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1
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A search for colocalization of serotonin 5-HT2A and 5-HT1A receptors in the rat medial prefrontal and entorhinal cortices-immunohistochemical studies

100%
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.
2
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Effect of cyclic adenosine monophosphate on the G protein-dependent inward rectifier Kplus-like channel current in medial prefrontal cortex pyramidal neurons

84%
Witkowski G., Rola R., Szulczyk P.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 5
3

Blockade on NMDA receptors in postnatal period decreased density of tyrosine hydroxylase immunoreactive axonal arbors in the medial prefrontal cortex of adult rats

84%
Wedzony K., Fijal K., Chocyk A.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 2
Malfunction of glutamatergic neurotransmission in postnatal period is considered to be a risk factor for development of schizophrenia. Thus, the present study investigates the impact of NMDA receptor blockade in the postnatal period on the density of tyrosine hydroxylase immunoreactive axonal arbors in the rat medial prefrontal cortex. Behavioral experiments revealed that adult rats (60 days old) treated in the postnatal period with a competitive antagonist of NMDA receptors, CGP 40116 (1.25 mg/kg on days 1, 3, 6, 9; 2.5 mg/kg on days 12, 15, 18; and finally 5 mg/kg on day 21, all injections s.c.), showed enhancement of the locomotor activity stimulated by quinpirole (0.3 mg/kg s.c.) and amphetamine (0.5 mg/kg s.c.), which suggests development of functional supersensitivity of dopaminergic systems. It has been found that CGP 40116, given in postnatal period decreased the density of tyrosine hydroxylase immunoreactive axonal arbors in the medial prefrontal cortex of adult animals. The decrease was observed in superficial (II/III) and deep (V/VI) layers of the medial prefrontal cortex, while the average length of tyrosine hydroxylase immunoreactive axonal arbors was increased in both superficial and deep cortical layers. Changes in the density of tyrosine hydroxylase immunoreactive axonal arbors have not been followed by a significant decrease in the content of tyrosine hydroxylase protein measured by Western blot. Thus, NMDA receptor blockade in the early period of life evokes changes in architecture of tyrosine hydroxylase immunoreactive axonal arbors and that malfunction of glutamatergic neurotransmission, in early period of life may produce anatomical changes which resemble those observed in the brains of schizophrenics.
4
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Glutamatergic neurons of rat medial prefrontal cortex innervating the ventral tegmental area are positive for serotonin 5-HT1A receptor protein

84%
Wedzony K., Chocyk A., Kolasiewicz W., Mackowiak M.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 4
The present study was designed to investigate whether serotonin 5-HT1A receptor protein (5-HT1A receptor-immunoreactivity), is present on cortical pyramidal neurons of the rat medial prefrontal cortex (MPC) innervating the ventral tegmental area (VTA). Recent data stress the role of serotonin 5-HT1A receptors in the pathology of schizophrenia, and in the mechanism of action of novel antipsychotic drugs. It was found that approximately 52% of cells in layers II/III of the MPC whose axons initial segments were immunoreactive for serotonin 5HT1A receptor were also labeled with Fluoro-Gold (FG), a retrograde tracer injected into the VTA, indicating that certain portion of neurons forming glutamatergic innervations of the VTA may be controlled by serotonin 5-HT1A receptors. In deep cortical layers (V/VI) retrogradely labeled neurons never colocalized with serotonin 5-HT1A receptor-mmunoreactivity. These anatomical data indicate that serotonin 5-HT1A receptors might potentially control the excitability and propagation of information transmitted by the pyramidal cells to the VTA. Moreover, our results indicate that the drugs operating via serotonin 5-HT1A receptors in the MPC, might control from this level the release of glutamate in the VTA and restore function of glutamate neurotransmission, whose dysfunction is observed for example in schizophrenia.
5

Alteration of spontaneous spectral powers and coherences of local field potential in prenatal valproic acid mouse model of autism

