Impaired exploration induced by type 1 diabetes is related to locomotor activity rather than a reduction in motivation


Here are the Impaired exploration induced by type 1 diabetes is related to locomotor activity rather than a reduction in motivation journals presenting the latest research across various disciplines. From social sciences to technology, each article is expected to provide valuable insights to our readers.

Impaired exploration place, impaired exploration merit, impaired exploration induced fit, impaired exploration induced by type 1 diabetes is an autoimmune, impaired exploration induced by type 1 diabetes is hereditary, impaired exploration peak, impaired exploration induced coma.

Impaired exploration induced by type 1 diabetes is related to locomotor activity rather than a reduction in motivation

Type 1 diabetes mellitus (T1D) is associated with cognitive impairments in humans. A well-established animal model of T1D is induced through the administration of streptozotocin (STZ), a glucose analog that induces pancreatic β-cell death, resulting in hyperglycemia and cognitive impairment linked to neuroinflammation and oxidative stress. Tumor necrosis factor (TNF)-α, a key inflammatory mediator, is elevated in the central nervous system (CNS) of diabetic animals. In this study, we utilized TNFR1 knockout mice to investigate the role of TNFR1 signaling in short-term T1D-related cognitive impairment. Our findings showed that diabetic animals did not develop cognitive damage within the first 2 weeks of T1D but exhibited reduced exploration in all behavioral tests. Our findings suggest that this reduction in exploration was attributable to motor impairment, as there was no reduction in motivated novelty-seeking behavior. Additionally, deletion of TNFR1 signaling attenuated g ait speed impairment in diabetic mice, but did not affect other motor-related or exploratory behaviors. © 2024 International Brain Research Organization (IBRO)

Authors : Amorim de Souza Lima T.; Raissa Ribeiro M.; Carneiro de Brito M.; Mitiko Kawamoto E.

Source : Elsevier Ltd

Article Information

Year 2024
Type Article
DOI 10.1016/j.neuroscience.2024.09.030
ISSN 03064522
Volume 560

You can download the article here


If You have any problem, contact us here


Support Us:

Download Now Buy me a coffee Request Paper Here