Microinjections of kainic acid into the midbrain reticular core were performed in chronically implanted, unanesthetized cats. The immediate effects of kainate excitation were studied during the first 8 h, in animals without any behavioral or EEG signs of epilepsy. Animals displayed pupillary dilatation, piloerection, accelerated respiration, a frozen attitude with a complete lack of facial expression, and no or only very slight orienting reactions. The most structural syndrome was a hallucinatory-type behavior that began in the first hour following the injection. Animals moved forward in a crouched position as if stalking a prey, vocalizing and opening their mouth in an attacking attitude, or moved back as if defending themselves against as imaginary menacer, seeming virtually terrified. The EEG desynchronization began 20-30 sec after the onset of injection and lasted for 12-14 h without any trace of alpha rhythm, spindles or slow waves. Control injections of buffer solution into the midbrain core and kainic acid in other cerebral structures were followed neither by the hallucinatory defense-attack syndrome, nor by comparably long-lasting EEG desynchronization. The hallucinatory-type behavior elicited during the waking state in the present experiments is compared to the oneiric behavior described by Jouvet and Delorme [21] during paradoxical sleep in animals with suppression of muscular atonia, and possible common mechanisms are discussed.

Download full-text PDF

Source
http://dx.doi.org/10.1016/0166-4328(81)90005-xDOI Listing

Publication Analysis

Top Keywords

kainic acid
12
midbrain reticular
8
reticular core
8
hallucinatory-type behavior
8
eeg desynchronization
8
behavioral effects
4
effects kainic
4
acid injections
4
injections midbrain
4
core microinjections
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!