ELECTROPHYSIOLOGICAL EFFECTS OF GLIBENCLAMIDE ON HIPPOCAMPAL AND BASOLATERAL AMYGDALA NEURONSIN RATS WITH
A Isoyan1, M Danielyan2, K Nebogova2
11Orbeli Institute of Physiology, National Academy of Sciences of Armenia, Yerevan, Armenia; 2Yerevan State Medical University named after M. Heratsi, Armenia.
Georgian Medical News
|January 9, 2026
Summary
High fructose intake harms brain function. Glibenclamide treatment helped restore normal neuronal activity in the hippocampus and amygdala, suggesting potential for metabolic syndrome complications.
Area of Science:
- Neuroscience
- Metabolic Research
- Pharmacology
Background:
- High fructose consumption disrupts metabolic homeostasis and impairs neuronal function.
- Metabolic syndrome is linked to neurodegenerative complications.
- Understanding the impact of fructose on neural networks is crucial.
Purpose of the Study:
- To investigate the effects of glibenclamide on hippocampal and basolateral amygdala neurons in rats with chronic fructose consumption.
- To evaluate glibenclamide's role in modulating neuronal activity and synaptic responses under metabolic stress.
Main Methods:
- Rats were divided into control, fructose-only, and fructose plus glibenclamide groups.
- Neuronal activity in the hippocampal CA1 region was recorded.
- Synaptic responses were classified as tetanic depression-posttetanic depression (TD-PTD), tetanic depression-posttetanic potentiation (TD-PTP), or tetanic potentiation-posttetanic potentiation (TP-PTP).
Main Results:
- Chronic fructose intake led to hyperglycemia and suppressed neuronal firing.
- Glibenclamide normalized neuronal firing rates and promoted inhibitory synaptic responses.
- Glibenclamide enhanced reduced tetanic potentiation and increased tetanic depression in fructose-fed rats.
Conclusions:
- Glibenclamide modulates the excitation-inhibition balance in neural networks experiencing metabolic stress.
- Glibenclamide shows therapeutic potential in mitigating neurodegenerative issues associated with metabolic syndrome.
