Acute effect of some psychotropic drugs on low-frequency amygdaloid kindled seizures

Minabe, Yoshio; Tanii, Yasuyuki; Kurachi, Masayoshi

doi:10.1016/0006-3223(87)90102-8

Cited by 12 publications

(4 citation statements)

References 19 publications

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“…This appeared to be a rebound phenomenon. In our experiment on single haloperidol treatment (Minabe et al 1987b), 0.7 mg/kg and 1.5 mg/kg IP haloperidol produced a PNT decrease selectively, 3 mg/kg IP haloperidol produced a PNT decrease, followed by an increase. Dose dependency of the effect of neuroleptics on seizure generation was also reported in previous studies (Chen et al 1968;Oliver et al 1982).…”

Section: Discussionmentioning

confidence: 96%

Effects of chronic haloperidol treatment on amygdaloid seizure generation in cats

1988

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We evaluated the effect of chronic haloperidol treatment (0.5-2 mg/kg/day, 21 day) on amygdala-generating seizures using a kindling procedure induced by low frequency electrical stimulations. The number of stimulating pulses required for triggering of epileptic afterdischarge (pulse-number threshold; PNT) is the indicator of the seizure generating threshold. A PNT decrease occurred, followed by a PNT increase toward the pre-treatment level during high-dose, chronic haloperidol treatment. A PNT increase occurred, followed by a PNT decrease toward the pre-treatment level during the withdrawal period after the high-dose treatment. A decrease of the triggered seizure duration occurred during the high-dose treatment. These results indicate that a transient decrease of seizure generating threshold occurs during chronic haloperidol treatment, and withdrawal of the drug is followed by what appears to be a rebound phenomenon. We suggest that this effect might be related to the antipsychotic potency and associated neurochemical changes known to be caused by chronic haloperidol treatment.

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Section: Discussionmentioning

confidence: 96%

Effects of chronic haloperidol treatment on amygdaloid seizure generation in cats

1988

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“…It is well established that drugs enhancing serotonergic or noradrenergic activity exert anticonvulsant activity in different seizure models ( Kilian & Frey, 1973 ; Peterson & Albertson, 1982 ; Przegalinski, 1985 ; Corcoran & Weiss, 1990 ). Antidepressant drugs, which block the uptake of NE, 5‐HT, or both biogenic amines, were consistently shown to exert anticonvulsant activity after acute administration in fully kindled animals ( Stach et al ., 1980 ; Knobloch et al ., 1982 ; Clifford et al ., 1985 ; Minabe et al ., 1987 ; Yacobi & Burnham, 1991 ). However, clinically many antidepressant drugs are thought to have the potential to provoke seizures, particularly in patients with a preexisting lowered seizure threshold ( Trimble, 1984 ; Lipka & Lathers, 1987 ; Brodie, 1992 ).…”

Section: Discussionmentioning

confidence: 99%

Anticonvulsant and proconvulsant effects of tramadol, its enantiomers and its M1 metabolite in the rat kindling model of epilepsy

Potschka

Friderichs

Löscher

2000

British J Pharmacology

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1 The centrally acting analgesic tramadol has recently been reported to cause seizures at recommended dosages in patients, whereas animal experiments had indicated that seizures only occur in high, toxic doses. Tramadol has a dual mechanism of action that includes weak agonistic eects at the mu-opioid receptor as well as inhibition of monoamine (serotonin, norepinephrine) re-uptake. Its major (M1) metabolite mono-O-desmethyltramadol, which is rapidly formed in vivo, has a markedly higher anity for mu receptors and may thus contribute to the eects of the parent compound. Furthermore, the pharmacological eects of tramadol appear to be related to the dierent, but complementary and interactive pharmacologies of its enantiomers. In the present study, we evaluated (+)-tramadol, its enantiomers, and its M1 metabolite ((+)-enantiomer) in the amygdala kindling model of epilepsy in rats. Adverse eects determined in kindled rats were compared to those in nonkindled rats. 2 At doses within the analgesic range, (+)-tramadol and its enantiomers induced anticonvulsant eects in kindled rats. However, at only slightly higher doses seizures occurred. With (+)-tramadol, generalized seizures were observed at 30 mg kg 71 in most kindled but not in nonkindled rats. The (7)-enantiomer induced myoclonic seizures at 30 mg kg 71 in most kindled but not in nonkindled rats, although myoclonic seizure activity was observed in some nonkindled rats at 10 or 20 mg kg 71 . Seizures were also observed after the (+)-enantiomer and the (+)-enantiomer of the M1 metabolite, but experiments with higher doses of these compounds were limited by marked respiratory depression. 3 The data demonstrate that kindling enhances the susceptibility of rats to convulsant adverse eects of tramadol and its enantiomers, indicating that a preexisting lowered seizure threshold increases the risk of tramadol-induced seizures.

