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  1. 26 Acta Neurobiologiae Experimentalis

  2. 2 Neuropatologia Polska

  3. 1 Polish Journal of Pharmacology

  4. 1 Postępy Higieny i Medycyny Doświadczalnej

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  1. 2 2009

  2. 3 2008

  3. 2 2007

  4. 1 2004

  5. 1 2003

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  1. 3 Lazarewicz J. W.

  2. 2 Koczyk D.

  3. 2 Rybkowski W.

  4. 2 Salinska E.

  5. 1 Adams J. P.

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1
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MAPK regulation of gene expression in the central nervous system

100%
Adams J. P., Roberson E. D., English J. D., Selcher J. C., Sweatt J. D.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 3
377-394
EN
Long-term potentiation (LTP), a cellular model for long-term memory, is generally acknowledged to consist of both a short-term phase that is characterized by a dependence on autonomous protein kinase activity, and a long-term phase that is characterized by a dependence on changes in gene expression and new protein synthesis. Similarly, long-term memory exhibits a dependence on gene expression and altered protein synthesis. Recent evidence indicates that the mitogen-activated protein kinase (MAPK) cascade plays a role in both LTP and long-term memory. The MAPK cascade has heretofore largely been studied in the context of cell division and proliferation and as such, mechanisms for the regulation of gene expression by the MAPK cascade have received considerable attention. Given the possible role of altered gene expression in the late phase of LTP and in long-term memory, we evaluated the capacity of the MAPK ERK (extracellular signal-regulated kinase) to regulate phosphorylation of the transcription factor cAMP response element binding protein (CREB) in hippocampal area CA1. Our studies indicate a critical role for the MAPK cascade in the regulation of CREB phosphorylation in the hippocampus.
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Electrical hippocampal activity during danger and safety signals in classical conditioning in the rat

80%
Kasicki S., Jelen P., Olszewski M., Slawinska U.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 1
119-128
EN
The effect of stimuli predicting danger (DS) and safety (SS) in Pavlovian aversive conditioning on hippocampal local field potentials (LFP) was studied in 25 partially restrained adult male rats (Long-Evans). DS lasting 5 s preceded tail-shock, while SS overlapping DS during DS last 3 s predicted omission of shock. The power spectra of LFPs during trials were analyzed in theta and delta frequency bands. In DS, theta frequency during the last 3 s was lower that in first 2 s. In danger and safety situation theta peak frequency was different for dorsal CA1 activity (5.99 Hz vs. 6.86 Hz, respectively), while delta peak frequency was different for ventral CA1 (1.56 Hz vs. 1.07 Hz) for the last 3 s of trial. Differences in theta frequency in danger and safety situation may reflect differences in sensory processing during induced emotional states and/or related differences in motor behavior.
3
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Differential expression of NMDA-evoked 45Ca release in rat hippocampal regions in vivo

80%
Lazarewicz J., Rybkowski W.
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EN
Recently we detected NMDA-induced 45Ca release in the rat dentate gyrus in vivo, attributable to the Ca2+ release (CICR) from the endoplasmic reticulum via ryanodine channels.In these experiments we compare expression of NMDA-evoked 45Ca release in the rat dentate gyrus (DG), CA1 and subiculum (SUB).The release of 45Ca was studied using in vivo prelabelled hippocampal regions.It was shown thet NMDA-induced 45Ca release, highly pronounced in the rat DG/CA4, is significantly less expressed in the CA1, whereas in the SUB and NMDA-evoked decrease in 45Ca efflux was noted.This corresponds to distribution of ryanodine receptors in the rat hippocampus, known from the literature.Expression of NMDA-evoked 45Ca release in these rat hippocampal regions which are enriched in ryanodine receptors supports our working hypothesis that CICR via ryanodine channels may be mainly responsible for 45Ca release.
4
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Changes of the acoustic startle reflex in rats with radiation-induced hippocampal lesion

