Site Of Neuronal Loss Research Articles

Interrelation structural and functional alterations in the dentate gyrus of rats with aging.

The process of natural aging is considered as a risk factor for the development of neurodegenerative pathology, in which decrease of physiological cognitive functions of the body is found. 2 groups were formed: group 1 - rats at the age of 12 months (n = 10), group 2 - rats at the age of 24 months (n = 10). We evaluated the neuropsychiatric state of animals and determined the degree injury of neurons. It was established that the motor and orientational-research activity of old rats (24 months) was lower than that of rats of mature age (12 months). Microscopic examination of rat brain sections stained with thionin according to the Nissl method in mature animals in the granular layer of dentate gyrus showed that the most of neuronal perikarya had a close to round shape with a centrally located nucleus and nucleolus, characterized by normochromic cytoplasm and compact arrangement. There were single neurons with hyperchromatosis of the cytoplasm and wrinkled hyperchromic neurons, which were mainly located on the border of granular and subgranular layers of dentate gyrus. Sites of neuronal loss were observed in senile age rats, a significant increase in both the specific number of hyperchromic shrunken neurons (p <0.05) and neurons with cytoplasm hyperchromatosis without shrinkage (p <0.05) was observed. Such neurons prevailed at the boundary of the granular and subgranular layers, as well as in the crest region. During aging in rats aged 24 months, pronounced changes in neurons of granular layer of dentate gyrus in the form of an increase in the number of hyperchromic shrunken neurons are found at the boundary of granular and subgranular layers and in the crest region. These changes are accompanied by more severe functional disorders in 24-month-old rats which may accelerate the process of aging.

Effects of Non-invasive, Targeted, Neuronal Lesions on Seizures in a Mouse Model of Temporal Lobe Epilepsy

Surgery to treat drug-resistant epilepsy can be quite effective but remains substantially underutilized. A pilot study was undertaken to test the feasibility of using a non-invasive, non-ablative, approach to produce focal neuronal loss to treat seizures in a rodent model of temporal lobe epilepsy. In this study, spontaneous, recurrent seizures were established in a mouse model of pilocarpine-induced status epilepticus. After post-status epilepticus stabilization, baseline behavioral seizures were monitored for 30 d. Non-invasive opening of the blood–brain barrier targeting the hippocampus was then produced by using magnetic resonance-guided, low-intensity focused ultrasound, through which a neurotoxin (quinolinic acid) administered intraperitoneally gained access to the brain parenchyma to produce focal neuronal loss. Behavioral seizures were then monitored for 30 d after this procedure, and brains were subsequently prepared for histologic analysis of the sites of neuronal loss. The average frequency of behavioral seizures in all animals (n = 11) was reduced by 21.2%. Histologic analyses along the longitudinal axis of the hippocampus revealed that most of the animals (n = 8) exhibited neuronal loss located primarily in the intermediate aspect of the hippocampus, while sparing the septal aspect. Two other animals with damage to the intermediate hippocampus also exhibited prominent bilateral damage to the septal aspect of the hippocampus. A final animal had negligible neuronal loss overall. Notably, the site of neuronal loss along the longitudinal axis of the hippocampus influenced seizure outcomes. Animals that did not have bilateral damage to the septal hippocampus displayed a mean decrease in seizure frequency of 27.7%, while those with bilateral damage to the septal hippocampus actually increased seizure frequency by 18.7%. The animal without neuronal loss exhibited an increase in seizure frequency of 19.6%. The findings indicate an overall decrease in seizure frequency in treated animals. And, the site of neuronal loss along the longitudinal axis of the hippocampus appears to play a key role in reducing seizure activity. These pilot data are promising, and they encourage additional and more comprehensive studies examining the effects of targeted, non-invasive, neuronal lesions for the treatment of epilepsy.