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1

Injury induced dendritic plasticity in the mature central nervous system

100%
Macias M.
Acta Neurobiologiae Experimentalis
|
2008
|
tom 68
|
nr 2
Injury to the mature central nervous system (CNS) induces a series of transient changes leading not only to death of neurons, but also to spontaneous rearrangement of the affected network. One of such pro plastic events, detected following injury, is an increased level of neurotrophins. Neurotrophins are a family of proteins involved in survival and outgrowth processes. The other one, more difficult to observe, is a change in the complexity of the dendritic tree, causing arborization or pruning, depending on many circumstances: i.e. lesion etiology. Subsequent therapies like enriched environment or locomotor exercise bring about a functional improvement, which was found to further increase the neurotrophin level and induced additional arborization of dendrites. Another important consequence of damage to CNS connections is deafferentation, shown to induce a down regulation of outgrowth inhibitors. Their suppression in turn may facilitate dendritic plasticity. Taken together, these factors may contribute to enhanced plasticity in the injured mature CNS. Thus the proper use of endogenously increased plastic potential seems to be important for design and optimizing therapeutic strategies. Further investigation of mechanisms involved in switching on plasticity may help to improve on existing therapies and find new ways to obtain better recovery following injury.
2

The influence of graded levels of Jerusalem artichokes and body weight on the digestibility of dietary components in a sugar cane molasses-based pig diet

63%
Macias M., Ly J.
Journal of Animal and Feed Sciences
|
1998
|
tom 07
|
nr 3
313-322
3

Regulation and cellular functions of mTORC1 in animal models of epilepsy

51%
Jaworski J., Macias M., Blazejczyk M., Urbanska M.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
Introduction: Mammalian target of rapamycin (mTOR) is a protein kinase that regulates cellular metabolism. Adequate mTOR activity is needed for development as well as proper physiology of mature neurons. Changes in mTOR activity are often observed in neuropathology. Several groups reported that seizures increase mTOR activity, and mTOR contributes to spontaneous seizures. However, the current knowledge about 1) the spatiotemporal and 2) the subcellular pattern of mTOR activation as well as 3) mTOR downstream effectorsin epilepsy is limited. Effects of mTOR insufficiency in seizures also remain under investigated. Aim: The aim of my team is to understand regulation and contribution of mTOR to epilepsy and pinpointing cellular mechanisms downstream mTOR. Methods: To study a role of mTOR in epilepsy we used models of pharmacological treatment with kainic acid (KA). We performed analysis of status epilepticus (SE) severity and progression. We analyzed with quantitative Western-blot and microarrays changes in signaling pathways and gene expression. Subcellular distribution of mTOR and its activity was analyzed by live microscopy. Results: We showed that SE induces mTOR first in neurons and next in astrocytes. At early times post seizures mTOR translocates to the nucleus, where its activity increases gradually. We showed that mTOR is involved in KA-dependent gene expression and genes regulated by mTOR regulate cytoskeleton. One of them, Elmo-1 regulates axonal growth and dendritic spine changes. Our research shows also that insufficient mTOR activity lead to increased sensitivity to KA. Conclusions: mTOR is an important player in epilepsy. One of the processes likely controlled by mTOR in epilepsy is transcription of genes responsible for cytoskeleton rearrangement. On the other hand, insufficient mTOR activity decreases threshold for epileptic-like neuronal activity. FINANCIAL SUPPORT: The research was supported by Polish National Science Centre (grants no. 2012/05/B/ NZ3/00429; 2012/07/E/NZ3/00503), 7FP grant (no. 602391, “EPISTOP”) and the Polish Ministerial funds for science (years 2014–2018) for the implementation of international co‑financed project. JJ is a recipient of the Foundation for Polish Science “Mistrz” Professorial Subsidy.
4

Spatio-temporal characterization mTOR kinase activity induced by kainic acid evoked seizures

