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- Onimus, O, et al.
(författare)
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Haloperidol-Induced Immediate Early Genes in Striatopallidal Neurons Requires the Converging Action of cAMP/PKA/DARPP-32 and mTOR Pathways
- 2022
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Ingår i: International journal of molecular sciences. - : MDPI AG. - 1422-0067. ; 23:19
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Tidskriftsartikel (refereegranskat)abstract
- Antipsychotics share the common pharmacological feature of antagonizing the dopamine 2 receptor (D2R), which is abundant in the striatum and involved in both the therapeutic and side effects of this drug’s class. The pharmacological blockade of striatal D2R, by disinhibiting the D2R-containing medium-sized spiny neurons (MSNs), leads to a plethora of molecular, cellular and behavioral adaptations, which are central in the action of antipsychotics. Here, we focused on the cell type-specific (D2R-MSNs) regulation of some striatal immediate early genes (IEGs), such as cFos, Arc and Zif268. Taking advantage of transgenic mouse models, pharmacological approaches and immunofluorescence analyses, we found that haloperidol-induced IEGs in the striatum required the synergistic activation of A2a (adenosine) and NMDA (glutamate) receptors. At the intracellular signaling level, we found that the PKA/DARPP-32 and mTOR pathways synergistically cooperate to control the induction of IEGs by haloperidol. By confirming and further expanding previous observations, our results provide novel insights into the regulatory mechanisms underlying the molecular/cellular action of antipsychotics in the striatum.
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- Picconi, B, et al.
(författare)
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Loss of bidirectional striatal synaptic plasticity in L-DOPA-induced dyskinesia
- 2003
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Ingår i: Nature Neuroscience. - : Springer Science and Business Media LLC. - 1546-1726 .- 1097-6256. ; 6:5, s. 501-506
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Tidskriftsartikel (refereegranskat)abstract
- Long-term treatment with the dopamine precursor levodopa (L-DOPA) induces dyskinesia in Parkinson's disease (PD) patients. We divided hemiparkinsonian rats treated chronically with L-DOPA into two groups: one showed motor improvement without dyskinesia, and the other developed debilitating dyskinesias in response to the treatment. We then compared the plasticity of corticostriatal synapses between the two groups. High-frequency stimulation of cortical afferents induced long-term potentiation (LTP) of corticostriatal synapses in both groups of animals. Control and non-dyskinetic rats showed synaptic depotentiation in response to subsequent low-frequency synaptic stimulation, but dyskinetic rats did not. The depotentiation seen in both L-DOPA-treated non-dyskinetic rats and intact controls was prevented by activation of the D1 subclass of dopamine receptors or inhibition of protein phosphatases. The striata of dyskinetic rats contained abnormally high levels of phospho[Thr34]-DARPP-32, an inhibitor of protein phosphatase 1. These results indicate that abnormal information storage in corticostriatal synapses is linked with the development of L-DOPA-induced dyskinesia.
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- Stagkourakis, S, et al.
(författare)
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Maternal Aggression Driven by the Transient Mobilisation of a Dormant Hormone-Sensitive Circuit
- 2024
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Ingår i: bioRxiv : the preprint server for biology. - : Cold Spring Harbor Laboratory.
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Aggression - a sexually dimorphic behavior, is prevalent in males and typically absent in virgin females. Following parturition, however, the transient expression of aggression in adult females ensures the pups’ defense from predators and infanticide. While maternal hormones are known to elicit nursing, whether they play a role in the expression of maternal aggression remains unknown. Here we show that a molecularly defined subset of ventral premammillary (PMvDAT) neurons, instrumental for intermale aggression, switch into a hyperexcitable state during lactation. We identify that the maternal hormones prolactin and oxytocin excite these cells, an effect mediated through T-type Ca2+channels. Optogenetic manipulation or genetic ablation of PMvDATneurons profoundly affects maternal aggression, while activation of these neurons impairs the expression of non-aggression-related behaviors. This work identifies a monomorphic neural substrate that incorporates hormonal cues to enable the transient expression of a dormant behavioral program in adult females.Graphical abstractIn BriefMaternal hormones activate a subset of hypothalamic “aggression neurons”, which are required for the transient expression of maternal aggression during lactation.HighlightsQuiescent PMvDATneurons in female mice become hyperexcitable in lactating dams.Manipulation of PMvDATcell activity bidirectionally regulates maternal aggression.The maternal hormones prolactin and oxytocin excite PMvDATcells.Activation of PMvDATneurons impairs the expression of non-aggression-related behavioral programs.
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- Bastide, Matthieu F, et al.
(författare)
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Pathophysiology of L-dopa-induced motor and non-motor complications in Parkinson's disease.
- 2015
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Ingår i: Progress in Neurobiology. - : Elsevier BV. - 1873-5118 .- 0301-0082. ; 132:Jul 21, s. 96-168
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Forskningsöversikt (refereegranskat)abstract
- Involuntary movements, or dyskinesia, represent a debilitating complication of levodopa (L-dopa) therapy for Parkinson's disease (PD). L-dopa-induced dyskinesia (LID) are ultimately experienced by the vast majority of patients. In addition, psychiatric conditions often manifested as compulsive behaviours, are emerging as a serious problem in the management of L-dopa therapy. The present review attempts to provide an overview of our current understanding of dyskinesia and other L-dopa-induced dysfunctions, a field that dramatically evolved in the past twenty years. In view of the extensive literature on LID, there appeared a critical need to re-frame the concepts, to highlight the most suitable models, to review the central nervous system (CNS) circuitry that may be involved, and to propose a pathophysiological framework was timely and necessary. An updated review to clarify our understanding of LID and other L-dopa-related side effects was therefore timely and necessary. This review should help in the development of novel therapeutic strategies aimed at preventing the generation of dyskinetic symptoms.
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- Briz, V, et al.
(författare)
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The non-coding RNA BC1 regulates experience-dependent structural plasticity and learning
- 2017
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 8:1, s. 293-
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Tidskriftsartikel (refereegranskat)abstract
- The brain cytoplasmic (BC1) RNA is a non-coding RNA (ncRNA) involved in neuronal translational control. Absence of BC1 is associated with altered glutamatergic transmission and maladaptive behavior. Here, we show that pyramidal neurons in the barrel cortex of BC1 knock out (KO) mice display larger excitatory postsynaptic currents and increased spontaneous activity in vivo. Furthermore, BC1 KO mice have enlarged spine heads and postsynaptic densities and increased synaptic levels of glutamate receptors and PSD-95. Of note, BC1 KO mice show aberrant structural plasticity in response to whisker deprivation, impaired texture novel object recognition and altered social behavior. Thus, our study highlights a role for BC1 RNA in experience-dependent plasticity and learning in the mammalian adult neocortex, and provides insight into the function of brain ncRNAs regulating synaptic transmission, plasticity and behavior, with potential relevance in the context of intellectual disabilities and psychiatric disorders.
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- Carta, AR, et al.
(författare)
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Dyskinesia in Parkinson's disease therapy
- 2012
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Ingår i: Parkinson's disease. - : Hindawi Limited. - 2042-0080 .- 2090-8083. ; 2012, s. 639080-
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