LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 34

Search options

  1. Article: Editorial: The cerebellar involvement in non cerebellar pathologies.

    Lippiello, Pellegrino / Montarolo, Francesca / Tanaka-Yamamoto, Keiko / Hoxha, Eriola

    Frontiers in cellular neuroscience

    2023  Volume 17, Page(s) 1232155

    Language English
    Publishing date 2023-06-13
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2023.1232155
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article: Elovl5 Expression in the Central Nervous System of the Adult Mouse.

    Balbo, Ilaria / Montarolo, Francesca / Boda, Enrica / Tempia, Filippo / Hoxha, Eriola

    Frontiers in neuroanatomy

    2021  Volume 15, Page(s) 669073

    Abstract: ... ...

    Abstract ELOVL5
    Language English
    Publishing date 2021-04-29
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452969-2
    ISSN 1662-5129
    ISSN 1662-5129
    DOI 10.3389/fnana.2021.669073
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: Effects of the administration of Elovl5-dependent fatty acids on a spino-cerebellar ataxia 38 mouse model.

    Balbo, Ilaria / Montarolo, Francesca / Genovese, Federica / Tempia, Filippo / Hoxha, Eriola

    Behavioral and brain functions : BBF

    2022  Volume 18, Issue 1, Page(s) 8

    Abstract: Background: Spinocerebellar ataxia 38 (SCA38) is a rare autosomal neurological disorder characterized by ataxia and cerebellar atrophy. SCA38 is caused by mutations of ELOVL5 gene. ELOVL5 gene encodes a protein, which elongates long chain ... ...

    Abstract Background: Spinocerebellar ataxia 38 (SCA38) is a rare autosomal neurological disorder characterized by ataxia and cerebellar atrophy. SCA38 is caused by mutations of ELOVL5 gene. ELOVL5 gene encodes a protein, which elongates long chain polyunsaturated fatty acids (PUFAs). Knockout mice lacking Elovl5 recapitulate SCA38 symptoms, including motor coordination impairment and disruption of cerebellar architecture. We asked whether, in Elovl5 knockout mice (Elovl5
    Results: The administration from birth of the diet containing PUFAs downstream Elovl5 led to a significant amelioration of the motor performance in the beam test of Elovl5
    Conclusions: These results suggest that the dietary intervention in SCA38, whenever possible, should be started from birth or as early as possible.
    MeSH term(s) Animals ; Cerebellum ; Disease Models, Animal ; Fatty Acid Elongases/metabolism ; Fatty Acids/administration & dosage ; Fatty Acids, Unsaturated ; Mice ; Mice, Knockout ; Spinocerebellar Ataxias/diet therapy
    Chemical Substances Fatty Acids ; Fatty Acids, Unsaturated ; Elovl5 protein, mouse (EC 2.3.1.-) ; Fatty Acid Elongases (EC 2.3.1.-)
    Language English
    Publishing date 2022-08-06
    Publishing country England
    Document type Journal Article
    ZDB-ID 2185773-8
    ISSN 1744-9081 ; 1744-9081
    ISSN (online) 1744-9081
    ISSN 1744-9081
    DOI 10.1186/s12993-022-00194-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article: Differential diagnosis of unipolar versus bipolar depression by GSK3 levels in peripheral blood: a pilot experimental study.

    Rosso, Gianluca / Maina, Giuseppe / Teobaldi, Elena / Balbo, Ilaria / Di Salvo, Gabriele / Montarolo, Francesca / Rizzo Pesci, Nicola / Tempia, Filippo / Hoxha, Eriola

    International journal of bipolar disorders

    2023  Volume 11, Issue 1, Page(s) 33

    Abstract: Background: The differential diagnosis of patients presenting for the first time with a depressive episode into unipolar disorder versus bipolar disorder is crucial to establish the correct pharmacological therapy (antidepressants vs mood stabilizers), ... ...

