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1

Sieci perineuronalne - zagadkowe struktury w ukladzie nerwowym

100%
Liguz-Lecznar M.
Postępy Biologii Komórki
|
2004
|
tom 31
|
nr 1
117-126
2

Vesicular glutamate transporters VGLUT1 and VGLUT2 in development of mouse barrel cortex

63%
Liguz-Lecznar M., Skangiel-Kramska J.
Acta Neurobiologiae Experimentalis
|
2006
|
tom 66
|
nr 4
3

Vesicular glutamate transporters (VGLUTs): The three musketeers of glutamatergic system

63%
Liguz-Lecznar M., Skangiel-Kramska J.
Acta Neurobiologiae Experimentalis
|
2007
|
tom 67
|
nr 3
Glutamate is the predominant excitatory neurotransmitter in the central nervous system (CNS) and glutamatergic transmission is critical for controlling neuronal activity. Glutamate is stored in synaptic vesicles and released upon stimulation. The homeostasis of glutamatergic system is maintained by a set of transporters present in plasma membrane and in the membrane of synaptic vesicles. The family of vesicular glutamate transporters in mammals is comprised of three highly homologous proteins: VGLUT1-3. The expression of particular VGLUTs is largely complementary with limited overlap and so far they are most specific markers for neurons that use glutamate as neurotransmitter. VGLUTs are regulated developmentally and determine functionally distinct populations of glutamatergic neurons. Controlling the activity of these proteins could potentially modulate the efficiency of excitatory neurotransmission. This review summarizes the recent knowledge concerning molecular and functional characteristic of vesicular glutamate transporters, their development, contribution to synaptic plasticity and their involvement in pathology of the nervous system.
4

Attenuation of inflammatory response after stroke allows to retain brain plasticity

51%
Liguz-Lecznar M., Jablonka J., Kossut M.
Acta Neurobiologiae Experimentalis
|
2013
|
tom 73
|
nr Suppl.1
Despite indications that brain plasticity may be enhanced after stroke, we have described impairment of experience-dependent plasticity in rodent cerebral cortex neighbouring the stroke-induced lesion. There is increasing evidence showing that inflammation accounts for stroke progression. Once activated, inflammatory cells can release a variety of cytotoxic agents that may induce more cell damage as well as disruption of the blood-brain barrier and extracellular matrix. We have shown that chronic treatment with anti-inflammatory drug ibuprofen restored plasticity of cortical representation of vibrissae induced by whisker deprivation. We have also the upregulation cyclooxygenase-2 (COX-2) and other proinflammatory factors, i.e. IL-1 and tumor necrosis factor TNFα shown in the acute poststroke phase. Since TNFα is one of the key players in stroke progression, we decided to reduce the TNFα signalling by introduction into the brain soluble TNFα receptors 1 that will compete for TNFα with receptors localized in the brain tissue. We have shown that such approach undertaken simultaneously with the stroke was successful in preserving the poststroke brain plasticity. Supported by Polish National Science Centre Grant: N N401 098739.
5

Associative learning modifies representation of vibrissae in SII cortex -A 2DG study

51%
Debowska W., Siucinska E., Liguz-Lecznar M., Kossut M.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Secondary somatosenory cortex (SII) in rodents receives input from vibrissae trough reciprocal cortico-cortical connections from the barrel cortex and directly from thalamic sensory nuclei. In humans, SII is activated bilaterally during attentional tasks and it is consider to play a role in tactile memory and sensimotor integration. We examined it behavioral paradigms that modifi es SI evokes also plasticity in SII. We measured area of SII activation by stimulation of a row of vibrissae previously activated in classical conditioning paradigm, in which stimulation of a row of vibrissae was paired with a tail shock. The training consisted of 3 daily 10 min sessions, during which 40 pairings were delivered. Activation was mapped with [14C]-2-deoxyglucose (2DG) autoradiography one day after the end of conditioning. The autoradiograms were analyzed with computerized image analysis system, which aligned the 2DG uptake pattern with Nissl stain. We reported previously that conditioning results in enlargement of cortical representation of the “trained” row of vibrissae in SI. Here we found that in SII the representation of the “trained” row is increased bilaterally, by 37% on the average. The increase was observed in cortical layers II/III and IV. Clearly, plasticity in SII is not simply a refl ection of changes in SI. It may be supposed that in response to activation of a pathway involved in conditioning, structures involved in attention respond more strongly to sensory stimuli.
6