80%
Blaszczyk J. W., Walasek G., Woznicka A., Seress L.
Acta Neurobiologiae Experimentalis
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1999
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vol. 59
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issue 3
171-176
EN
The main question of the study was: to what extent does a neonatal radiation-induced hippocampal lesion lead to emotional changes in adulthood? Acoustic startle response (ASR) was studied in two groups of adult rats. The rats from the first group (14 animals) were exposed to neonatal x-ray irradiation. Their ASR were compared with those from the 10 intact rats that formed a control group. The ASR was tested during two sessions with different illumination of the acoustic chamber. During the first session the rats were tested in the darkness while during the second test the acoustic chamber was illuminated with a 15 W bulb. Irradiation resulted in a significant reduction of granule cells of the hippocampus (about 55%). The lesion resulted in emotional and behavioral changes evidenced by modification of the ASR. The irradiated rats exhibited a significantly increased amplitude of the startle response. In contrast to the light condition, the darkness context caused a decline of the ASR amplitude in the control group and failed to elicit significant changes in the lesioned animals. The results support the hypothesis that hippocampal lesions disrupt motor inhibition.
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Neurogenesis in gerbil hippocampus following brain ischemia: Focus on the involvement of metalloproteinases

80%
Wojcik L., Sawicka A., Rivera S., Zalewska T.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 1
52-61
EN
Accumulating evidence indicates that cerebral ischemia enhances neurogenesis in the adult brain. The mechanisms responsible for stem-cell development are poorly understood. Recent in vitro studies indicate the involvement of metalloproteinase (MMPs) in the regulation of proliferation and differentiation of neural progenitor cells. To elucidate if MMPs participate in neurogenesis-associated processes after ischemic insult, we aimed to establish spatial and temporal relationships between neural stem-cell development and the activity of MMPs in the adult brain hippocampus. Our results show that post ischemic acceleration in the proliferation of progenitors in the dentate gyrus is accompanied by increased activity of MMPs. On the contrary, in the damaged CA1 pyramidal layer the neurogenesis seems to be rather elusive.Simultaneously, the activity of MMPs fell below the control level. In conclusion, our results show that the activation of MMPs may, at least in part, contribute to ischemia-induced neurogenesis in the dentate gyrus of the adult brain.
6

Calcium accumulation in synapses of the rat hippocampus after cerebral ischemia

80%
Gajkowska B., Mossakowski M. J.
Neuropatologia Polska
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1992
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vol. 30
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issue 2
111-126
EN
The ultrastructural localization of calcium deposits in the synapses of rat hippocampus after 10 min global cerebral ischemia was evaluated. Oxalate-pyroantimonate technique was applied. After 24 hours of postischemic recirculation enhancement of intracellular (pre- and postsynaptic parts) and extracellular (synaptic clefts) calcium deposits was found in great proportion of synapses in CA1 sector. Abundant Ca-precipitates appeared specially in synaptics clefts and in the postsynaptic parts near synaptic densities. Increased calcium deposits in some changed mitochondria were also observed, The results presented in this paper suggest synaptic modulation of calcium homeostasis, disturbed after ischemic incident. Presence of Ca-precipitates in synaptic clefts and postsynaptic parts seems to be a sensitive indicator of increased calcium influx from the extracellular to the intracellular compartments.
7
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Erythropoietin preconditioning suppresses neuronal death following status epilepticus in rats

80%
Yang J., Huang Y., Yu X., Sun H., Li Y., Deng Y.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 2
141-148
EN
Status epilepticus (SE) is a grave condition in which the brain undergoes lasting seizures which can lead to neuronal loss. Our previous study suggested that preconditioning with erythropoietin (Epo) suppressed neuronal apoptosis in hippocampus of rats following SE in vivo by inhibiting caspase-3. In this study, we investigated the mechanisms by which Epo preconditioning may exert its anti-apoptotic effects using a lithium-pilocarpine induced SE model in rats. The effects of Epo on neuronal cell death were evaluated using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the role of the Bcl-2 protein family, which have been shown to be anti- (Bcl-2, Bcl-w) or pro- (Bid, Bim) apoptotic, was examined with immunofluorescence. We found Epo preconditioning decreased the total number of TUNEL, Bim and Bid positive cells, but increased the total number of Bcl-w and Bcl-2 positive cells. These results suggest that systemic Epo pretreatment protects neurons in an acute phase of SE and may result in further suppression of neuronal apoptosis in hippocampus by regulating the balance between pro- and anti-apoptotic Bcl-2 family proteins.
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Early postnatal ethanol exposure induces fluctuation in the expression of BDNF mRNA in the developing rat hippocampus

