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Implications of Kindling And Quenching For the Possible Frequency Dependence Of rTMS

Published online by Cambridge University Press:  07 November 2014

R. M. Post ,
T. Kimbrell ,
M. Frye ,
M. George ,
U. McCann ,
J. Little ,
R. Dunn ,
H. Li  and
S.R.B. Weiss
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Abstract

Kindling involves repeated administration of brief high-frequency electrophysiological stimulation of the brain at initially subthreshold intensities that eventually evoke full-blown seizures. It has thus been used not only as a model of epileptogenesis, but of long-term neuronal memory. Quenching is a phenomenon that utilizes low-frequency stimulation for much longer periods of time (eg, 1 Hz for 15 minutes), and appears to exert preventive effects on the development of kindling and inhibit the manifestation of full-blown kindled seizures by markedly increasing the amygdala afterdischarge and seizure threshold. (See also “Kindling and Quenching: Conceptual Implications for rTMS,” by Weiss and Post, page 32). The parameters of kindling and quenching with intracerebral stimulation of the amygdala in vivo are highly similar to those achieved in vitro in hippocampai slice preparations for inducing long-term potentiation (LTP) and longterm depression (LTD), respectively. These neuroplastic changes are relatively long lasting and appear reversible at the level of synaptic function with either LTD or LTP capable of countering the effects of the other.

Type
Feature Articles
Information
CNS Spectrums , Volume 2 , Issue 1: Transcranial Magnetic Stimulation: Mapping & Modifying Brain-Behavior Relationships , January 1997 , pp. 54 - 60
Copyright
Copyright © Cambridge University Press 1997