51%
Macias M., Blazejczyk M., Jaworski J.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
The common effects of epileptic seizures are aberrant plastic changes in synaptic connectivity and morphological rearrangements in hippocampal mossy fi bers. This phenomenon is believed to be a basis of facilitation of further epileptic episodes, however its molecular mechanism remains elusive. mTOR kinase is crucial for rearrangements of neuronal morphology and for long term synaptic plasticity. Overactivation of mTOR was reported in brain pathologies associated with seizures (tuberous sclerosis, cortical dysplasia). Experimental evidence supports causative role of mTOR in these forms of epilepsy. So far, however, links of mTOR signaling pathway to other types of epilepsy are unknown. To address this issue we investigated activation of mTOR and its downstream effectors in rat brain after kainic acid (KA) induced epilepsy. Animals were sacrifi ced 2, 6, 12, 24 and 72 hours after KA administration and levels of phosphorylated mTOR and S6 has been examined. Both, biochemical methods and immunohistochemistry proved S6 activation in hippocampus and cerebral cortex at all time points after KA. Immunohistochemical analysis additionally revealed that 2 h after KA, activities of mTOR and S6 are upregulated mainly in neurons while after 6 h there was also enhancement of glial S6 immunoreactivity. Our data suggest that KA induced seizures activate mTOR signaling in various cell types with specifi c spatio-temporal pattern. This work has been fi nanced by PNRF-96-AI-1/07 grant.
5

A note on the pattern of feed intake in pigs fed Jerusalem artichoke [Helianthus tuberosus L.]

51%
Ly J., Macias M., Figueroa V., Piloto J. L.
Journal of Animal and Feed Sciences
|
1994
|
tom 03
|
nr 3
201-205
6

Ileal and faceal digestibility of Jerusalem artichokes [Helianthus tuberosus L.] in pigs

51%
Ly J., Macias M., Reyes J. L., Figueroa V.
Journal of Animal and Feed Sciences
|
1995
|
tom 04
|
nr 3
195-205
7

Confocal visualization of the effect of short-term locomotor exercise on BDNF and TrkB distribution in the lumbar spinal cord of the rat: The enhancement of BDNF in dendrites?

51%
Macias M., Dwornik A., Skup M., Czarkowska-Bauch J.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 2
8

A note on the use of Jerusalem artichokes [Helianthus tuberosus L.] in diets for growing pigs

45%
Piloto J. L., Figueroa V., Macias M., Rosabal M., Ly J.
Journal of Animal and Feed Sciences
|
1998
|
tom 07
|
nr 2
213-217
9

Kainic acid causes mTOR activation and translocation from cytosol to the nucleus – Live imaging study

45%
Macias M., Janusz-Kaminska A., Tarkowski B., Gozdz A., Jaworski J.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: The mechanistic target of rapamycin (mTOR) is a protein kinase, which integrates eukaryotic cell growth, metabolism and external stimuli. Most research link mTOR with control of protein translation but recent studies revealed additional mTOR function in cell nucleus. Previously, we showed that phosphorylation of mTOR (Ser2448; P-mTOR) is upregulated in neuronal nucleus upon kainate (KA) induced status epilepticus. Whether other stimuli have the same effect on nuclear mTOR phosphorylation and if increased nuclear import of mTOR contributes to this phenomenon remained unknown. Also it was not known if nuclear transport of other proteins affects mTOR signaling. AIM(S): To analyze effects of neuronal activity on nuclear translocation of mTOR and its nuclear activity. To analyze importance of nuclear transport for mTOR signaling. METHOD(S): Cultured hippocampal neurons were treated with: KA, BDNF; NMDA and chemical LTP (cLTP) protocol or TTX. mTOR activity was measured with FRET method. mTOR nuclear translocation was assessed using FRAP. Nuclear import was blocked with importazole. Immunofluorescence of P-S6 protein was used as a marker of mTOR activity. RESULTS: We found that KA, BDNF, NMDA and cLTP caused nuclear upregulation of P-mTOR. However, TTX or cLTD had no effect. FRAP and FRET revealed that mTOR activity due to KA treatment is first observed in cytosol and then in nucleus, where mTOR is translocated upon treatment. Blocking nuclear import silenced mTOR activity in response to KA and inhibited P-mTOR upregulation in the nucleus. CONCLUSIONS: Our experiments showed that increased neuronal activity upregulates nuclear P-mTOR and increases nuclear activity of mTOR due to nuclear translocation of the kinase. FINANCIAL SUPPORT: The research was supported by PNSC grants no. 2012/05/B/NZ3/00429 and 2012/07/E/ NZ3/00503.
10