80%
Miki T., Kuma H., Yokoyama T., Sumitani K., Matsumoto Y., Kusaka T., Warita K., Wang Y.-Y., Hosomi N., Imagawa T., Bedi K. S., Itoh S., Nakamura Y., Takeuchi Y.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 4
484-493
EN
Effects of early postnatal ethanol exposure on brain-derived neurotrophic factor (BDNF) mRNA expression in the rat hippocampus were investigated. Wistar rats were assigned to either ethanol treatment (ET), separation control (SC) or mother-reared control (MRC) groups. Ethanol exposure was achieved by a vapor inhalation method for 3 hours a day between postnatal days (PND) 10-15. On PND 16, 20, 30, and 60, the expression of BDNF mRNA in the hippocampus was determined using real-time RT-PCR analysis. There was a significant age-related increase in the BDNF mRNA expression between PND 3060 in MRC animals. The BDNF mRNA expression in ET rats was increased at both PND 16 and 20 and thereafter decreased at PND 60 compared to SC animals. Such age-related fluctuation in the expression of BDNF mRNA differed from that of MRC animals. The exact functional implications, if any, of these ethanol-induced changes in BDNF mRNA expression remain unknown although it can be speculated that they may have an effect on the behaviors known to be influenced by the hippocampal formation.
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NMDA receptors and nitric oxide regulate prostaglandin D2 synthesis in the rabbit hippocampus in vivo

80%
Lazarewicz J. W., Salinska S. E., Salinska E., Stafiej S. A., Stafiej A., Ziembowicz Z. A., Ziembowicz A., Zieminska Z. E., Zieminska E.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 4
427-435
EN
The aim of this in vivo microdialysis study was to characterise the regulation of prostaglandin D2 (PgD2) synthesis by NMDA receptors in the rabbit hippocampus in relation to changes in extracellular Ca2+ concentration ([Ca2+]e) and nitric oxide (NO) levels. Samples of dialysate were analysed for changes in PgD2 concentration, in [Ca2+]e and in the level of NO. The results demonstrated that a 20-min pulse application of 0.1 - 2.5 mM NMDA via a microdialysis probe induced a prolonged stimulation of PgD2 release that was sensitive to competitive NMDA receptor antagonists. An inhibitor of voltage-sensitive Na+ channels, tetrodotoxin, did not influence this effect but significantly suppressed basal PgD2 production, whereas a NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), prevented NMDA-evoked NO release and inhibited NMDA-induced PgD2 release in an L-arginine-sensitive manner. NO donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside, stimulated PgD2 release. NMDA-evoked decrease in [Ca2+]e was insensitive to TTX and L-NAME. These results demonstrate an in vivo NMDA receptor-mediated modulation of PgD2 synthesis in the brain, in which NO participates.
10
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Differential response of microtubule-associated protein 2 (MAP-2) in rat hippocampus after exposure to trimethyltin (TMT):an immunocytochemical study

80%
Koczyk D.
Acta Neurobiologiae Experimentalis
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1994
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vol. 54
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issue 1
55-58
11

Comparative anatomy of the arterial vascularization of the hippocampus in man and in experimental animals /cat, rabbit and sheep/

