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2 results on '"Zaniani, N"'

1. Identification of an epilepsy-linked gut microbiota signature in a pediatric rat model of acquired epilepsy

Author

Riva, A, Sahin, E, Volpedo, G, Petretto, A, Lavarello, C, Di Sapia, R, Barbarossa, D, Zaniani, N, Craparotta, I, Barbera, M, Sezerman, U, Vezzani, A, Striano, P, Ravizza, T, Riva A., Sahin E., Volpedo G., Petretto A., Lavarello C., Di Sapia R., Barbarossa D., Zaniani N. R., Craparotta I., Barbera M. C., Sezerman U., Vezzani A., Striano P., Ravizza T., Riva, A, Sahin, E, Volpedo, G, Petretto, A, Lavarello, C, Di Sapia, R, Barbarossa, D, Zaniani, N, Craparotta, I, Barbera, M, Sezerman, U, Vezzani, A, Striano, P, Ravizza, T, Riva A., Sahin E., Volpedo G., Petretto A., Lavarello C., Di Sapia R., Barbarossa D., Zaniani N. R., Craparotta I., Barbera M. C., Sezerman U., Vezzani A., Striano P., and Ravizza T.

Abstract

A dysfunctional gut microbiota-brain axis is emerging as a potential pathogenic mechanism in epilepsy, particularly in pediatric forms of epilepsy. To add new insights into gut -related changes in acquired epilepsy that develops early in life, we used a multi-omics approach in a rat model with a 56% incidence of epilepsy. The presence of spontaneous seizures was assessed in adult rats ( n = 46) 5 months after status epilepticus induced by intra-amygdala kainate at postnatal day 13, by 2 weeks (24/7) ECoG monitoring. Twenty-six rats developed epilepsy (Epi) while the remaining 20 rats (No-Epi) did not show spontaneous seizures. At the end of ECoG monitoring, all rats and their sham controls ( n = 20) were sacrificed for quantitative histopathological and immunohistochemical analyses of the gut structure, glia and macrophages, as well as RTqPCR analysis of inflammation/oxidative stress markers. By comparing Epi, No-Epi rats, and sham controls, we found structural, cellular, and molecular alterations reflecting a dysfunctional gut, which were specifically associated with epilepsy. In particular, the villus height -tocrypt depth ratio and number of Goblet cells were reduced in the duodenum of Epi rats vs both No-Epi rats and sham controls ( p < 0.01). Villus height and crypt depth in the duodenum and jejunum (p < 0.01) were increased in No-Epi vs both Epi and sham controls. We also detected enhanced Iba1-positive macrophages, together with increased IL1b and NFE2L2 transcripts and TNF protein, in the small intestine of Epi vs both No-Epi and sham control rats ( p < 0.01), denoting the presence of inflammation and oxidative stress. Astroglial GFAPimmunostaining was similar in all experimental groups. Metagenomic analysis in the feces collected 5 months after status epilepticus showed that the ratio of two dominant phyla ( Bacteroidota-to-Firmicutes ) was similarly increased in Epi and No-Epi rats vs sham control rats. Notably, the relative abundance of families

Published
2024

2. Use of colchicine in cortical area 1 of the hippocampus impairs transmission of non-motivational information by the pyramidal cells

Author

Zaniani, N. R., Manizheh Karami, and Porkhodadad, S.

Subjects
Behavior, Pyramidal Cell, Colchicine, Research Papers, Hippocampus, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, lcsh:RC321-571
Abstract

Colchicine, a potent neurotoxin derived from plants, has been recently introduced as a degenerative toxin of small pyramidal cells in the cortical area 1 of the hippocampus (CA1). In this study, the effect of the alkaloid in CA1 on the behaviors in the conditioning task was measured. Injections of colchicine (1,5 µg/rat, intra-CA1) was performed in the male Wistar rats, while the animals were settled and cannulated in a stereotaxic apparatus. In the control group solely injection of saline (1 µl/rat, intra-CA1) was used. One week later, all the animals passed the saline conditioning task using a three-day schedule of an unbiased paradigm. They were administered saline (1 ml/kg, s.c.) twice a day throughout the conditioning phase. To evaluate the possible effects of cell injury by the toxin on the pyramidal cells, both the motivational signals while in the conditioning box and the non-motivational locomotive signs of the treated and control rats were measured. Based on the present study the alkaloid caused no change in the score of place conditioning, but affected both the sniffing and grooming behaviors in the group that received colchicine. However, the alkaloid did not show the significant effect on the rearing or compartment entering in the rats. According to the findings, the intra-CA1 injection of colchicine may impair the neuronal transmission of non-motivational information by the pyramidal cells in the dorsal hippocampus.

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