bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interaction between glucocorticoid hormones, stress and psychostimulant drugs*
Authors: Marinelli Michela , Piazza Pier Vincenzo 
Published: March 2003

AbstractIn this review we summarize data obtained from animal studies showing that glucocorticoid hormones have a facilitatory role on behavioural responses to psychostimulant drugs such as locomotor activity, self‐administration and relapse. These behavioural effects of glucocorticoids involve an action on the meso‐accumbens dopamine system, one of the major systems mediating the addictive properties of drugs of abuse. The effects of glucocorticoids in the nucleus accumbens are site‐specific; these hormones modify dopamine transmission in only the shell of this nucleus without modifying it in the core. Studies with corticosteroid receptor antagonists suggest that the dopaminergic effects of these hormones depend mostly on glucocorticoid, not on mineralocorticoid receptors. These data suggest that an increase in glucocorticoid hormones, through an action on mesolimbic dopamine neurons, could increase vulnerability to drug abuse. We also discuss the implications of this finding with respect to the physiological role of glucocorticoids. It is proposed that an increase in glucocorticoids, by activating the reward pathway, could counteract the aversive effects of stress. During chronic stress, repeated increases in glucocorticoids and dopamine would result in sensitization of the reward system. This sensitized state, which can persist after the end of the stress, would render the subject more responsive to drugs of abuse and consequently more vulnerable to the development of addiction.
Mesencephalic and diencephalic afferent connections to the thalamic nucleus rotundus in the lizard, Psammodromus algirus
Authors: Dávila José Carlos , Andreu Manuel José. , Real M. Ángeles , Puelles Luis. , Guirado Salvador 
Published: March 2003

AbstractThe present work is an analysis of the afferent projections to the thalamic nucleus rotundus in a lizard, both at the light‐ and electron‐microscopic level, using biotinylated dextran amine (BDA) as a neuroanatomical tracer. This study has confirmed previously reported afferent projections to nucleus rotundus in reptiles and has also identified a number of new cellular aggregates projecting to this dorsal thalamic nucleus. After BDA injections into nucleus rotundus, retrogradely labelled neurons were observed consistently within the following neuronal groups in the midbrain and the diencephalon: (i) the stratum griseum centrale of the optic tectum; (ii) the nucleus subpretectalis in the pretectum; (iii) the nucleus ansa lenticularis posterior, the posterior nucleus of the ventral supraoptic commissure, and the posteroventral nucleus, in the dorsal thalamus and (iv) the lateral suprachiasmatic nucleus and part of the reticular complex in the ventral thalamus. Tectal axons entering nucleus rotundus were fine and varicose and formed exclusively asymmetric synaptic contacts, mainly on small dendritic profiles. Rotundal neurons had symmetric synapses made by large boutons probably of nontectal origin. After comparing our results with those in other reptiles, birds and mammals, we propose that the sauropsidian nucleus rotundus forms part of a visual tectofugal pathway that conveys mesencephalic visual information to the striatum and dorsal ventricular ridge, and is similar to the mammalian colliculo‐posterior/intralaminar–striatoamygdaloid pathway, the function of which may be to participate in visually guided behaviour.
Activation of histaminergic H3 receptors in the rat basolateral amygdala improves expression of fear memory and enhances acetylcholine release
Authors: Cangioli Iacopo , Baldi Elisabetta , Mannaioni Pier Francesco , Bucherelli Corrado , Blandina Patrizio , Passani M. Beatrice 
Published: March 2003

AbstractThe basolateral amygdala (BLA) is involved in learning that certain environmental cues predict threatening events. Several studies have shown that manipulation of neurotransmission within the BLA affects the expression of memory after fear conditioning. We previously demonstrated that blockade of histaminergic H3 receptors decreased spontaneous release of acetylcholine (ACh) from the BLA of freely moving rats, and impaired retention of fear memory. In the present study, we examined the effect of activating H3 receptors within the BLA on both ACh release and expression of fear memory. Using the microdialysis technique in freely moving rats, we found that the histaminergic H3 agonists R‐α‐methylhistamine (RAMH) and immepip, directly administered into the BLA, augmented spontaneous release of ACh in a similar manner. Levels of ACh returned to baseline on perfusion with control medium. Rats receiving intra‐BLA, bilateral injections of the H3 agonists at doses similar to those enhancing ACh spontaneous release, immediately after contextual fear conditioning, showed stronger memory for the context–footshock association, as demonstrated by longer freezing assessed at retention testing performed 72 h later. Post‐training, bilateral injections of 15 ng oxotremorine also had a similar effect on memory retention, supporting the involvement of the cholinergic system. Thus, our results further support a physiological role for synaptically released histamine, that in addition to affecting cholinergic transmission in the amygdala, modulates consolidation of fear memories
Electroconvulsive seizures increase hippocampal neurogenesis after chronic corticosterone treatment
Authors: Hellsten Johan , Wennström Malin , Mohapel Paul , Ekdahl Christine T. , Bengzon Johan , Tingström Anders 
Published: March 2003