Somatostatin receptors on parvalbumin interneurons in mouse somatosensory cortex

51%
Lukomska A., Dobrzanski G., Liguz-Lecznar M., Kossut M.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: Cortical interneurons containing somatostatin (SST-INs) are the second most numerous subtype of GABA-ergic cells in the somatosenory cortex of rodents. SST‑INs inhibit excitatory cells and also other inhibitory interneurons. They are involved in disinhibitory circuits, in which SST-INs inhibit interneurons containing parvalbumin (PV-INs) which, in turn, stop inhibiting excitatory neurons. Somatostatin is present in synapses in a separate pool of vesicles and may be released together with GABA. Activation of somatostatin receptors in the brain may cause inhibition of adenylyl cyclase, decrease of intracellular Ca2+ levels, hyperpolarization of cells mediated by K+ channels, protein phosphatases activation and MAP kinases modulation. Somatostatin action on PV‑INs is poorly understood. AIM(S): To get a picture of possible sites of somatostatin action upon PV-INs, we examined the distribution of five subtypes of somatostatin receptors (SSTRs1‑5) on genetically labeled PV‑INs in the barrel cortex. METHOD(S): The experiment was conducted on PV‑ires‑Cre driver mice lines crossed with the Ai14 line to obtain tdTomato expression following Cre-mediated recombination. Cre‑dependent cell labeling was verified by immunocytochemical reaction with anti-PV antibody. A series of immunofluorescent staining using antibodies against SSTR1‑5 were performed on coronal and tangential brain sections. RESULTS: We found that SSTR1, SSTR3, and SSTR5 were present on PV‑INs in all cortical layers (74% to 96% of PV neurons showed colocalization with these SSTRs). SSTR4 was found only on 36% to 62% of PV neurons, depending on the layer. Immunolabeling was found on cell bodies and dendrites. Surprisingly, we did not observe SSTR2 presence on PV‑INs in any cortical layer. CONCLUSION: Apparently, somatostatin acts on PV-INs through only four receptor subtypes, excluding SSTR2. FINANCIAL SUPPORT: Supported by National Science Center grant OPUS 2015/17B/NZ/02016 to MK.
7

Gabaergic system in aging. Focus on somatostatin containing interneurons

51%
Rozycka A., Zakrzewska R., Liguz-Lecznar M.
Acta Neurobiologiae Experimentalis
|
2017
|
tom 77
|
nr Suppl.1
INTRODUCTION: Molecular aging, defined as an age‑related transcriptome changes, and biochemical protein-related alterations within synapses weaken the plastic potential of neurons. Previously, we have shown an age-related impairment of learning-related functional plasticity in mouse somatosensory cortex (SI), induced by associative fear learning and visualized with brain mapping using 2-deoxyglucose technique. AIM(S): The aim of the study was to investigate age-related changes in somatostatin-containing GABAergic interneurons, which are involved in learning – related plasticity in mouse SI. METHOD(S): Learning-related plasticity was induced with classical conditioning, where tactile stimulus to large sensory whiskers was coupled to the tail shock. Two groups of mice were used in the experiments: young (3 months old) and aged (1 year old). We have investigated mRNA and protein level of GAD67 (enzyme synthesizing GABA) and SOM (somatostatin) in mouse SI using q-RT-PCR and ELISA, respectively. Using immunofluorescence we compared the number of both types of neurons in SI. RESULTS: Analysis of q-RT-PCR results revealed no change in investigated mRNAs levels between young and aged mice. We also observed an upregulation of GAD67 and GABA levels after training in young but not in aged animals. Immunohistochemistry results showed an increase in the number of GAD67+ cells, however, we did not observe an elevation in the number of SOM+/GAD67+ cells. CONCLUSIONS: Increase in GAD67+ neurons density after sensory training in aged animals without parallel upregulation in GAD67 and GABA levels suggests lower GABA synthesis resulting in reduced effectiveness of aged GABAergic neurons. Lack of increase in SOM+ neurons density after sensory training in aged mice, suggest that upregulation of SOM+ cells is necessary for training induced plasticity. FINANCIAL SUPPORT: Supported by National Science Centre grant 2013/09/B/NZ3/00540.
8

The response of main subclasses of GABAergic interneurons to plasticity induction and aging: changes in mRNA levels

