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DTSTART;TZID=Europe/Paris:20221212T090000
DTEND;TZID=Europe/Paris:20221212T090000
DTSTAMP:20260424T031742
CREATED:20221103T132537Z
LAST-MODIFIED:20221208T131409Z
UID:151735-1670835600-1670835600@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Keri-Ann Charles
DESCRIPTION:Venue: CGFB \n\nSupervisor:\nDr. Abdelhamid Benazzouz\, IMN \nTitle\nThe pathophysiology of nociceptive abnormalities in the context of Parkinson’s Disease \nAbstract\nPain is one of the most common causes of disability in public health\, not only does it significantly impacts the quality of life of patients both physically and financially\, yet it also remains inadequately treated specially in patients with neurological diseases\, for example\, Parkinson’s disease (PD). PD is the second most common neurodegenerative disorder\, present in 1-3% of the world’s population over 60 years of age. It is primarily characterised by its disabling motor symptoms\, including but not limited to\, tremors\, rigidity and bradykinesia. PD also presents a wide range of non-motor symptoms that are usually apparent long before the development of clinical motor signs of the disease. One of the main symptoms is pain\, which is experienced by about 80% of PD patients. \nGenerally\, it is admitted that PD is due to the degeneration of dopamine neurons in the substantia nigra pars compacta (SNpc) of the central nervous system. In addition\, the pathophysiology of pain in PD also seems to be\, at least in part\, dependent on this loss of dopamine. The restoration of dopaminergic neurotransmission by L-Dopa has been used successfully for many years in the treatment of motor symptoms. However\, its efficacy in the treatment of PD pain forms is not clearly determined. The present study focused on the role of dopamine\, especially the dopaminergic A11-spinal cord descending pathway\, in pain perception using an animal model of PD. \nFirst\, we have shown that unilateral lesion of dopamine neurons after the injection of 6-OHDA into the Medial Forebrain Bundle (MFB) decreased paw withdrawal threshold and latency\, which corresponds to an increased mechanical allodynia and thermal hyperalgesia\, respectively\, in hemiparkinsonian rats. In parallel\, electrophysiological results showed increased responses of c-fibre’s evoked action potentials of wide dynamic range (WDR) neurons\, recorded in the dorsal horn of the spinal cord (DHSC)\, to electrical nociceptive stimuli of the sciatic nerve.  Then\, we showed that behavioural and electrophysiological abnormalities in dopamine depleted animals were reversed by intrathecal injections of dopamine agonists with a more pronounced improvement when targeting D2 than D1 dopamine receptors. Finally\, we investigated the role of the direct descending pathway from the hypothalamic A11 nucleus to the spinal cord\, the only dopaminergic descending projection evidenced as of now. We have shown that partial lesion of A11 neurons significantly reduced nociceptive thresholds. \nSecond\, we investigated the role of the subthalamic nucleus (STN) in nociception in normal conditions and in the context of PD. Our electrophysiological results showed that STN neurons presented different responses to the electrical stimulation of the sciatic nerve in a similar way in the two conditions. Furthermore\, as chronic deep brain stimulation (DBS) of the STN has been shown to improve pain in the context of PD\, we have investigated the influence of STN DBS on nociceptive integration in the spinal cord. We have shown that STN DBS induced a decrease in the number of spike C of WDR neurons demonstrating a normalization of nociceptive integration in the DHSC. This effect was reversed by the microinjection of lidocaine in the raphe magnus nucleus. \nResults of these studies show first\, that dopamine projections to the spinal cord are involved in pain hypersensitivity in our rat model of PD\, highlighting the primary role of the hypothalamic nucleus A11 in the pathophysiology of pain in PD. Second our results support also the idea that the STN\, which is known to play an important role in the pathophysiology of PD motor disabilities\, is also involved in the nociceptive abnormalities associated to PD. \nOur study provides new insights into the pathophysiology of pain in PD and opens the way to new therapeutic approaches targeting this disabling non-motor symptom of the disease. \n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-keri-ann-charles/
CATEGORIES:Thesis
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DTSTART;TZID=Europe/Paris:20221212T140000
DTEND;TZID=Europe/Paris:20221212T140000
DTSTAMP:20260424T031742
CREATED:20221118T143734Z
LAST-MODIFIED:20221209T141427Z
UID:152879-1670853600-1670853600@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Shri Vidhya SESHADRI SRINIVASAN
DESCRIPTION:Venue: Institut François Magendie (salle de conférence) \nAnd on teams :\nClick here to join the meeting\nMeeting ID: 358 976 077 001\nPasscode: oD8oL4 \nDefense in english \n\nThesis supervisor: Mireille Montcouquiol\nTeam: Planar polarity and plasticity (Montcouquiol / Sans) – Neurocentre Magendie \nTitle\nLoss of Multiple PDZ domain containing protein has sensory and cognitive consequences \nAbstract\nMultiple PDZ domain containing protein (MPDZ or MUPP1) is a large cytosolic polarity protein with thirteen PDZ domains present at the tight junction of epithelial cells and at the synapses of neurons. In both systems (epithelial and neuronal) it functions as a scaffolding protein to participate in the maturation and in the function of the cell and tissues. Genetic variations within MPDZ have been associated with various pathologies including congenital hydrocephalus with brain and eye anomalies (HYC2\, OMIM #603785) or alcohol and sedative dependence. Some patients with MPDZ variants were diagnosed with sensorineural hearing loss and mild intellectual disability (ID)\, but these aspects received little attention. Notably\, while many studies report different aspects of the gene/protein characteristics\, there is no study of the consequences of the early deletion of the gene within the inner ear and the brain within the same genetic model. This thesis focuses on evaluating the structural and functional consequences of an early conditional deletion of MPDZ in the inner ear and in the brain of a mouse\, in the hope of better understanding the pleiotropic effect of the deletion on some developmental mechanisms controlled by MPDZ.  We generated two mice models: one with a deletion in the inner ear (MPDZear) and one with a deletion in the brain (MPDZbrain). In the MPDZear mutant\, I evaluated the consequences of loss of MPDZ using hearing tests and balance vestibular test\, revealing deficits in both systems. Next\, I identified structural deficit domain-containings in the auditory hair cells\, both in their apical and their synaptic compartments. I found a clear disruption of the hair bundle structure\, consistent with a reduction and a mislocalisation of some apical surface markers\, as well as a disorganization of some of the synaptic components. Functional correlates confirmed a disrupted intake of FM1-43 uptake at the hair bundle and an abnormal Ca2+ increase associated with decreased exocytosis efficiency at the synapse side of the hair cell. In the MPDZbrain mutant\, while we did not identify gross anatomical deficits\, our data revealed a deficits\, and notably a decreased prepulse inhibition (PPI) response\, typical of a disruption in sensory gating. \nTaken together\, these data identify a number of epithelial and synaptic disruptions in the inner ear supporting the hearing and balance deficits of our model\, and further show brainspecific deficits that could participate to the sensory deficit but are also consistent with the ID observed in patients. \nJury\nPr. Paul Avan\, Dr. Aziz El Amraoui\, Dr. Susanna Pietropaolo\, Dr. Regis Nouvian\, Dr. Didier Dulon\, Dr Mireille Montcouquiol \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-shri-vidhya-seshadri-srinivasan/
CATEGORIES:Thesis
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