AbstractMajor depression is often associated with elevated glucocorticoid levels. High levels of glucocorticoids reduce neurogenesis in the adult rat hippocampus. Electroconvulsive seizures (ECS) can enhance neurogenesis, and we investigated the effects of ECS in rats where glucocorticoid levels were elevated in order to mimic conditions seen in depression. Rats given injections of corticosterone or vehicle for 21 days were at the end of this period treated with either a single or five daily ECSs. Proliferating cells were labelled with bromodeoxyuridine (BrdU). After 3 weeks, BrdU‐positive cells in the dentate gyrus were quantified and analyzed for co‐labelling with the neuronal marker neuron‐specific nuclear protein (NeuN). In corticosterone‐treated rats, neurogenesis was decreased by 75%. This was counteracted by a single ECS. Multiple ECS further increased neurogenesis and no significant differences in BrdU/NeuN positive cells were detected between corticosterone‐ and vehicle‐treated rats given five ECS. Approximately 80% of the cells within the granule cell layer and 10% of the hilar cells were double‐labelled with BrdU and NeuN.We therefore conclude that electroconvulsive seizures can increase hippocampal neurogenesis even in the presence of elevated levels of glucocorticoids. This further supports the hypothesis that induction of neurogenesis is an important event in the action of antidepressant treatment.
Cerebellar LTD facilitates but is not essential for long‐term adaptation of the vestibulo‐ocular reflex
Authors: Van Alphen A. M. , De Zeeuw C. I. 
Published: March 2003

AbstractThe induction of cerebellar long‐term depression (LTD) at the parallel fibre–Purkinje cell synapse is selectively blocked in L7‐PKCi transgenic mice, rendering these mice unable to adaptively modify their vestibulo‐ocular reflex (VOR) during visuo‐vestibular training for a few hours. Despite this deficit, their eye movement performance as well as their general motor behaviour appears unaffected. This combination suggests that, in the long term, residual forms of plasticity in the vestibulo‐cerebellar circuitry can compensate for the absence of cerebellar LTD. To investigate whether LTD‐deficient mice exhibit motor learning in the long run, we subjected L7‐PKCi transgenic mice to visuo‐vestibular training paradigms that were aimed at either increasing or decreasing the VOR response in the course of eight consecutive days. During the increasing paradigm, the VOR gain of transgenic mice increased significantly, while VOR gain decreased and VOR phase‐lead increased during the decreasing paradigm. The impact of these long training periods on the VOR was significantly smaller in LTD‐deficient mice than in wild type littermates. Thus, while LTD may be necessary for short‐term VOR adaptation, it facilitates but is not required for long‐term adaptation of the VOR.
The genetic basis for psychiatric illness in man*
Authors: Tandon Kopal , McGuffin Peter 
Published: March 2003

AbstractFollowing the influential genetic studies of Heston and Kety, there has been growing acceptance of the role of genes in determining behaviour. It is now recognized that most types of behaviour, from normal variations in traits such as personality to complex psychiatric disorders, are influenced not only by environmental factors but also by multiple genes. While twin and adoption studies have been vital in demonstrating the heritability of behaviour, the focus is now on the identification of the genes involved using the molecular genetic strategies linkage analysis and allelic association. This article will discuss techniques that have been used in psychiatric genetics, and how they have advanced our understanding of complex behaviour.
Differences in GABAergic transmission between two inputs into the perirhinal cortex
Authors: Garden Derek L. F. , Kemp Nicola , Bashir Zafar I. 
Published: March 2003