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References

1.Goddard, GV, McIntyre, DC, Leech, CK. A permanent change in brain function resulting from daily electrical stimulation. Exp Neurol. 1969;25:295–330.CrossRefGoogle ScholarPubMed
2.Racine, R. Kindling: the first decade. Neurosurgery. 1978;3:234–252.CrossRefGoogle ScholarPubMed
3.Goddard, GV, Douglas, RM. Does the engram of kindling model the engram of normal long term memory? Can J Neurol Sci. 1975;2:385–394.CrossRefGoogle ScholarPubMed
4.Weiss, SRB, Li, XL, Rosen, JB, et al.Quenching: inhibition of development and expression of amygdala kindled seizures with low frequency stimulation. NeuroReport. 1995;6:2171–2176.Google Scholar
5.Weiss, SRB, Li, X-L, Noguera, EC, et al.Quenching: persistent alterations in seizure and afterdischarge threshold following low-frequency stimulation. In: M., Corcoran and S., Moshe, eds. Kindling V. New York, NY: Plenum Publishing. In press.Google Scholar
6.Christie, BR, Kerr, DS, Abraham, WC. Flip side of synaptic plasticity: long-term depression mechanisms in the hippocampus. Hippocampus. 1994;4:127–135.CrossRefGoogle ScholarPubMed
7.Linden, DJ. Long-term synaptic depression in the mammalian brain. Neuron. 1994;12:457–472.CrossRefGoogle ScholarPubMed
8.Malenka, RC. Synaptic plasticity in the hippocampus: LTP and LTD. Cell. 1994;78:535–538.CrossRefGoogle ScholarPubMed
9.Cain, D. Long-term potentiation and kindling: how similar are the mechanisms? TINS. 1989;12:6–10.Google Scholar
10.Racine, RJ, Moore, KA, Evans, C. Kindling-induced potentiation in the piriform cortex. Brain Res. 1991;556:218–225.Google Scholar
11.Cain, DP, Corcoran, ME. Kindling with low-frequency stimulation: Generality, transfer, and recruiting effects. Exp Neurol, 1981;73:219–232.Google Scholar
12.Corcoran, ME, and Cain, DP. Kindling of seizures with low frequency electrical stimulation, Brain Res. 1980;196:262–265.Google Scholar
13.Clark, M, Post, RM, Weiss, SRB, Cain, CJ, Nakajima, T. Regional expression of c-fos mRNA in rat brain during the evolution of amygdala-kindled seizures. Mol Brain Res. 1991;11:55–64.Google Scholar
14.Dragunow, M, Currie, RW, Faull, RL, Robertson, HA, Jansen, K. Immediate-early genes, kindling and long-term potentiation. Neurosci Biobehav Rev. 1989;13:301–313.Google Scholar
15.Rosen, JB, Cain, CJ, Weiss, SR, Post, RM. Alterations in mRNA of enkephalin, dynorphin and thyrotropin releasing hormone during amygdala kindling: an in situ hybridization study. Brain Res Mol Brain Res. 1992;15:247–255.Google Scholar
16.Weiss, SRB, Clark, M, Rosen, JB, Smith, MA, Post, RM. Contingent tolerance to the anticonvulsant effects of carbamazepine: relationship to loss of endogenous adaptive mechanisms. Brain Res Rev. 1995;20:305–325.Google Scholar
17.Post, RM, Weiss, SRB, Leverich, GS. Recurrent affective disorder: roots in developmental neurobiology and illness progression based on changes in gene expression. In: D., Cicchetti and D., Tucker, eds. Development and Psychopathology. New York, NY: Cambridge University Press; 1994:781–813.Google Scholar
18.Post, RM, Weiss, SRB, Leverich, GS, et al.Developmental psychobiology of cyclic affective illness: implications for early therapeutic intervention. In: D., Cicchetti and D., Tucker, eds. Development and Psychopathology. New York, NY: Cambridge University Press; 1996:273–305.Google Scholar
19.Wada, JA, Sato, M, Corcoran, ME. Persistent seizure susceptibility and recurrent spontaneous seizures in kindled cats. Epilepsia. 1974;15:465–478.Google Scholar
20.Pinel, JPJ, Rovner, LI. Experimental epileptogenesis: kindling-induced epilepsy in rats. Exp Neurol. 1978;58:190–202.Google Scholar
21.Post, RM, Weiss, SRB. Endogenous biochemical abnormalities in affective illness: therapeutic vs. pathogenic. Biol Psychiatry. 1992;32:469–484.Google Scholar
22.Byrne, JH, Kandel, ER. Presynaptic facilitation revisited: state and time dependence. J Neurosci. 1996;16:425–435.Google Scholar
23.Post, RM, Putnam, FW, Contel, NR, Goldman, B. Electroconvulsive seizures inhibit amygdala kindling: implications for mechanisms of action in affective illness. Epilepsia. 1984;25:234–239.CrossRefGoogle ScholarPubMed
24.Sackeim, HE, Devanand, DP. Electroconvulsive therapy. 1123-1142. 1995. In: FE, Bloom and DJ, Kupfer, eds. Psychopharmacology: The Fourth Generation of Progress. New York, New York: Raven PressGoogle Scholar
25.Sackeim, HA, Decina, P, Portnoy, S, Neeley, P, Malitz, S. Studies of dosage, seizure threshold, and seizure duration in ECT. Biol Psychiatry. 1987;22:249–268.Google Scholar
26.Coffey, CE, Lucke, J, Weiner, RD, Krystal, AD, Aque, M. Seizure threshold in electroconvulsive therapy: I. Initial seizure threshold. Biol Psychiatry. 1995;37:713–720.CrossRefGoogle ScholarPubMed
27.Enns, M, Karvelas, L. Electrical dose titration for electroconvulsive therapy: a comparison with dose prediction methods. Convuls Ther. 1995;11:86–93.Google ScholarPubMed
28.McCall, WV, Reid, S, Ford, M. Electrocardiographic and cardiovascular effects of subconvulsive stimulation during titrated right unilateral ECT. Convuls Ther. 1994;10:25–33.Google Scholar
29.George, MS, Wassermann, EM, Williams, WA, et al.Daily repetitive transcranial magnetic stimulation (rTMS) improves mood in depression. NeuroReport. 1995;6:1853–1856.CrossRefGoogle ScholarPubMed
30.Pascual-Leone, A, Rubio, B, Pallardo, F, Catala, MD. Rapid-rate transcranial magnetic stimulation of left dorsolateral prefrontal cortex in drug-resistant depression. Lancet. 1996;348:233–237.Google Scholar
31.Pascual-Leone, A, Catala, MD, Pascual-Leone Pascual A Lateralized effect of rapid-rate transcranial magnetic stimulation of the prefrontal cortex on mood. Neurology. 1996;46:499–502.CrossRefGoogle ScholarPubMed
32.George, MS, Wassermann, EM, Williams, WA, et al.Daily left prefrontal repetitive transcranial magnetic stimulation in outpatient depression: initial results of a double-blind placebo controlled crossover trial. APA New Research Program and Abstracts. 1996:280. Abstract.Google Scholar
33.McCann, UD, Kimbrell, TA, Morgan, CM, et al. Repetitive transcranial magnetic stimulation for the hypermetabolism of posttraumatic stress disorder: a case report. Unpublished manuscript.Google Scholar
34.Ketter, TA, Kimbrell, TA, George, MS, et al.Baseline hypermetabolism may predict carbamazepine response, and hypometabolism nimodipine response in mood disorders. Abstracts of the XXth CINP Congress. 1996:10. Abstract.Google Scholar
35.Semple, WE, Goyer, P, McCormick, R, et al.Preliminary report: brain blood flow using PET in patients with posttraumatic stress disorder and substance-abuse histories. Biol Psychiatry. 1993;34:115–118.CrossRefGoogle ScholarPubMed
36.Shin, LM, Kosslyn, SM, McNally, RJ, et al. A positron emission tomography study of combat-related post-traumatic stress disorder. Presented at the 10th Annual Meeting of the International Society for Traumatic Stress Studies, November 8, 1994, Chicago, Illinois.Google Scholar
37.Rauch, SL, van der Kolk, BA, Fisler, RE, et al.A symptom provocation study of posttraumatic stress disorder using positron emission tomography and script-driven imagery. Arch Gen Psychiatry. 1996;380–387.Google Scholar
38.Van der Kolk, BA. The psychobiology of traumatic memory: lesions from neuroimaging studies. Presented at Psychobiology of Posttraumatic Stress Disorder, a New York Academy of Sciences Conference, September 7-10, 1996, New York, New York. Speaker Abstract.Google Scholar
39.Rush, AJ, Beck, AT, Kovacs, M. Comparative efficacy of cognitive therapy and pharmacotherapy in the treatment of depressed outpatients. Cog Ther Res. 1977;1:17–37.Google Scholar
40.Elkin, I, Shea, MT, Watkins, JT, et al.National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments. Arch Gen Psychiatry. 1989;46:971–82.CrossRefGoogle ScholarPubMed
41.Dudek, SM, Bear, MF. Homosynaptic long-term depression in area CA, of hippocampus and effect of N-methyt D-aspartate receptor blockade, PNAS. 1992;89:4363–4367.Google Scholar