were confirmed in a parallel experiment in the rat using electrical stimulation and field‐potential recordings. Future studies are needed to provide a direct link between the rTMS‐induced modulation of cortical connectivity and its effects on specific behaviours.
Differences in auditory and physiological properties of HVc neurons between reproductively active male and female canaries (Serinus canaria)
Authors: Del Negro Catherine , Edeline Jean‐Marc 
Published: March 2003

AbstractBased on neuronal recordings in the HVc, this study investigated differences between reproductively active male and sexually receptive female canaries. It is the first study to describe auditory responses and cell characteristics of HVc neurons in female songbirds and to compare them with the responses and characteristics obtained in males. Extracellular single unit recordings showed that in males HVc cells exhibited two types of auditory responses to conspecific and heterospecific song playbacks: tonic and phasic responses. The major finding of the present study is the absence of tonic responses in females. Neurons in the HVc of females only responded phasically to song playbacks. In both sexes, neurons exhibiting auditory responses had thinner action potentials than the others. As all the tonic cells recorded in males were thin spike cells (action potential = 0.6 ms) and had high firing rates (6 Hz in average), they are potentially interneurons. In both sexes, two categories of nonresponsive cells were found: neurons that did not fire at song onset and had the lowest spontaneous firing rate; and neurons that did not exhibit changes in activity in response to song playbacks. Analyses of physiological characteristics of HVc neurons revealed that the rate of spontaneous activity was higher in males than in females. This study is a first step towards in dentifying the cellular bases of the sexual dimorphism in HVc function and highlights the pivotal role of interneurons in HVc auditory processing.
Catalepsy induced by a blockade of dopamine D1 or D2 receptors was reversed by a concomitant blockade of adenosine A2A receptors in the caudate‐putamen of rats
Authors: Hauber Wolfgang , Neuscheler Patric , Nagel Jens , Müller Christa E. 
Published: March 2003

AbstractThe present study sought to determine, in more detail, the effects of an unselective and a selective adenosine A2A receptor blockade on catalepsy induced by a blockade of dopamine D1 or D2 receptors in rats. The results demonstrated that systemic administration of the unselective A1/A2 receptor antagonist, theophylline and the selective A2A receptor antagonist, CSC potently reversed catalepsy induced by a systemic D2 receptor blockade with raclopride or by a bilateral blockade of D2 receptors in the caudate‐putamen (CPu) with S(–)sulpiride. Likewise, systemic administration of theophylline and CSC reversed catalepsy induced by a systemic D1 receptor blockade with SCH23390; theophylline also counteracted catalepsy after an intra‐CPu D1 receptor blockade with SCH23390. Intracerebral co‐microinfusions of the selective A2A receptor antagonist, MSX‐3 together with a D1 (SCH23390) or D2 receptor [S(–) sulpiride] antagonist revealed that catalepsy due to intra‐CPu D1 or D2 receptor blockade can be potently reversed by an intra‐CPu A2A receptor blockade. In conclusion, our results with systemic and intra‐CPu drug administration demonstrate that D1 and D2 receptor‐mediated catalepsy can both be reversed by a concomitant blockade of A2A receptors. Our results implicate that the CPu is a critical neural substrate for antagonistic interactions of a D1/D2 receptor blockade and an A2A receptor blockade in control of motor activity. The present results provide further support for the view that A2A receptor antagonists may be potential therapeutics for the treatment of Parkinson's disease.
The projections of the midbrain periaqueductal grey to the pons and medulla oblongata in rats
Authors: Odeh Francis , Antal Miklós 
Published: March 2003

AbstractIt is now established that stimulation of the ventrolateral midbrain periaqueductal grey (PAG) evokes inhibition of nociceptive spinal neurons, which results in analgesia and a powerful attenuation of pain behaviour. It is postulated that the PAG exerts this inhibitory effect on spinal nociceptive functions through the activation of descending serotonergic and noradrenergic pathways that arise from the rostral ventromedial medulla (RVM) and pontine noradrenergic nuclei. To investigate the neuroanatomical substrate of this functional link between the PAG and RVM, as well as the pontine noradrenergic nuclei in the rat, we labelled axons that project from the ventrolateral PAG to various regions of the pons and medulla oblongata using the anterograde tracing substance, Phaseolus vulgaris leucoagglutinin. We demonstrated that some of PAG efferents really do terminate in the RVM and pontine noradrenergic nuclei, but a substantial proportion of them project to the intermediate subdivision of the pontobulbar reticular formation. Combining the axonal tracing with serotonin‐ and tyrosine‐hydroxylase‐immunohistochemistry, we also found that, in contrast to previous results, PAG efferents make relatively few appositions with serotonin‐ and tyrosine‐hydroxylase‐immunoreactive neurons in the RVM and pontine noradrenergic nuclei; most of them terminate in nonimmunoreactive territories. The results suggest that the ventrolateral PAG may activate a complex pontobulbar neuronal assembly including neurons in the intermediate subdivision of the pontobulbar reticular formation, serotonin‐ and tyrosine‐hydroxylase‐immunoreactive and nonimmunoreactive neurons in the RVM and pontine noradrenergic nuclei. This pontobulbar neural circuitry, then, may mediate the PAG‐evoked activities towards the spinal dorsal horn resulting in the inhibition of spinal nociceptive functions.
Detection and discrimination of chromatic targets in hemianopic macaque monkeys and humans
Authors: Cowey Alan , Stoerig Petra 
Published: March 2003

AbstractWe measured the ability of three macaque monkeys with unilateral removal of primary visual cortex to detect 9°, 200‐ms targets presented at random in the upper or lower quadrants of the normal and hemianopic visual fields. The white or variously coloured target could differ from the background in both colour and luminance, or in either of them. Blue and red targets were detectable at any luminance contrast, but green and white targets were barely or not at all detectable at and near isoluminance in the hemianopic field. Blue and red targets were better detected than white targets at the same luminance difference. However, when both the target and the background were dynamically luminance‐masked, detection in the hemianopic field failed at isoluminance whatever the colour. In addition, the monkeys were unable to discriminate between simultaneously presented red and green or blue and green targets in the hemianopic field when both targets had similar luminance contrast with the background. Two hemianopic patients tested on a subset of the tasks performed similarly to the monkeys. Together, the results indicate that the residual colour‐opponent system that survives damage to V1 is involved in the detection of chromatic changes but cannot sustain simultaneous discrimination between pairs of colours.