AbstractWe have investigated properties of GABAergic synaptic transmission in perirhinal cortex evoked by stimulation of temporal and entorhinal cortex sides. GABAA IPSCs were isolated by blockade of glutamatergic transmission in slices of adult perirhinal cortex; IPSC decay was best fitted with two exponentials. Interestingly, temporal IPSCs had a larger slow component of decay (P < 0.05) compared to entorhinal IPSCs. Depression of IPSCs by the GABAB receptor agonist baclofen was greater (P < 0.05) in the temporal input (79 ± 4% depression) than the entorhinal input (65 ± 3% depression). Furthermore, baclofen abolished the slow component of IPSC decay in both inputs. Activity‐dependent depression of IPSCs at 5 Hz was greater (P < 0.05) in the temporal input [paired pulse ratio (PPR) 0.5 ± 0.04] compared to that in the entorhinal input (PPR 0.67 ± 0.02, n = 10). The differences in paired pulse depression between the inputs were removed by the GABAB receptor antagonist CGP55845A. This study demonstrates several differences in GABA transmission between temporal and entorhinal inputs including the differential activation of presynaptic GABAB receptors and differential regulation of inhibitory synaptic transmission. These properties may be important in the control of neuronal activity within perirhinal cortex.
Evaluation of Affymetrix Gene Chip sensitivity in rat hippocampal tissue using SAGE analysis*
Authors: Evans Simon J. , Datson Nicole A. , Kabbaj Mohamed , Thompson Robert C. , Vreugdenhil Erno , De Kloet E. Ronald , Watson Stanley J. , Akil Huda 
Published: March 2003

AbstractDNA microarrays are a powerful tool for monitoring thousands of transcript levels simultaneously. However, the use of DNA microarrays in studying the central nervous system faces several challenges. These include the detection of low‐abundance transcripts in highly complex tissue as well as estimating relatively low‐magnitude changes in transcript levels in response to experimental manipulation. Many transcripts important to brain function have low expression levels or are expressed in relatively few cells, making them difficult to detect in the complex background of brain tissue. The aim of the present study is to evaluate the sensitivity of Gene Chip detection of transcripts in brain by using results from serial analysis of gene expression (SAGE) studies. The results of this comparison indicate that Affymetrix Gene Chips, like SAGE, only reliably detect medium‐ to high‐abundance transcripts and that detection of low‐abundance transcripts, many of which have great relevance to biological function in brain, is inconsistent. Specifically, we estimate that Gene Chips reliably detect no more than 30% of the hippocampal transcriptome when using a gross hippocampal dissection as the source tissue. This report provides the first broad evaluation of Affymetrix Gene Chip sensitivity relevant to studying the brain.
Group I and II metabotropic glutamate receptors modulate respiratory activity in the lamprey
Authors: Bongianni Fulvia , Mutolo Donatella , Carfì Marco , Pantaleo Tito 
Published: March 2003

AbstractThe respiratory role of group I and II metabotropic glutamate receptors (mGluRs) was investigated in the in vitro lamprey brainstem preparation by analysing changes in respiratory activity induced by bath application of specific agonists (10 and 25 µm) and antagonists (500 µm). Respiratory responses reached their maximum within 10 or 15 min, without any obvious further changes during application periods of 60 min The broad‐spectrum mGluR agonist (1S,3R)‐1‐aminocyclopentane‐1,3‐dicarboxylic acid (ACPD) and the specific group I mGluR agonist (S)‐3,5‐dihydroxyphenylglycine (DHPG) caused dose‐dependent increases in respiratory frequency and peak vagal activity. DHPG at higher concentrations (50–100 µm) did not cause any further consistent change in respiratory variables. Two different agonists acting on group II mGluRs, i.e. (2S,3S,4S)‐CCG/(2S,1′S,2′S)‐2‐(carboxycyclopropyl)‐glycine (L‐CCG‐I) and (2S,2′R,3′R)‐2‐(2′,3′‐dicarboxycyclopropyl)glycine (DCG‐IV), were employed. At 10 µm DCG‐IV increased respiratory frequency, whilst L‐CCG‐I did not produce any significant effect. Both drugs increased respiratory frequency and peak vagal amplitude at 25 µm. The nonselective group I and II antagonist (S)‐α‐methyl‐4‐carboxyphenylglycine (MCPG) as well as the specific group I antagonist (RS)‐1‐aminoindan‐1,5‐dicarboxylic acid (AIDA) elicited reversible reductions in respiratory frequency. Blockade of group II mGluRs by (2S)‐α‐ethylglutamic acid (EGLU) increased both frequency and peak amplitude of vagal bursts. The results indicate that both group I and II mGluRs have an important modulatory role in the control of the lamprey pattern of breathing, probably through an action on the rhythm generating mechanisms. They support the view that these receptors are activated under physiological conditions and differentially affect the frequency and intensity of respiratory bursts.
Dehydroepiandrosterone (DHEA) stimulates neurogenesis in the hippocampus of the rat, promotes survival of newly formed neurons and prevents corticosterone‐induced suppression
Authors: Karishma K. K. , Herbert J. 
Published: March 2003