80%
Goetzen B., Sztamska E.
Neuropatologia Polska
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1992
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vol. 30
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issue 2
173-184
EN
The studies were performed by the authors' injection method on 30 human brains and 80 animal ones. The cerebral arteries were infected with synthetic coloured latex and then prepared in an operating microscope. It was found that the main source of arterial supply of both the human and animal hippocampus is the posterior cerebral artery. However, this artery has different origins in the arterial circle of the brain in man, cat, rabbit and sheep. Comparative investigations have also proved that the hippocampal vascular system in man and animals is very similar. It is formed by branches of the posterior cerebral artery and of the anterior choroidal artery, called the hippocampal arteries, and by numerous internal hippocampal arterioles arising from them at right angle. The regional distribution of these arterioles is impossible to describe because of their variable course in the hippocampal cortex and of the similar vascularization of different cortical areas of the hippocampus. The studies have also shown that the hippocampal arterial system is very well developed and makes collateral circulation possible. Extracerebral segments of the hippocampal arterioles in human senile brains and chefly in brains with atherosclerosis showed different deformations in the form of siphon-like structures, knot-loops and vascular glomeruli.
12
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Dilatation of the lateral part of the transverse fissure of the brain in Alzheimer's disease

80%
Narkiewicz O., Leon M., Convit A., George A. E., Wegiel J., Morys J., Bobinski M., Colomb J., Miller D. C., Wisniewski H. M.
Acta Neurobiologiae Experimentalis
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1993
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vol. 53
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issue 3
457-465
EN
Post-morten MRI (magnetic resonance images) studies followed by histopathological examination were used to study the size and the shape of the of the of the in seven individuals with Alzheimer disease (AD) and five controls. Incontrol brains, the lateral part of the transverse fissure is a narrow cleft protruding laterally as choroid and hippocampal recesses. In AD-affected brains, the lateral part of the transverse fissure becomes a large subarachnoid space as a result of different degrees of atrophy of various hippocampal and parahippocampal structures. Our findings directly indicate the relationship between changes in the hippocampal and parahippocampal structures and the size of the lateral part of the transverse fissure. Sector CA1, the subiculum, the entorhinal cortex, and the parahippocampal isocortex are the most affected, whereas the dentate gyrus is much less affected. Adjacent thalamic structures, which are less vulnerable to the AD pathology, do not appear to contribute to transverse fissure changes. The size and the shape of the lateral part of the transverse fissure of the brain in AD reflect the atrophy of the hippocampus and parahippocampal structures.
13
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Extracellular ATP as a neurotransmitter: its role in synaptic plasticity in the hippocampus

80%
Wieraszko A.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 2
637-648
EN
Growing evidence indices that ATP may play a very important role in Long-Term Potentiation (LTP), a neurophysiological process that has been implicated in memory formation.LTP is an enhancement of synaptic strength induced by a specific pattern of high frequency stimulation, or by application of exogenous ATP.In the hippocampus LTP-inducing stimulation is accompanied by a massive Ca2+ -dependent release of ATP from presympatic terminals.Released extracellular ATP may either intract with numerous types of ATP receptors present on the neuronal surface, or serve as a substrate for ecto-protein phosphorylation.The results of combined electrophysiological and biochemical experiments indicate that participation of extracellular ATP in the ecto-protein phosphorylation process is most likely involved in the permanent amplification of the synaptic response in the hippocampus.
14

The effect of chronic treatment with imipramine on the G-proteins mRNA level in the rat hippocampus - an interaction with a calcium channel antagonist

80%
Lason W., Przewlocki R.
Polish Journal of Pharmacology
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1993
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vol. 45
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issue 2
219-226
EN
The effect of long-term administration of imipramine (10 mg/kg po, twice daily, 30 days) with or without nifedipine (5 mg/kg ip, twice daily, 28 days) on the G protein alfa subunit, Gs-alfa, Go-alfa and Gi-alfa mRNA levels was investigated in the rat hippocampus. An in situ hybridization histochemistry showed that imipramine decreased the Go-alfa mRNA level in CA1 (by ca. 40%) and CA3 (by ca. 37%) hippocampal fields and, to a lesser extent, in the dentate gyrus (by ca. 25%), but had no effect on the Gs-alfa and Gi-alfa mRNA levels in those structures. Nifedipine decreased (by ca. 30%) the Gs-alfa level in the studied fields of hippocampal formation, having no imfluence on the level of mRNA which codes other subunits of G protein, Coadministration of nifedipine and imipramine reversed the imipramine effect on Go-alfa, but had no effect on the nifedipine induced decrease at the Gs-alfa mRNA level. These results suggest that inhibition of L calcium channels modifies the effect of imipramine at the level of intracellular signal transduction.
15