Unilateral photothrombotic stroke in the frontal cerebral cortex causes biiateral impairment of skilled movements of the rat forelimb

45%
Sulejczak D., Skup M., Stzralkowski R., Macias M., Czarkowska-Bauch J.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
11

Distribution of TrkB receptors in motor-sensory cortical areas in the rat

45%
Macias M., Dwornik A., Sulejczak D., Czarkowska-Bauch J., Skup M.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
12

Cutaneous reflexes in chronic spinal rats

45%
Dwornik A., Macias M., Wiater M., Skup M., Czarkowska-Bauch J.
Acta Neurobiologiae Experimentalis
|
1999
|
tom 59
|
nr 3
13

Neurons and glia npregulate FIk1 following various cortical injuries

39%
Sulejczak D., Nosecka E., Macias M., Skup M., Czarkowska-Bauch J., Walski M., Frontczak-Baniewicz M.
Acta Neurobiologiae Experimentalis
|
2005
|
tom 65
|
nr 3
14

What locomotor training brings to intact and injured spinal cord?

39%
Skup M., Macias M., Dwornik A., Ziemlinska E., Strzalkowski R., Czarkowska-Bauch J.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 3
15

Locomotor training is an effective tool to stimulate BDNF and NT-4 neurotrophins in rat spinal cord

39%
Dwornik A., Macias M., Sulejczak D., Wiater M., Skup M., Czrkowska-Bauch J.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
16

Stimulation of TrkB receptor protein expression in the spinal cord by locomotor training:contribution of oligodendroglia

39%
Macias M., Dwornik A., Sulejczak D., Wiater M., Czarkowska-Bauch J., Skup M.
Acta Neurobiologiae Experimentalis
|
2001
|
tom 61
|
nr 3
17

Locomotion induces changes in Trk B receptors in small diameter cells of the spinal cord

39%
Skup M., Czarkowska-Bauch J., Dwornik A., Macias M., Sulejczak D., Wiater M.
Acta Neurobiologiae Experimentalis
|
2000
|
tom 60
|
nr 3
18

Spatiotemporal characterization of mTOR kinase activity following kainic acid induced status epilepticus and analysis of rat brain response to chronic rapamycin treatment

33%
Macias M., Blazejczyk M., Kazmierska P., Caban B., Skalecka A., Tarkowski B., Konopacki J., Jaworski J.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Mammalian target of rapamycin (mTOR) is a protein kinase that senses nutrient availability, trophic factors support, cellular energy level, cellular stress, neurotransmitters and adjusts cellular metabolism accordingly. Recently, several groups reported that seizures increase mTOR activity, and such increased activity in genetic models can contribute to spontaneous seizures. However, the current knowledge about the spatiotemporal pattern of mTOR activation induced by proconvulsive agents is rather rudimentary. Also consequences of insufficient mTOR activity on a status epilepticus are poorly understood. Here, we investigated these two issues. We showed that mTOR signaling was activated by kainic acid (KA)-induced status epilepticus through several brain areas as well as revealed two waves of mTOR activation: an early wave (2 h) that occurs in neurons and a late wave that predominantly occurs in astrocytes. Unexpectedly, we found that pretreatment with rapamycin, a potent mTOR inhibitor, gradually (1) sensitized animals to KA treatment and (2) induced gross anatomical changes in the brain. Supported by Polish National Science Center OPUS grant (2012/05/B/ NZ3/00429)
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