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1

The rhythmic slow activity recorded from entorhinal cortex in freely moving cats

100%
Blaszczyk M., Grabowski R., Eckersdorf B., Golebiewski H., Konopacki J.
Acta Neurobiologiae Experimentalis
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1996
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tom 56
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nr 1
2
Content available remote

A search for colocalization of serotonin 5-HT2A and 5-HT1A receptors in the rat medial prefrontal and entorhinal cortices-immunohistochemical studies

75%
Wedzony K., Chocyk A., Mackowiak M.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 2
Recently developed antipsychotic drugs ameliorating the negative symptoms of schizophrenia act not only on dopamine D2 receptors but also on serotonin 2A (5-HT2A) and 1A (5-HT1A) receptors in specific regions of the cerebral cortex. Since it is not yet known whether serotonin 5-HT1A and 5-HT2A receptors coexist in the same population of neurons in the cortex, the present study investigated their colocalization in the rat medial prefrontal (MPC) and entorhinal (EC) cortices. Using antibodies that recognize epitopes specific to the serotonin 5-HT2A or 5-HT1A receptors, studies employing confocal microscopy have shown that in the MPC 5-HT2A receptors are preferentially, if not exclusively, present on the pyramidal neurons and that 5-HT1A-immunopositive material is present in the axonal hillocks and, to lower extend, in cytoplasm of presumably pyramidal cell bodies. With the regard of labeling of active receptors (i.e. present in shafts and axonal hillocks) we found that about 38% of neurons positive for the presence of serotonin 5-HT2A receptors, are also positive for serotonin 5-HT1A receptors in the MPC. In the EC, only 22% of serotonin 5-HT2A-positive neurons were positive for serotonin 5-HT1A receptor-immunoreactivity. In the respect of cytoplasmatic serotonin 5-HT1A receptor-immunoreactivity (possibly inactive receptors), 65% and 73% of serotonin 5-HT2A receptor-positive neurons were colocalized with serotonin 5-HT1A receptors in the MPC and EC, respectively. Data obtained on serotonin 5-HT2A and 5-HT1A receptor localization provide anatomical grounds for at least three distinct populations of pyramidal neurons, one governed only by 5-HT2A, one only by 5-HT1A and one by both types of serotonin receptors.
3

How does trimethyltin affect the brain: facts and hypotheses

63%
Koczyk D.
Acta Neurobiologiae Experimentalis
|
1996
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tom 56
|
nr 2
4

In vitro recorded theta-like activity in the limbic cortex: comparison with spontaneous theta and epileptiform discharges

51%
Konopacki J., Golebiewski H., Eckersdorf B., Kowalczyk T., Bocian R.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 1
The generation of EEG theta rhythm in the mammalian limbic cortex is a prime example of rhythmic activity that involves central mechanisms of oscillations and synchrony. This EEG pattern has been extensively studied since 1938, when Jung and Kornmuller (1938) demonstrated the first theta recordings in the hippocampal formation of rabbits. In 1986 in collaboration with Drs. B.H. Bland, S.H. Roth and B.M. Maclver we demonstrated for the first time that bath perfusion of hippocampal slices with the cholinergic agonist, carbachol, resulted in theta-like oscillations. Since this initial demonstration of in vitro theta-like activity, we have carried out a number of experiments in an attempt to answer the basic question: what are the similarities between cholinergic-induced in vitro theta-like activity and theta rhythm which naturally occurs in the in vivo preparation. Thus far, our studies have provided strong evidence that theta-like activity recorded in vitro shares many of the physiological and pharmacological properties of theta rhythm observed in vivo. The question whether in vitro theta-like oscillations reflect features of epileptiform activity is also adressed in this review.
5

Trimethyltin - induced plastic neuronal changes in rat hippocampus are accompanied by astrocytic trophic activity

51%
Koczyk D., Skup M., Zaremba M., Oderfeld-Nowak B.
Acta Neurobiologiae Experimentalis
|
1996
|
tom 56
|
nr 1
6

The second layer neurones of the entorhinal cortex and the perforant path in physiological ageing and Alzheimer's disease

45%
Morys J., Sadowski M., Barcikowska M., Maciejewska B., Narkiewicz O.
Acta Neurobiologiae Experimentalis
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1994
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tom 54
|
nr 1
7

Development of oscillatory activity in the limbic cortex in vitro

45%
Konopacki J.
Acta Neurobiologiae Experimentalis
|
1996
|
tom 56
|
nr 1
8

Brain injury: prolonged induction of transcription factors

38%
Pennypacker K. R., Kassed C. A., Eidizadeh S., O'Callaghan J. P.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 4
A specific temporal order of events at the cellular and molecular level occurs in response to injury to the brain. Injury-compromised neurons degenerate while surviving neurons undergo neuritogenesis and synaptogenesis to establish neuronal connectivity destroyed in the injury. Several genes, such as those coding cytoskeletal proteins and growth factors, have been shown to be regulated by AP-1 and NF-kB transcription factors, two of the most studied DNA binding regulatory proteins. Our laboratory has discovered that Fos-related antigen-2 from AP-1 transcription factor family and NF-kB p65 and p50 subunits are induced long-term (days to months) in the brain after neurotoxic, excitotoxic or ischemic insult. Fos-related antigen-2 is induced in neurons in several models of injury and its elevated expression lasts days to months, corresponding to the severity. The time-course of FRA-2 induction is abbreviated with less severe insult (terminal damage) relative to the cell death, but the induction occurs during the period of regeneration and repair in both models. NF-kB p65 is basally expressed in hippocampal and cortical neurons, but is elevated in reactive astrocytes in hippocampus and entorhinal cortex starting at two days and lasting at least two weeks after kainate treatment. Neurons of the hippocampus surviving ischemic or neurotoxic injury increase expression of NF-kB p50 for at least a week after injury, suggesting a function for p50 in neuronal survival and/or repair. The extended expression of these transcription factors implies a role in the activation of genes related to repair and regeneration, such as growth factors and synaptic proteins, after injury to the CNS.
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