Electrophysiological studies on the effects of antidepressant drugs and corticosterone on serotonin receptors in the hippocampus

80%
Zahorodna A., Tokarski K., Bijak M.
Postępy Higieny i Medycyny Doświadczalnej
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2000
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vol. 54
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issue 3
391-401
EN
Disturbances in the serotonin (5-HT) system and the limbic-hypothalamo-pituitary-adrenal axis (LHPA) have been implicated in the pathophysiology of depression. It is well established that hippocampus is a central component of limbic circuitry that participates in the modulation of cognition, mood and behavior, and is involved in the control of the LHPA axis. Therefore, the hippocampus provides a unique environment to study the interplay between serotonergic system, antidepressants and corticosteroids. Activity of hippocampal cells can be modulated by 5-HT via inhibitory 5-HT1A and excitatory 5-HT4 receptors. Repeated treatment with antidepressants increases the responsiveness of hippocampal pyramidal neurons to the 5-HT1A and attenuates the responsiveness to the 5-HT4 receptor agonists, with a time course which correlates with the delayed onsed of the therapeutic effect of antidepressants in humans. Moreover, repeated corticosterone, which may constitute a model of a prolonged nonadaptable stress, has opposite effect on hippocampal responsiveness to the 5-HT1A and 5-HT4 receptor activation. Such an action results in an enhancement of the 5-HT-mediated inhibition by antidepressants and a reduction in the inhibitory effect of 5-HT by corticosterone which may be relevant to antidepressant/antiaxiety and proaxiety effects, respectively, of both treatments.
16
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The effects of chronic corticosterone on hippocampal astrocyte numbers: A comparison of male and female Wistar rats

71%
Bridges N., Slais K., Sykova E.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 2
131-138
EN
Chronic stress and/or glucocorticoid administration produces atrophy of hippocampal neurons. However, evidence of the impact of glucocorticoids on glial cells, especially in both males and females, is limited. In the present study, we investigated the total percentage body weight, hippocampal volume and hippocampal astrocyte numbers following chronic corticosterone treatment in male and female Wistar rats. Males had greater left and right hippocampal volumes overall, but no effect on hippocampal volume was seen after corticosterone treatment. Total body weight was dose-dependently lower in both sexes, but the decrease was more prominent in male rats. Corticosterone treatment dose-dependently increased astrocyte numbers in the CA1 region, but not in the lateral and medial CA3 hippocampal regions. This increase was similar in both male and female rats. The astrogliosis observed following chronic corticosterone may have implications for extrasynaptic communication and neuron-glia interactions and is similar to changes in the astrocytic population observed in aged rats.
17
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Effects of the anterior temporal lobe lesions, separate or combined with hippocampal damage, on spatial delayed responses guided by auditory stimulus

71%
Kowalska D. M.
Acta Neurobiologiae Experimentalis
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1999
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vol. 59
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issue 4
303-313
EN
Seventeen dogs were trained in a three-choice auditory spatial delayed response task, guided by auditory stimulus, at a 10 s delay to a criterion of 90% correct responses in 90 consecutive trials. Four dogs then received bilateral anterior temporal lobe lesions (AT), 6 dogs received hippocampal lesions (H), and 7 dogs served as controls (C). Group C reached postoperative criterion immediately while groups AT and H needed additional training. When subsequently tested at longer delays and with distractions, the group H animals performed more poorly than either the AT or C animals. Further, the group H dogs were again impaired when they retrained at a 10 s delay. In the second phase, the group H and AT animals received a second lesion forming a group (HAT) with bilateral lesions to both the hippocampus and the anterior temporal lobe. Unexpectedly, dogs from group HAT were unimpaired in either postoperative retraining or during performance task and distractions. The results emphasize the importance of the hippocampus in spatial delayed response with an acoustic cue. Effect of combined lesions after extensive training is discussed. Data might support the view, that the hippocampus plays time limited role in memory storage.
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Effects of DAGO on the rodent hippocampal evoked potentials using different perfusion solutions