51%
Rozycka A., Zakrzewska R., Liguz-Lecznar M.
Acta Neurobiologiae Experimentalis
|
2019
|
tom 79
|
nr Suppl.1
INTRODUCTION: Inhibitory interneurons undergo age-related alterations that may have tremendous consequences on cellular and network computations and account for cognitive and behavioral deficits. Accordingly, we have shown that mechanisms governing fear learning‑induced plasticity were weakened in aged (1 y.o.) mice somatosensory cortex, hampering manifestation of plastic changes, while in old (2 y.o.) mice the plasticity was absent. AIM(S): To investigate age-related mRNA changes of distinct markers that are characteristic of GABAergic interneurons, define their main subtypes, and correlate potential changes with age‑related plasticity impairments. METHOD(S): Plasticity was induced with a classical conditioning paradigm, in which tactile stimulus to one row of whiskers was paired with a tail electric shock. Three groups of mice were used: young (3 months old), aged (1 y.o.) and old (2 y.o.). Using qRT‑PCR, we investigated mRNA levels of GAD67, GAD65, parvalbumin (PV), somatostatin (SST), calretinin (CR), calbindin (CB), vasoactive intestinal polypeptide (VIP), and Neuropeptide Y (NPY). RESULTS: qRT‑PCR analysis showed changes in mRNA levels, resulting from both aging itself and from plasticity induction. mRNA level of CB decreased in aged and old animals, whereas PV increased in the old group. After plasticity induction, we observed a reduction of NPY in the young group, while aged animals presented a decline of VIP mRNA levels. We observed decrease in CB along with an increase in PV mRNA levels, which may result in calcium homeostasis disruption in neurons and may consequently be involved in the plasticity impairments observed in aged and old animals. CONCLUSIONS: Being a part of the VIP-SST disinhibitory circuit that exist in many cortical areas, VIP mRNA changes may contribute to dysregulation of this important mechanism controlling plasticity. FINANCIAL SUPPORT: National Science Centre grant 2013/09/B/NZ3/00540.
9

Influance of age upon photothrombotic stroke in mice

51%
Liguz-Lecznar M., Aleksy M., Skangiel-Kramska J., Kossut M.
Acta Neurobiologiae Experimentalis
|
2009
|
tom 69
|
nr 3
Stroke is one of the leading causes of death and disability in humans. Animal models of stroke simulate the human pathology and can help to develop the effective therapies. One of such models is the photothrombosis model in which cerebral ischemia is induced photochemically by injecting the photosensitive dye. The advantages of this model are the small infarct size, minimal surgical manipulation of the animal. Despite the strong connection of stroke with aging process, the majority of experimental studies are conducted in young or adult animals. Here we have used young (3 months old) and aged (12 months old) mice to produce the small (about 2 mm in diameter) infarct neighboring the primary somatosensory barrel cortex area and including the whole depth of cortex. After 7-day reconvalescence we have analyzed the presence and size of the evoked infarct. In both groups stroke has evoked similar changes in cortex cytoarchitecture, however we found that aging has decreased the method effectiveness of about 25%. Moreover, comparing to young animals, in old mice size and extent of infarct evoked with the same parameters and conditions were much less unrepeatable. It can be associated with changes of the nervous system physiology with age that concern the blood fl ow, diameter of blood vessels, metabolism and physiology of neurons and glial cells. Alternatively, older mice may have adapted functionally to age-dependent damage. Supported by the Scientifi c Network: Biovision SNB-504-8.
10

A surface antigen delineating a subset of neurons in the primary somatosensory cortex of the mouse

51%
Nowicka D., Liguz-Lecznar M., Skangiel-Kramska J.
Acta Neurobiologiae Experimentalis
|
2003
|
tom 63
|
nr 3
11

Somatostatin expressing cells in experience - dependent plasticity in the somatosensory cortex of adult mice

45%
Nowak K., Liguz-Lecznar M., Cybulska-Klosowicz A., Zakrzewska R., Kossut M.
Acta Neurobiologiae Experimentalis
|
2011
|
tom 71
|
nr S
Synaptic plasticity in the nervous system is associated with rapid state-dependent changes that require constant adaptation of the balance between excitation and inhibition. Increasing neuronal activity has been shown to stimulate the inhibitory system to preserve the excitation/inhibition homeostasis. Experimental data suggest an increased inhibitory GABA-ergic neurotransmission in brain structures involved in the learning process. Previously we have shown that classical conditioning involving stimulation of a row of facial vibrissae in adult mice results in an increased density of GABAergic interneurones and increased cortical expression of glutamic acid decarboxylase in granular layer of trained row representation. Also, we have found that parvalbumin containing subpopulation was not involved in the observed changes. From numerous subpopulations of GABAergic neurons, somatostatin (SST) containing cells seem to be likely involved in regulation of activity and plasticity of neuronal networks. To test this hypothesis we have used the sensory training protocol that was based on the classical conditioning where tactile stimulation of one row of sensory whiskers (CS) was paired with a tail shock (UCS). The training was continued for 3 consecutive days and lasted 10 min each day (40 trials). Cells expressing SST were assessed using stereology-based counting in both hemispheres in the barrel cortex. We have shown the substantial (22%) increase of SST-containing cells in the trained row representation. The result suggests that somatostatin is involved in learning induced changes of inhibitory cortical network. Supported by grant No. 2486/B/P01/2010/39 (M.K.) N N301 248639.
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