AbstractTreating adult male rats with subcutaneous pellets of dehydroepiandrosterone (DHEA) increased the number of newly formed cells in the dentate gyrus of the hippocampus, and also antagonized the suppressive of corticosterone (40 mg/kg body weight daily for 5 days). Neither pregnenolone (40 mg/kg/day), a precursor of DHEA, nor androstenediol (40 mg/kg/day), a major metabolite, replicated the effect of DHEA (40 mg/kg/day). Corticosterone reduced the number of cells labelled with a marker for neurons (NeuN) following a 28‐day survival period, and this was also prevented by DHEA. DHEA by itself increased the number of newly formed neurons, but only if treatment was continued throughout the period of survival. Subcutaneous DHEA pellets stimulated neurogenesis in a small number of older rats (≈ 12 months old). These results show that DHEA, a steroid prominent in the blood and cerebral environment of humans, but which decreases markedly with age and during major depressive disorder, regulates neurogenesis in the hippocampus and modulates the inhibitory effect of increased corticoids on both the formation of new neurons and their survival.
Impaired spatial and sequential learning in rats treated neonatally with d‐fenfluramine
Authors: Morford L. L. , Inman‐Wood S. L. , Gudelsky G. A. , Williams M. T. , Vorhees C. V. 
Published: March 2003

Abstractd‐Fenfluramine, a serotonin releaser, was administered to neonatal rats on postnatal days 11–20 (a stage of hippocampal development analogous to third trimester human ontogeny). As adults, the d‐fenfluramine‐treated offspring exhibited dose‐related impairments of sequential and spatial learning and reference memory in the absence of sensorimotor impairments. Procedures to minimize stress and to control for other performance effects prior to testing for spatial learning demonstrated that nonspecific factors did not account for the selective effects of d‐fenfluramine on learning and memory. Developmental d‐fenfluramine‐induced spatial and sequential learning deficits are similar to previous findings with developmental MDMA treatment. By contrast, recent findings with developmental d‐methamphetamine treatment showed spatial learning deficits while sparing sequential learning. The spatial learning effects common to all three drugs suggest that they may share a common mechanism of action, however, the effects are not related to long‐lasting changes in hippocampal 5‐HT levels as no differences were found in adulthood. Whether the cognitive deficits are related to the effects of substituted amphetamines on corticosteroids, other aspects of the 5‐HT system, or some unidentified neuronal substrates is not known, but the data demonstrate that these drugs are all capable of inducing long‐term adverse effects on learning.
Vasopressin from hypothalamic magnocellular neurons has opposite actions at the adenohypophysis and in the supraoptic nucleus on ACTH secretion
Authors: Wotjak Carsten T. , Ludwig Mike , Ebner Karl , Russell John A. , Singewald Nicolas , Landgraf Rainer , Engelmann Mario 
Published: March 2003

