Introduction: Memantine as N-Methyl-D-Aspartic Acid (NMDA) receptor antagonist is used in some neurological disorders. Moreover, memantine presents modulatory effects on the somatosensory information processing in healthy subjects. This study investigated the effects of memantine on electrophysiological properties of barrel cortex neurons in male rats.
Methods: Single unit recording was used to evaluate the electrophysiological properties of barrel cortex neurons. The neural responses to the Principal Whisker (PW), Adjacent Whisker (AW), and combined displacement of two whiskers [20 ms Inter-Stimulus Intervals (ISIs)] were recorded before and 2 hours after memantine gavage (10 mg/kg). A Condition Test Ratio (CTR) was calculated for assessing inhibitory interactions.
Results: Two hours after memantine gavage, neuronal ON and OFF responses to PW deflection were decreased. Furthermore, CTR for both ON and OFF responses was decreased following memantine administration.
Conclusion: The current study demonstrated that memantine modified neural response properties in the rat barrel cortex.
Highlights: Memantine modulated excitatory receptive fields in the rat somatosensory cortex.Memantine decreased integrative receptive fields in rat somatosensory cortex.
Plain Language Summary: As an NMDA receptor antagonist, memantine is used to treat moderate to severe Alzheimer's disease. Memantine has beneficial effects on cognition, mood, and perform daily activities. However, the current study results suggested that memantine may affect information processing in the somatosensory system. This should be considered for future research in the clinic.
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http://dx.doi.org/10.32598/bcn.2021.1156.2 | DOI Listing |
Curr Treat Options Oncol
January 2025
Breast Oncology Program, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Breast cancer metastasizing to the central nervous system (CNS) encompasses two distinct entities: brain metastases involving the cerebral parenchyma and infiltration of the leptomeningeal space, i.e., leptomeningeal disease.
View Article and Find Full Text PDFJ Alzheimers Dis
January 2025
Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Stockholm, Sweden.
Background: Medications for comorbid conditions may affect cognition in Alzheimer's disease (AD).
Objective: To explore the association between common medications and cognition, measured with the Mini-Mental State Examination.
Methods: Cohort study including persons with AD from the Swedish Registry for Cognitive/Dementia Disorders (SveDem).
Nutrients
December 2024
Foodomics Lab, Institute of Food Science Research (CIAL, CSIC), 28049 Madrid, Spain.
Systematic Alzheimer's disease (AD) is a neurodegenerative disease increasingly prevalent in the aging population. AD is characterized by pathological features such as -amyloid (A) plaque accumulation, tau neurofibrillary tangles formation, oxidative stress, an impaired cholinergic system, and neuroinflammation. Many therapeutic drugs have been developed to slow the progression of AD by targeting these pathological mechanisms.
View Article and Find Full Text PDFJ Clin Med
December 2024
Division of Biostatistics and Neural Networks, Medical University of Gdansk, Debinki 1 St., 80-211 Gdansk, Poland.
: Deep brain stimulation (DBS) is employed to adjust the activity of impaired brain circuits. The variability in clinical trial outcomes for treating Alzheimer's disease with memantine is not yet fully understood. We conducted a randomized in silico study comparing virtual DBS therapies with treatment involving an NMDA antagonist combined with DBS in patients with Alzheimer's disease.
View Article and Find Full Text PDFLife (Basel)
November 2024
EuroEspes Biomedical Research Center, International Center of Neuroscience and Genomic Medicine, Bergondo, 15165 Corunna, Spain.
Alzheimer's disease (AD) is a complex/multifactorial brain disorder involving hundreds of defective genes, epigenetic aberrations, cerebrovascular alterations, and environmental risk factors. The onset of the neurodegenerative process is triggered decades before the first symptoms appear, probably due to a combination of genomic and epigenetic phenomena. Therefore, the primary objective of any effective treatment is to intercept the disease process in its presymptomatic phases.
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