67%
Cheaha D., Kumarnsit E.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
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nr 4
Previously, autism spectrum disorder (ASD) has been identified mainly by social communication deficits and behavioral symptoms. However, a link between behaviors and learning process in the brain of animal model of autism remained largely unexplored. Particularly, spontaneous neural signaling in learning-related brain areas has not been studied. This study investigated local field potential (LFP) of the hippocampus (HP), the olfactory bulb (OB) and the medial prefrontal cortex (mPFC) in mice prenatally exposed to valproic acid (VPA) on gestational day 13. Adult male Swiss albino mouse offspring implanted with intracranial electrodes were used. VPA-exposed mice exhibited ASD-associated behaviors. Hippocampal LFP analysis revealed that VPA group significantly increased low gamma activity (25–45 Hz) during awake immobility. Regression analyses confirmed positive correlations between locomotor speed and hippocampal theta oscillations in control but not VPA group. VPA group exhibited increases in delta (1–4 Hz) and beta (25–35 Hz) activities in OB during awake immobility and active exploring, respectively. Moreover, significantly increased and decreased coherences between HP and OB of VPA animals were seen within gamma (active exploration) and theta (awake immobility) ranges, respectively. In addition, significant increase in coherence between HP and mPFC was seen within delta range during active exploration. In addition to three ASD symptoms, VPA animals also exhibited differential patterns of olfacto-hippocampal LFP, altered locomotor speed-related hippocampal theta activities and distinct interplays between HP and learning-related brain areas. The altered olfacto-hippocampal and medial prefrontal cortex-hippocampal networks may underlie impairments in autism mouse model.
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Degeneration of astrocytes in the prefrontal cortex induces depressive-like behavior in rats: Behavioral, immunochemical and histological studies

67%
Smialowska M., Szewczyk B., Wawrzak-Wlecial A., Domin H.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
Postmortem studies of depressed patients showed that one of the most consistent findings is a decrease in the density of glial cells in human brain cortical regions, especially in the prefrontal and cingular areas. Furthermore, a decline in the number of astrocytes in the prefrontal cortex was found in rats after chronic unpredictable stress – one of the generally accepted animal models of depression. An important function of astrocytes in the brain tripartite synapse is the uptake of released glutamate. Hence the basic consequence of the loss of astrocytes is a reduction in glutamate uptake and an excess of glutamate in the synaptic cleft. The glutamatergic predominance in the excitator-inhibitory balance is postulated to be involved in the pathogenesis of depression. Recently, depressive-like behavior have been demonstrated in rats after astrocytes ablation. Therefore in the present study we tried to ascertain whether astroglial degeneration in the prefrontal cortex was sufficient to induce a depressive-like behavior and could serve as an animal model of depression. Astrocytic toxin L- or D,Lalpha-aminoadipic acid (AAA), 100 µg/2 µl, was microinjected bilaterally into rat medial prefrontal cortex (PFC). The toxins were injected twice, on day 1 and 2; afterwords depressive-like behavior was assessed by a forced swim test on day 5 of the experiment. Some rats were additionally treated with the antidepressant imipramine (30 mg/kg, i.p.) 24, 5 and 1 h before the forced swim test. The rats’ brains were taken out for an analysis on day eight. Histological verifications of the injection sites and immunohistochemical staining for the astrocytic marker glial fibrillary acidic protein (GFAP), were carried out. The GFAP positive cells were stereologically counted in the PFC. Also the level of GFAP expression was determined by the Western blot analysis in all the experimental groups. It was found that both L-AAA and DL-AAA induced a significant increase in immobility time in the forced swim test, without changing the overall locomotor activity, which indicates depressive-like effects of these compounds. The immunohistochemical and Western blot analyses showed a significant decrease in the number of GFAP-positive cells and GFAP level in the PFC of toxin-treated rats. The decrease amounted to ca. 50%. Both the behavioral and the GFAP changes were reversed or partially inhibited by imipramine injection. The obtained results suggest an important role of astrocytes in the PFC in mood regulation; moreover, they indicate that the degeneration of astrocytes in this structure may be used as an animal model of depression. This study was supported by Grant POIG.01.01.02-12-004/09Friday, November 23, 2012
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