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“…For the most part this is true, although there are some notable exceptions (Table VI). Two good examples are provided by kindling and FEADs, both of which are insensitive to apomorphine but are strongly suppressed by amphetamine (Bigler and Fleming, 1976;Bigler et al, 1974;Fleming et al, 1972;King and Burham, 1980;Minabe et al, 1987;Sat0 et al, 1980). However, more Jobe et al, 1973aKellogg, 1976KO et al, 1982Koslow and Roth, 1971Maynert et al, 1975KO et al, 1981Loscher, 1985Lazarova and Roussinov, 1979Meldrum et al, 1972, 1975cAltshuler et al, 1976Chen et al, 1968De Schaepdryver et al, 1962Kilian and Frey, 1973Maynert et al, 1975McKenzie and Soroko, 1973Prockop et al, 1959Waller and Buterbaugh, 1985Johnson et al, 1979Dadkar et al, 1979Kilian and Frey, 1973Maynert et al, 1975Yoshimura et al, 1991Meldrum et al, 1986Liischer and Honack, 1990Maj, 1982Meldrum et al, 1986Meldrum et al, 1986Meldrum et al, 1986Meldrum et al, 1986McLean et al, 1987Hara et al, 1993Renming et al, 1992Sasa et al, 1988 recent work in this field by…”

Section: Indirectly Acting Dopamine Agonistsmentioning

confidence: 99%

The role of dopamine in epilepsy

Starr

1996

Synapse

241

157

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The clinical benefits of dopamine agonists in the management of epilepsy can be traced back over a century, whilst the introduction of neuroleptics into psychiatry practice 40 years ago witnessed the emergence of fits as a side effect of dopamine receptor blockade. Epidemiologists noticed a reciprocal relationship between the supposed dopaminergic overactivity syndrome of schizophrenia and epilepsy, which came to be regarded as a dopamine underactivity condition. Early pharmacological studies of epilepsy employed nonselective drugs, that often did not permit dopamine's antiepileptic action to be clearly dissociated from that of other monoamines. Likewise, the biochemical search for genetic abnormalities in brain dopamine function, as predeterminants of spontaneous epilepsy, proved largely inconclusive. The discovery of multiple dopamine receptor families (D1 and D2), mediating opposing influences on neuronal excitability, heralded a new era of dopamine‐epilepsy research. The traditional anticonvulsant action of dopamine was attributed to D2 receptor stimulation in the forebrain, while the advent of selective D1 agonists with proconvulsant properties revealed for the first time that dopamine could also lower the seizure threshold from the midbrain. Whilst there is no immediate prospect of developing D2 agonists or D1 antagonists as clinically useful antiepileptics, there is a growing awareness that seizures might be precipitated as a consequence of treating other neurological disorders with D2 antagonists (schizophrenia) or D1 agonists (parkinsonism). © 1996 Wiley‐Liss, Inc.

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Acute effect of some psychotropic drugs on low-frequency amygdaloid kindled seizures

Cited by 12 publications

References 19 publications

Effects of chronic haloperidol treatment on amygdaloid seizure generation in cats

Effects of chronic haloperidol treatment on amygdaloid seizure generation in cats

Anticonvulsant and proconvulsant effects of tramadol, its enantiomers and its M1 metabolite in the rat kindling model of epilepsy

The role of dopamine in epilepsy

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