    Abstract Background: The differential diagnosis of patients presenting for the first time with a depressive episode into unipolar disorder versus bipolar disorder is crucial to establish the correct pharmacological therapy (antidepressants vs mood stabilizers), but no biological markers are currently available. Several lines of evidence indicate an involvement of Glycogen Synthase Kinase-3 (GSK3) in the pathophysiology of depression. However, previous reports about GSK3 in peripheral blood were incomplete or inconsistent, so a specific marker is not yet available. The aim was to search for consistent differences in GSK3α and GSK3β or of their phosphorylated forms in samples of peripheral blood from patients with unipolar and bipolar depression.
    Methods: Mononucleate peripheral blood cells (PBMCs) of samples from patients presenting with a depressive episode were analyzed with the western blot technique.
    Results: The total amount of GSK3β in PBMCs was significantly lower in patients with bipolar disorder than in patients with unipolar depression. The sensitivity based on GSK3β was 85%. GSK3α was not significantly different but allowed a correct detection of 57% of BD patients. The combination in series of GSK3β and GSK3α yields a sensitivity of about 100%, but with 26.7% false negatives.
    Conclusions: Our results suggest that PBMC GSK3β could be a candidate biomarker for the differential diagnosis of bipolar disorder versus unipolar depression. This finding may help in implementing the still limited panel of peripheral biomarkers for differential diagnosis between unipolar and bipolar disorder in patients presenting with a depressive episode.
    Language English
    Publishing date 2023-10-08
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2732954-9
    ISSN 2194-7511
    ISSN 2194-7511
    DOI 10.1186/s40345-023-00314-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: GIRK1-Mediated Inwardly Rectifying Potassium Current Is a Candidate Mechanism Behind Purkinje Cell Excitability, Plasticity, and Neuromodulation.

    Lippiello, Pellegrino / Hoxha, Eriola / Tempia, Filippo / Miniaci, Maria Concetta

    Cerebellum (London, England)

    2020  Volume 19, Issue 6, Page(s) 751–761

    Abstract: G-protein-coupled inwardly rectifying potassium (GIRK) channels contribute to the resting membrane potential of many neurons and play an important role in controlling neuronal excitability. Although previous studies have revealed a high expression of ... ...

    Abstract G-protein-coupled inwardly rectifying potassium (GIRK) channels contribute to the resting membrane potential of many neurons and play an important role in controlling neuronal excitability. Although previous studies have revealed a high expression of GIRK subunits in the cerebellum, their functional role has never been clearly described. Using patch-clamp recordings in mice cerebellar slices, we examined the properties of the GIRK currents in Purkinje cells (PCs) and investigated the effects of a selective agonist of GIRK1-containing channels, ML297 (ML), on PC firing and synaptic plasticity. We demonstrated that GIRK channel activation decreases the PC excitability by inhibiting both sodium and calcium spikes and, in addition, modulates the complex spike response evoked by climbing fiber stimulation. Our results indicate that GIRK channels have also a marked effect on synaptic plasticity of the parallel fiber-PC synapse, as the application of ML297 increased the expression of LTP while preventing LTD. We, therefore, propose that the recruitment of GIRK channels represents a crucial mechanism by which neuromodulators can control synaptic strength and membrane conductance for proper refinement of the neural network involved in memory storage and higher cognitive functions.
    MeSH term(s) Action Potentials/drug effects ; Action Potentials/physiology ; Animals ; Animals, Newborn ; Excitatory Postsynaptic Potentials/drug effects ; Excitatory Postsynaptic Potentials/physiology ; Female ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/agonists ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/physiology ; Male ; Mice ; Neuronal Plasticity/drug effects ; Neuronal Plasticity/physiology ; Neurotransmitter Agents/pharmacology ; Phenylurea Compounds/pharmacology ; Purkinje Cells/drug effects ; Purkinje Cells/physiology ; Pyrazoles/pharmacology
    Chemical Substances CID 56642816 ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; Neurotransmitter Agents ; Phenylurea Compounds ; Pyrazoles
    Language English
    Publishing date 2020-07-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2112586-7
    ISSN 1473-4230 ; 1473-4222
    ISSN (online) 1473-4230
    ISSN 1473-4222
    DOI 10.1007/s12311-020-01158-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: NURR1-deficient mice have age- and sex-specific behavioral phenotypes.

    Montarolo, Francesca / Martire, Serena / Chiara, Francesco / Allegra, Sarah / De Francia, Silvia / Hoxha, Eriola / Tempia, Filippo / Capobianco, Marco Alfonso / Bertolotto, Antonio

    Journal of neuroscience research

    2022  Volume 100, Issue 9, Page(s) 1747–1754

    Abstract: The transcription factor NURR1 is essential to the generation and maintenance of midbrain dopaminergic (mDA) neurons and its deregulation is involved in the development of dopamine (DA)-associated brain disorders, such as Parkinson's disease (PD). The ... ...

