Hippocampal kindling-induced after-discharge and behavioural depression: immediate and long-term attenuation by opiate antagonists

Cottrell, G. A.; Nyakas, Csaba; Bohus, B.

doi:10.1016/0014-2999(88)90743-1

Cited by 14 publications

(5 citation statements)

References 20 publications

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“…Postictal effects vary from a total loss of awareness, posture, and responsiveness to a mild confusion and cognitive disruption. Similar postictal behavioral depression could follow an electrically evoked seizure in animals (Frenk et al., 1979; Caldecott‐Hazard et al., 1983; Cottrell et al., 1988).…”

mentioning

confidence: 73%

Behavioral depression induced by an amygdala seizure and the opioid fentanyl was mediated through the nucleus accumbens

Long

Ma²,

Leung

2009

Epilepsia

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SUMMARYPurpose: To study the behavioral depression induced by a generalized limbic seizure and by an opioid. The hypothesis that an opioid fentanyl and an amygdala-evoked seizure induced behavioral depression through the nucleus accumbens was tested. Methods: The behavioral depression induced by an amygdala-kindled seizure was studied in fully kindled rats, with or without prior injection of fentanyl (0.05 mg/kg, s.c.). Local infusion of a nonspecific opioid antagonist, naloxone, or saline, was made bilaterally in the nucleus accumbens. The durations of loss of righting reflex (LORR), loss of tailpinch response, and catalepsy were assessed. Results: Fentanyl induced an LORR following a generalized kindled seizure. The combination of fentanyl and a generalized seizure, as compared to fentanyl alone or a generalized seizure alone, resulted in a prolonged duration of LORR, catalepsy, and loss of tail pinch response. Infusion of naloxone as compared to saline in the nucleus accumbens reduced the duration of catalepsy and LORR induced by fentanyl, with or without a generalized seizure. Conclusions: Postictal depression that follows a generalized kindled seizure enhanced the behavioral effects of the opioid fentanyl. Network synaptic depression induced by the seizure acted synergistically with fentanyl to produce analgesia, catalepsy, and LORR, in part through the nucleus accumbens.

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mentioning

confidence: 73%

Behavioral depression induced by an amygdala seizure and the opioid fentanyl was mediated through the nucleus accumbens

Long

Ma²,

Leung

2009

Epilepsia

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“…This behavioral depression that followed a convulsive seizure has been well documented, following amygdala or hippocampal stimulation [46,53]. The behavioral depression was pronounced for minutes after the seizure [32], but it was observed up to 2 days [40]. Opiate antagonists were effective in alleviating postictal behavioral depression [32,40,46].…”

Section: Postictal Behavioral Depression After Convulsive Limbic Seizures Is Mediated By Opiates and Frontal Cortical Activitymentioning

confidence: 95%

“…The behavioral depression was pronounced for minutes after the seizure [32], but it was observed up to 2 days [40]. Opiate antagonists were effective in alleviating postictal behavioral depression [32,40,46].…”

Section: Postictal Behavioral Depression After Convulsive Limbic Seizures Is Mediated By Opiates and Frontal Cortical Activitymentioning

confidence: 99%

Behaviors induced or disrupted by complex partial seizures

Leung

McLachlan

2000

Neuroscience & Biobehavioral Reviews

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We reviewed the neural mechanisms underlying some postictal behaviors that are induced or disrupted by temporal lobe seizures in humans and animals. It is proposed that the psychomotor behaviors and automatisms induced by temporal lobe seizures are mediated by the nucleus accumbens. A non-convulsive hippocampal afterdischarge in rats induced an increase in locomotor activity, which was suppressed by the injection of dopamine D(2) receptor antagonist in the nucleus accumbens, and blocked by inactivation of the medial septum. In contrast, a convulsive hippocampal or amygdala seizure induced behavioral hypoactivity, perhaps by the spread of the seizure into the frontal cortex and opiate-mediated postictal depression. Mechanisms underlying postictal psychosis, memory disruption and other long-term behavioral alterations after temporal lobe seizures, are discussed. In conclusion, many of the changes of postictal behaviors observed after temporal lobe seizures in humans may be found in animals, and the basis of the behavioral change may be explained as a change in neural processing in the temporal lobe and the connecting subcortical structures.

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“…Opioid peptides have been implicated in the mechanisms of seizure suppression and in some of the behav-ioral disturbances induced by kindling such as rigidity, analgesia, and immobility observed during the postictal period, as well as interictal enhanced locomotion (Caldecott-Hazard et al, 1982Caldecott-Hazard and Engel, 1987;Cotrell and Bohus, 1987;Caldecott-Hazard, 1988;Cottrell et al, 1988). The administration of fentanyl, a R-opioid receptor agonist, reduces the duration and severity of amygdaloid kindled seizures (Schwark et al, 1986), whereas naloxone, an opiate antagonist, facilitates kindling development in cats and rats (Hardy et al, 1980;Fernández-Guardiola et al, 1989).…”

mentioning

confidence: 99%

Amygdala Kindling Modifies Extracellular Opioid Peptide Content in Rat Hippocampus Measured by Microdialysis

Rocha

Evans²,

Maidment³

1997

Journal of Neurochemistry

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Opioid peptide release in the hippocampus was shown to be increased immediately following amygdala kindling stimulation in freely moving rats using microdialysis combined with a universal opioid peptide radioimmunoassay (RIA). Extracellular opioid peptide levels were elevated (55% above basal levels) within the first 10 min after electrical stimulation‐induced partial seizures in previously nonkindled animals. Fully kindled rats showed lower extracellular opioid peptide levels (40% reduction) during the interictal period [16 ± 2.1 days (mean ± SEM) after the last stage V seizure], in comparison with values obtained from the sham‐kindled group under basal conditions. However, opioid peptide release in fully kindled rats increased above 152% of interictal levels within the first 20 min after onset of fully kindled seizures, attaining peak levels equal to that of the partial kindled group and returning to prestimulation conditions 40–60 min following the ictal events. The majority of the immunoreactive material recovered from the hippocampus within the first 20 min following partial and generalized kindled seizures coeluted with dynorphin‐A (1–6), dynorphin‐A (1–8), and Leu‐enkephalin by HPLC/RIA analysis. It is proposed that the enhanced opioid peptide release in hippocampus induced by amygdala kindling stimulation might be associated with either enhanced excitability or seizure suppression as seizure susceptibility fluctuates. The reduced interictal opioid peptide levels may also underlie some interictal behavioral disturbances.

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Hippocampal kindling-induced after-discharge and behavioural depression: immediate and long-term attenuation by opiate antagonists

Cited by 14 publications

References 20 publications

Behavioral depression induced by an amygdala seizure and the opioid fentanyl was mediated through the nucleus accumbens

Behavioral depression induced by an amygdala seizure and the opioid fentanyl was mediated through the nucleus accumbens

Behaviors induced or disrupted by complex partial seizures

Amygdala Kindling Modifies Extracellular Opioid Peptide Content in Rat Hippocampus Measured by Microdialysis

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