71%
San_ M. S., Menendez L., Gutierrez M., Hidalgo A., Baamonde A.
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EN
Opioid receptor agonists exert excitatory effects in the hippocampus by inhibiting GABA release. We report that the mu-opioid agonist, DAGO, increases the amplitude of the population spikes (PS) measured in the stratum pyramidale of the CA1 cell layer in mouse and rat hippocampal slices perfused with an artificial cerebrospinal fluid (ACSF), but not when perfused in Krebs solution. The GABA A agonist, 3-APS, induces inhibitory responses when perfused in either ACSF or Krebs. Also, the field excitatory postsynaptic potentials (EPSP) measured on stratum radiatum do not differ when the slice is perfused with either ACSF or Krebs. The increase in the amplitude of the PS induced by DAGO is not obtained when perfused in a modified ACSF whose concentration of MgSO4 was lowered to its concentration in the Krebs solution (from 2.4 mM to 1.2 mM). Thus, changes in the concentration of MgSO4 seem to be responsible for the different responses induced by DAGO.
19
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Different developmental rates of selected brain structures in humans

71%
Dambska M., Kuchna I.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
83-93
EN
Various rates of development are characteristic for particular structures of the human central nervous system (CNS). The differences of the maturing brain steam and telencephalon are evident in routine neuropathological examination. The fetal and postnatal archi- and neocortex also reveals uneven levels of maturation. In order to precisely describe those differences in humans we performed a morphological and morphometric study on the dorsal vagal nucleus of the medulla oblongata, on Ammon's horn and on neocortex from midgestation to the 18th postnatal month. The numerical density of neurones, cell perikarya andnuclear cross-sectional area, and the ratio of nucleus to perikaryon area were measured. The results demonstrate a development-dependent decrease in cell density and progressive differentiation of neurones according to their changing size. They express a process of maturation which differs in rate across the CNS structures examined.
20
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Ischemia-related alteration of GABAA-operated chloride channel properties in gerbil hippocampus and cerebral cortex

71%
Strosznajder J., Koladkiewicz I., Chalimoniuk M., Samochocki M.
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|
issue 2
95-102
EN
The properties of GABA-gated chloride (Cl^-) channels in ischemia-reperfusion injury were studied by determination of the binding and dissociation kinetics of a specific Cl^- channel ligand, tert-butylbicyclophosphoro[^35S]thionate (TBPS) and by determination of ^36Cl^- uptake in the presence of the GABAA receptor agonist, muscimol. Four days after ischemia a small but insignificant decrease of [^35S]TBPS binding to synaptic plasma membranes (SPM) was observed in the hippocampus and cerebral cortex as compared to control. The effect of ischemia was larger and statistically significant after the first and second month of reperfusion, constituting 20% inhibition of [^35S]TBPS binding to SPM of sham-operated gerbils. On the other hand, the half-life of fast phase [^35S]TBPS dissociation four days after ischemia was markedly diminished by about 40%-50% as compared to its control value and persisted during the first and second month of reperfusion in the hippocampal SPM. A similar but less potent reduction of the half-life of the fast phase of [^35S]TBPS dissociation (about 30% versus control) appeared one and two months after ischemia in cerebral cortex SPM. One month after ischemia muscimol-stimulated ^36Cl^- uptake into cerebral cortex synaptoneurosomes was lowered as compared with control uptake, but remained statistically insignificant in the whole range of muscimol concentrations tested. Our results indicated that ischemia-reperfusion injury significantly decreases opening time of GABAA receptor-gated Cl^- channels in the hippocampus and cerebral cortex, which may lower the hyperpolarization ability of this receptor complex leading to an imbalance between excitatory and inhibitory neurotransmitter pathways in these brain areas, and in consequence to neuronal dysfunction or degeneration.
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