    Abstract The transcription factor NURR1 is essential to the generation and maintenance of midbrain dopaminergic (mDA) neurons and its deregulation is involved in the development of dopamine (DA)-associated brain disorders, such as Parkinson's disease (PD). The old male NURR1 heterozygous knockout (NURR1-KO) mouse has been proposed as a model of PD due to its altered motor performance that was, however, not confirmed in a subsequent study. Based on these controversial results, we explored the effects of the NURR1 deficiency on locomotor activity, motor coordination, brain and plasma DA levels, blood pressure and heart rate of old mice, also focusing on the potential effect of sex. As a probable consequence of the role of NURR1 in DA pathway, we observed that the old NURR1-KO mouse is characterized by motor impairment, and increased brain DA level and heart rate, independently from sex. However, we also observed an alteration in spontaneous locomotor activity that only affects males. In conclusion, NURR1 deficiency triggers sex- and age-specific alterations of behavioral responses, of DA levels and cardiovascular abnormalities. Further studies in simplified systems will be necessary to dissect the mechanism underlying these observations.
    MeSH term(s) Animals ; Dopamine/metabolism ; Dopaminergic Neurons/metabolism ; Female ; Male ; Mice ; Mice, Knockout ; Nuclear Receptor Subfamily 4, Group A, Member 2/genetics ; Parkinson Disease/metabolism ; Phenotype ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Nuclear Receptor Subfamily 4, Group A, Member 2 ; Transcription Factors ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2022-05-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 195324-2
    ISSN 1097-4547 ; 0360-4012
    ISSN (online) 1097-4547
    ISSN 0360-4012
    DOI 10.1002/jnr.25067
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Maternal treatment with sodium butyrate reduces the development of autism-like traits in mice offspring.

    Cristiano, Claudia / Hoxha, Eriola / Lippiello, Pellegrino / Balbo, Ilaria / Russo, Roberto / Tempia, Filippo / Miniaci, Maria Concetta

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2022  Volume 156, Page(s) 113870

    Abstract: Several studies indicate a relationship between maternal gut microbiota alteration and increased risk of autism spectrum disorders (ASD) in offspring. The possibility of compensating for such metabolic dysfunction at a very early stage of disease via ... ...

    Abstract Several studies indicate a relationship between maternal gut microbiota alteration and increased risk of autism spectrum disorders (ASD) in offspring. The possibility of compensating for such metabolic dysfunction at a very early stage of disease via maternal treatment has not been enough explored. Here, we examined in BTBR mouse model of ASD the effect of maternal treatment with the gut microbial metabolite butyrate (BUT) on the behavioral and synaptic plasticity deficits in juvenile and adult offspring. We show that BUT treatment of BTBR dams rescues the social and partially the repetitive behavior deficits in the offspring. In addition, maternal BUT implementation prevents the cerebellar cortex hypertrophy as well as the Purkinje cells firing and long-term synaptic plasticity deficits in BTBR mice. Our results demonstrate, for the first time, that maternal BUT treatment can improve ASD-like symptoms in offspring thus providing new directions for the early treatment of neurodevelopmental disorders.
    MeSH term(s) Mice ; Animals ; Autistic Disorder/drug therapy ; Butyric Acid/pharmacology ; Social Behavior ; Autism Spectrum Disorder/drug therapy ; Autism Spectrum Disorder/prevention & control ; Autism Spectrum Disorder/metabolism ; Mice, Inbred Strains ; Disease Models, Animal ; Mice, Inbred C57BL ; Behavior, Animal
    Chemical Substances Butyric Acid (107-92-6)
    Language English
    Publishing date 2022-10-21
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2022.113870
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article: Purkinje Cell Signaling Deficits in Animal Models of Ataxia.

    Hoxha, Eriola / Balbo, Ilaria / Miniaci, Maria Concetta / Tempia, Filippo

    Frontiers in synaptic neuroscience

    2018  Volume 10, Page(s) 6

    Abstract: Purkinje cell (PC) dysfunction or degeneration is the most frequent finding in animal models with ataxic symptoms. Mutations affecting intrinsic membrane properties can lead to ataxia by altering the firing rate of PCs or their firing pattern. However, ... ...

