Neurochemistry International, Год журнала: 2024, Номер unknown, С. 105895 - 105895
Опубликована: Окт. 1, 2024
Язык: Английский
Neurochemistry International, Год журнала: 2024, Номер unknown, С. 105895 - 105895
Опубликована: Окт. 1, 2024
Язык: Английский
Frontiers in Neuroscience, Год журнала: 2024, Номер 18
Опубликована: Окт. 30, 2024
Olfactory dysfunction has emerged as a hallmark feature shared among several neurological conditions, including both neurodevelopmental and neurodegenerative disorders. While diseases of categories have been extensively studied for decades, their association with olfaction only recently gained attention. deficits often manifest already during prodromal stages these diseases, yet it remains unclear whether common pathophysiological changes along olfactory pathways cause such impairments. Here we probe into the intricate relationship between disorders, shedding light on commonalities underlying mechanisms. We begin by providing brief overview circuit its connections to higher-associated brain areas. Additionally, discuss in focusing potential mechanisms that may contribute across types further debate disease propagation or are simply an epiphenomenon. conclude emphasizing significance function pre-clinical diagnostic tool identify individuals disorders offers opportunity preventive intervention before other symptoms manifest.
Язык: Английский
Процитировано
2Molecular Brain, Год журнала: 2024, Номер 17(1)
Опубликована: Сен. 27, 2024
Abstract Abnormalities in gamma-aminobutyric acid (GABA)ergic neurotransmission play a role the pathogenesis of autism, although mechanisms responsible for alterations specific brain regions remain unclear. Deficits social motivation and interactions are core symptoms likely due to defects dopaminergic neural pathways. Therefore, investigating morphology functional roles GABAergic neurons within projection areas could elucidate underlying etiology autism. The aim this study was (1) compare arborization glutamate decarboxylase (GAD)-positive from midbrain tegmentum; (2) evaluate synaptic activity primary striatum; (3) assess postsynaptic puncta ventral striatum wild-type (WT) Shank3 -deficient mice. We found significant decrease number short neurites GAD positive tegmentum application blocker GABA A receptors (GABA R) revealed significantly increased frequency spontaneous currents (sPSCs) striatal compared their WT counterparts. mean absolute amplitude events higher also observed reduction gephyrin/GABA R γ2 colocalization adult male gene expression collybistin lower nucleus accumbens while gephyrin were tegmental area (VTA) Shank3- deficient In conclusion, deficiency leads impaired function areas. These changes may underlie autistic symptoms, potential interventions modulating pathways represent new treatment modality.
Язык: Английский
Процитировано
0Neurochemistry International, Год журнала: 2024, Номер unknown, С. 105895 - 105895
Опубликована: Окт. 1, 2024
Язык: Английский
Процитировано
0