We made an animal model of cerebellar ataxia by injections of kainic acid into the cerebellar hemispheres on both sides of male rats. The histological and behavioral changes were observed at 4 weeks following the injections. The concentrations of catecholamines and the disappearance rates of alpha-MPT-induced catecholamines were measured in discrete regions of the brain of sham-operated and kainic acid-lesioned rats. A lowered dopamine disappearance rate was seen in the accumbens nucleus of the lesioned rats, but no change in norepinephrine. These findings suggest that the decrease in dopamine turnover in the accumbens nucleus is involved in the development of ataxic behavior.

Download full-text PDF

Source

Publication Analysis

Top Keywords

kainic acid
8
accumbens nucleus
8
cerebellar ataxic
4
ataxic rat
4
rat produced
4
produced kainic
4
acid changes
4
changes concentration
4
concentration turnover
4
turnover rates
4

Similar Publications

We hypothesized that active outer hair cells drive cochlear fluid circulation. The hypothesis was tested by delivering the neurotoxin, kainic acid, to the intact round window of young gerbil cochleae while monitoring auditory responses in the cochlear nucleus. Sounds presented at a modest level significantly expedited kainic acid delivery.

View Article and Find Full Text PDF

Background: Neurodegeneration due to neurotoxicity is one of the phenomena in temporal lobe epilepsy. Experimentally, hippocampal excitotoxicity process can occur due to kainic acid exposure, especially in the CA3 area. Neuronal death, astrocyte reactivity and increased calcium also occur in hippocampal excitotoxicity, but few studies have investigated immediate effect after kainic acid exposure.

View Article and Find Full Text PDF

Mice deficient in TWIK-1 are more susceptible to kainic acid-induced seizures.

iScience

January 2025

School of Biosystems and Biomedical Sciences, College of Health Sciences, Korea University, Seoul 02841, Republic of Korea.

TWIK-1 belongs to the two-pore domain K (K2P) channel family, which plays an essential role in the background K conductance of cells. Despite the development of exon 2-deleted knockout (KO) mice, the physiological role of TWIK-1 has remained largely unknown. Here, we observed that the exon 2-deleted KO mice expressed an internally deleted TWIK-1 (TWIK-1 ΔEx2) protein, which unexpectedly acts as a functional K channel.

View Article and Find Full Text PDF

Activation of glutamine synthetase (GS) as a new strategy for the treatment of major depressive disorder and other GS-related diseases.

Acta Pharmacol Sin

January 2025

Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Medical Science, Tyrosine Peptide Multiuse Research Group, Anti-aging Bio Cell Factory Regional Leading Research Center, Gyeongsang National University, Jinju, Gyeongnam, Republic of Korea.

Glutamine synthetase (GS) plays a crucial role in the homeostasis of the glutamate-glutamine cycle in the brain. Hypoactive GS causes depressive behaviors. Under chronic stress, GS has no change in expression, but its activity is decreased due to nitration of tyrosine (Tyr).

View Article and Find Full Text PDF

Regulation of Glutamate Transporter Type 1 by TSA and the Antiepileptic Mechanism of TSA.

Neurochem Res

January 2025

Huazhong University of Science and Technology, Tongji Medical College, Wuhan, Hubei, 430000, China.

Epilepsy (EP) is a neurological disorder characterized by abnormal, sudden neuronal discharges. Seizures increase extracellular glutamate levels, causing excitotoxic damage. Glutamate transporter type 1 (GLT-1) and its human homologue excitatory amino acid transporter-2 (EAAT2) clear 95% of extracellular glutamate.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!