AbstractMagnocellular vasopressinergic and oxytocinergic neurons of the hypothalamic supraoptic (SON) and paraventricular nuclei comprise the hypothalamic–neurohypophysial system, which is crucially involved in the regulation of body fluid and electrolyte homeostasis. However, still controversial is to what extent the same system influences the secretion of adrenocorticotropic hormone (ACTH) from the adenohypophysis. Therefore, we selectively stimulated magnocellular neurons of the SON of conscious male Wistar rats via retrodialysis. As expected, dialysis of the SON with hypertonic medium increased both the release of vasopressin within the SON and the secretion of vasopressin and oxytocin into the systemic blood circulation. This activation of the hypothalamic–neurohypophysial system was accompanied by a fivefold increase in plasma ACTH concentration. This effect was observed only if the tip of the microdialysis probe was within the SON. Intravenous infusion of the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP significantly attenuated the effects of local osmotic stimulation of the SON on ACTH secretion. In contrast, administration of the same antagonist directly into the SON significantly enhanced the osmotically stimulated secretion of ACTH and corticosterone, primarily by delaying the restoration of the hormone secretion to prestimulation levels. We conclude from these findings that vasopressin from the hypothalamic–neurohypophysial system participates in the regulation of the hormonal stress response in a counterbalanced manner at the level of the SON and the adenohypophysis.
Spatial and temporal variation of passer Per2 gene expression in two distinct cell groups of the suprachiasmatic hypothalamus in the house sparrow (Passer domesticus)
Authors: Abraham Ute , Albrecht Urs , Gwinner Eberhard , Brandstätter Roland 
Published: March 2003

AbstractIn mammals, the major pacemaker controlling circadian rhythmicity is located in the hypothalamic suprachiasmatic nuclei. Although there is evidence for the presence of a hypothalamic circadian oscillator in birds from lesioning studies, neuroanatomical, neurochemical and functional investigations have failed to identify its exact location. Two cell groups in the avian hypothalamus have been shown to bear characteristics of the mammalian suprachiasmatic nucleus: the suprachiasmatic nucleus and the lateral hypothalamic retinorecipient nucleus. We cloned an avian period homologue (pPer2) and investigated the temporal and spatial expression pattern of this gene in the house sparrow hypothalamus using in situ hybridization. Applying quantitative morphometry, we found rhythmic expression of pPer2 during light–dark as well as in constant conditions in the suprachiasmatic nucleus and in the lateral hypothalamus. The temporal and spatial distribution of pPer2 expression in the suprachiasmatic nucleus suggest a longitudinal compartmentalization of the nucleus with period gene expression being initiated in the most rostral portion of the suprachiasmatic nucleus before lights on. In the lateral hypothalamus, phasing of pPer2‐rhythmicity appeared different from the suprachiasmatic nucleus. The major difference between light–dark and constant conditions was a decrease in the amplitude of pPer2 rhythmicity in the suprachiasmatic nucleus. Our data demonstrate that, unlike in mammals, Per gene expression in the suprachiasmatic hypothalamus of the house sparrow is not confined to a single cell group, indicating a more complex organization of the circadian oscillator in the hypothalamus of birds.
Memory impairment following status epilepticus in immature rats: time‐course and environmental effects
Authors: Rutten Annemarieke , Van Albada Mirjam , Silveira Diosely C. , Cha Byung Ho , Liu Xianzeng , Hu Yingchu N. , Cilio Maria Roberta , Holmes Gregory L. 
Published: March 2003

AbstractStatus epilepticus (SE) has a high mortality and morbidity rate in children. Disturbances in learning and memory are frequently associated with SE although it is not clear when the cognitive deficits occur. If cognitive dysfunction occurs immediately following the seizure, the window of opportunity for therapeutic intervention is limited. The first goal of this study was to determine the timing of cognitive dysfunction following SE in weanling rats. As there is evidence that enriching the environment can improve cognitive and motor deficits following brain injury, our second goal was to determine whether environmental enrichment improves cognitive function following SE. Rats underwent lithium‐pilocarpine‐induced SE at postnatal (P) day 20 and were then tested for visual‐spatial memory in the water maze at P22, P25, P30, or P50. Rats with SE performed significantly worse in the water maze than control rats at all time points. Once the time‐courses of visual‐spatial memory deficits were determined, a second group of P20 rats were subjected to SE and were then placed in an enriched environment (enriched group) or remained in standard cages in the vivarium (nonenriched group) for 28 days. Following environmental manipulation, the animals were tested in the water maze. Rats housed in an enriched environment following the SE performed substantially better in the water maze than rats housed in standard cages. However, no differences were found between the enriched and nonenriched groups in EEG or histological evaluation. Although SE results in cognitive impairment within days of the seizure, housing in an enriched environment after SE has a beneficial effect on cognitive performance in rats.