Abstract
The effects of the neurotoxin kainic acid on a food-producing habit were studied in Wistar rats in an experimental chamber. Single doses of kainic acid at a subconvulsive dose (8 mg/kg, i.p.) were found to impair the habit, onset of impairment being delayed by several weeks rather than immediate. Conversely, administration of the neurotoxin at the convulsive dose (10 mg/kg) impaired reproduction of the habit with onset within several hours after treatment and persistence for periods of up to 10 days, though this dose did not prevent the acquisition of a new food-procuring habit. These defects in the reproduction of long-term memory traces were explained in terms of the characteristics of the effects of kainic acid on the hippocampal system, which is the most susceptible to systemic administration of the neurotoxin.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
REFERENCES
V. I. Arkhipov, “Reproduction of traces of long-term memory,” Zh. Vyssh. Nerv. Deyat., 48, No.5, 836–845 (1998).
V. I. Arkhipov, D. G. Sochivko, and O. V. Godukhin, “Mechanisms of memory impairment in models of epileptogenesis,” Usp. Sovrem. Biol., 121, No.2, 211–222 (2001).
V. I. Arkhipov and N. A. Shevchenko, “Experimental extinction of a habit as a test of cognitive impairments evoked by kainic acid,” Byull. Eksperim. Biol. Med., 133, No.6, 640–642 (2002).
A. R. Luriya, The Neuropsychology of Memory. Memory Impairments in Local Brain Lesions [in Russian], Pedagogika, Moscow (1974).
I. A. Sytinskii and V. S. Turovskii, “Kainic acid — a tool for studies of the brain,” Usp. Sovrem. Biol., 93, No.2, 253–269 (1982).
V. Arkhipov, “Delayed impairment of response extinction after single seizures induced by picrotoxin,” Behav. Brain Res., 128, 109–111 (2002).
A. Becker, A. Tiedge, and G. A. Grecksch, “Diazepam — its effect on pentylentetrazol-kindled seizures and on related cognitive disturbances,” Pharmacol. Res., 35, No.1, 27–32 (1997).
Y. Ben-Ari, “Limbic seizure and brain damage produced by kainic acid: mechanisms and relevance to human temporal lobe epilepsy,” Neurosci., 14, No.2, 375–402 (1985).
Y. Ben-Ari, “Cell death and synaptic reorganizations produced by seizure,” Epilepsia, 42, No.3, 5–7 (2001).
Y. Ben-Ari and R. Cossort, “Kainate, a double agent that generates seizures: two decades of progress,” TINS, 23, No.11, 580–587 (2000).
G. Bing, B. Wilson, P. Hudson, L. Jin, Z. Feng, W. Zhang, R. Bing, and J.-S. Hong, “A single dose of kainic acid elevates the levels of enkephalins and activator protein-1 transcription factors in the hippocampus for up to 1 year,” Proc. Natl. Acad. Sci. USA, 94, 9422–9427 (1997).
L. M. Brown-Croyts, P. W. Caton, D. T. Radecki, and S. L. McPherson, “Phenobarbital pre-treatment prevents kainic acid-induced impairments in acquisition learning,” Life Sci., 67, No.6, 643–650 (2000).
A. A. Farooqui, W. Y. Ong, X.-R. Ong, B. Halliwell, and L. A. Horrocks, “Neurochemical consequences of kainite-induced toxicity in brain: involvement of arachidonic acid and prevention of toxicity by phospholipase A2 inhibitors,” Brain Res. Rev., 38, 61–78 (2001).
W. Frerking and R. A. Niccol, “Synaptic kainite receptors,” Curr. Opin. Neurobiol., 10, 342–351 (2000).
M. J. Gayos, C. Primo, A. al-Majdalawi, J. M. Fernandez, M. Garrosa, and C. Iniguez, “Brain lesions and water-maze learning deficits after systemic administration of kainic acid to adult rats,” Brain Res., 653, No.1, 92–100 (1994).
D. K. Hannesson and M. E. Corcoran, “The mnemonic effects of kindling,” Neurosci. Biobehav. Res., 24, No.7, 725–751 (2000).
G. L. Holmes, Y. Yang, Z. Liu, J. M. Cermak, M. R. Sarkisian, C. E. Stafstrom, J. C. Neill, and K. Jan Blusztajn, “Seizure-induced memory impairment is reduced by choline supplementation before or after status epilepticus,” Epilepsy Res., 48, No.1–2, 3–13 (2001).
B. Kaminska, R. K. Filipowski, I. W. Bidermann, D. Konopka, D. Nowicka, M. Hetman, M. Dabrowski, D. C. Gorecki, K. Lukasiuk, and A. Szklarczyk, “Kainate-evoked modulation of gene expression in rat brain,” Acta Biochim. Polonica, 44, No.4, 781–790 (1997).
M. D. Lopelman, “Disorders of memory,” Brain, 125, 2152–2190 (2002).
E. W. Lothman and R. C. Collins, “Kainic acid induced limbic seizure: metabolic, behavioural, electroencephalographic and neuropathological correlates,” Brain Res., 218, 299–318 (1981).
A. Mikulecka, P. Krsek, and P. Mares, “Nonconvulsive kainic acid-induced seizures elicit age-dependent impairment of memory for the elevated plus-maze,” Epilepsy Behav., 1, No.6, 418–426 (2000).
M. A. Mikati, S. Tarif, L. Lteif, and M. A. Jawad, “Time sequence and types of memory deficits after experimental status epilepticus,” Epilepsy Res., 42, 97–101 (2001).
T. Myhrer, “Neurotransmitter systems involved in learning and memory in the rat: a meta-analysis based on studies of four behavioral tasks,” Brain Res. Rev., 41, 268–287 (2003).
J. W. Olney, V. Rhee, and O. L. Ho, “Kainic acid: a powerful neurotoxic analogue of glutamate,” Brain Res., 77, No.3, 507–512 (1974).
L. R. Squire, “Memory and hippocampus: a synthesis from findings with rats, monkeys, and humans,” Psychol. Rev., 99, 195–231 (1992).
O. S. Vinogradova, “Hippocampus as comparator: role of the two input and two output systems of the hippocampus in selection and registration of information,” Hippocampus, 11, 578–598 (2001).
Author information
Authors and Affiliations
Additional information
__________
Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 90, No. 7, pp. 849–856, July, 2004.
Rights and permissions
About this article
Cite this article
Arkhipov, V.I., Shevchenko, N.A. Studies of the Reproduction of Long-Term Memory During Exposure to Kainic Acid. Neurosci Behav Physiol 35, 829–834 (2005). https://doi.org/10.1007/s11055-005-0132-z
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/s11055-005-0132-z