    Abstract Purkinje cell (PC) dysfunction or degeneration is the most frequent finding in animal models with ataxic symptoms. Mutations affecting intrinsic membrane properties can lead to ataxia by altering the firing rate of PCs or their firing pattern. However, the relationship between specific firing alterations and motor symptoms is not yet clear, and in some cases PC dysfunction precedes the onset of ataxic signs. Moreover, a great variety of ionic and synaptic mechanisms can affect PC signaling, resulting in different features of motor dysfunction. Mutations affecting Na
    Language English
    Publishing date 2018-04-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2592086-8
    ISSN 1663-3563
    ISSN 1663-3563
    DOI 10.3389/fnsyn.2018.00006
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article ; Online: Role of β3-adrenergic receptor in the modulation of synaptic transmission and plasticity in mouse cerebellar cortex.

    Lippiello, Pellegrino / Hoxha, Eriola / Cristiano, Claudia / Malvicini, Emilia / Stanley, Adrien / Russo, Roberto / Tempia, Filippo / Miniaci, Maria Concetta

    Journal of neuroscience research

    2020  Volume 98, Issue 11, Page(s) 2263–2274

    Abstract: Convergent lines of evidence have recently highlighted β3-adrenoreceptors (ARs) as a potentially critical target in the regulation of nervous and behavioral functions, including memory consolidation, anxiety, and depression. Nevertheless, the role of β3- ... ...

    Abstract Convergent lines of evidence have recently highlighted β3-adrenoreceptors (ARs) as a potentially critical target in the regulation of nervous and behavioral functions, including memory consolidation, anxiety, and depression. Nevertheless, the role of β3-ARs in the cerebellum has been never investigated. To address this issue, we first examined the effects of pharmacological manipulation of β3-ARs on motor learning in mice. We found that blockade of β3-ARs by SR 59230A impaired the acquisition of the rotarod task with no effect on general locomotion. Since the parallel fiber-Purkinje cell (PF-PC) synapse is considered to be the main cerebellar locus of motor learning, we assessed β3-AR modulatory action on this synapse as well as its expression in cerebellar slices. We demonstrate, for the first time, a strong expression of β3-ARs on Purkinje cell soma and dendrites. In addition, whole-cell patch-clamp recordings revealed that bath application of β3-AR agonist CL316,243 depressed the PF-PC excitatory postsynaptic currents via a postsynaptic mechanism mediated by the PI3K signaling pathway. Application of CL316,243 also interfered with the expression of PF long-term potentiation, whereas SR 59230A prevented the induction of LTD at PF-PC synapse. These results underline the critical role of β3-AR on cerebellar synaptic transmission and plasticity and provide a new mechanism for adrenergic modulation of motor learning.
    MeSH term(s) Animals ; Cerebellar Cortex/metabolism ; Cerebellar Cortex/physiology ; Excitatory Postsynaptic Potentials ; Female ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Male ; Mice ; Neuronal Plasticity/physiology ; Patch-Clamp Techniques ; Phosphatidylinositol 3-Kinases/metabolism ; Purkinje Cells/metabolism ; Receptors, Adrenergic, beta-3/metabolism ; Receptors, Adrenergic, beta-3/physiology ; Rotarod Performance Test ; Synapses/physiology ; Synaptic Transmission/physiology
    Chemical Substances Receptors, Adrenergic, beta-3
    Language English
    Publishing date 2020-08-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 195324-2
    ISSN 1097-4547 ; 0360-4012
    ISSN (online) 1097-4547
    ISSN 0360-4012
    DOI 10.1002/jnr.24712
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article: Modulation, Plasticity and Pathophysiology of the Parallel Fiber-Purkinje Cell Synapse.

    Hoxha, Eriola / Tempia, Filippo / Lippiello, Pellegrino / Miniaci, Maria Concetta

    Frontiers in synaptic neuroscience

    2016  Volume 8, Page(s) 35

    Abstract: The parallel fiber-Purkinje cell (PF-PC) synapse represents the point of maximal signal divergence in the cerebellar cortex with an estimated number of about 60 billion synaptic contacts in the rat and 100,000 billions in humans. At the same time, the ... ...

    Abstract The parallel fiber-Purkinje cell (PF-PC) synapse represents the point of maximal signal divergence in the cerebellar cortex with an estimated number of about 60 billion synaptic contacts in the rat and 100,000 billions in humans. At the same time, the Purkinje cell dendritic tree is a site of remarkable convergence of more than 100,000 parallel fiber synapses. Parallel fiber activity generates fast postsynaptic currents via α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, and slower signals, mediated by mGlu
    Language English
    Publishing date 2016-11-03
    Publishing country Switzerland
    Document type Review ; Journal Article
    ZDB-ID 2592086-8
    ISSN 1663-3563
    ISSN 1663-3563
    DOI 10.3389/fnsyn.2016.00035
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top