Opioid peptides, particularly dynorphin, after amygdaloid-kindled seizures

Przew, R.; klocki,; Lasoń, Władysław; Stach, R; Kacz, D.

doi:10.1016/0167-0115(83)90268-9

Cited by 28 publications

(5 citation statements)

References 19 publications

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“…These observations were also consistent with greater hippocampal cell loss in the first group of patients. This study has focused on alterations in the location of Dyn-IR elements in TLE specimens, but previous studies of experimental seizure models suggest that the intensity of dynorphin immunoreactivity (Lason et al, 1983;Przewlocki et al, 1983;Iadarola et al, 1986;Kanamatsu et al, 1986a, b;Gall, 1988) and zinc labeling (Sloviter, 1985;Frederickson et al, 1988) can also vary according to the prior seizure history. In the present study, there was only one case in which prior seizure activity may have led to a detectable decrease in the intensity of staining in the inner molecular layer.…”

Section: Discussionmentioning

confidence: 99%

Altered patterns of dynorphin immunoreactivity suggest mossy fiber reorganization in human hippocampal epilepsy

et al. 1990

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Dynorphin A(1-17), an opioid peptide that is normally present in the hippocampal mossy fiber system, was localized immunocytochemically in the hippocampal formation of control autopsy and temporal lobe epilepsy (TLE) specimens. In control tissue, dynorphin-like immunoreactive (Dyn-IR) structures were confined to the mossy fiber path and were most highly concentrated in the polymorph (hilar) region of the dentate gyrus. Very few Dyn-IR structures were present in the molecular and granule cell layers of the dentate gyrus. In contrast, in all TLE specimens, Dyn-IR elements were present in these layers. The extent of aberrant staining varied among the TLE specimens, and 2 major patterns were observed. The first was a relatively wide band of reaction product in the inner one-third to one-fourth of the molecular layer (8 cases), and the second was a more limited distribution of immunoreactive fibers and presumptive terminals in the granule cell and immediately adjacent supragranular regions (2 cases). The extent of aberrant Dyn-IR structures appeared to be related to the amount of cell loss in the polymorph and CA3 fields and to dispersion of the granule cell somata. Specimens processed with the Timm's sulfide silver method for heavy metals provided independent evidence for the distribution of mossy fibers. In both control and TLE specimens, the patterns of labeling were virtually identical to those of dynorphin localization. These findings suggest that sprouting of mossy fibers or their axon collaterals has occurred in hippocampal epilepsy and that the reorganized fibers contain at least one of the neuropeptides that are normally present in this system. Such fibers could form recurrent excitatory circuits and contribute to synchronous firing and epileptiform activity, as suggested in studies of experimental models of epilepsy.

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Section: Discussionmentioning

confidence: 99%

Altered patterns of dynorphin immunoreactivity suggest mossy fiber reorganization in human hippocampal epilepsy

et al. 1990

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“…It was recently reported that the level of hippocampal dynorphin is increased in amygdaloid-kindled rabbits (Przewlocki et al, 1983) and in rats receiving intra-amygdaloid kainic acid (Lason et al, 1983). These observations suggest that, like enkephalin, the metabolic state of dynorphin stored in hippocampal neurons can change in response to seizure activities.…”

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confidence: 88%

Dynorphin- and enkephalin-like immunoreactivity is altered in limbic- basal ganglia regions of rat brain after repeated electroconvulsive shock

Kanamatsu¹,

McGinty²,

Mitchell³

et al. 1986

J. Neurosci.

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In an attempt to determine whether the opioid peptides derived from prodynorphin participate in the effects of electroconvulsive shock (ECS), we used radioimmunoassay and immunocytochemistry to measure dynorphin-like immunoreactivity (DN-LI) in various rat brain regions after repeated ECS treatments. Ten daily ECSs caused a significant increase in dynorphin A (1-8)-LI in most limbic-basal ganglia structures, including hypothalamus (50%), striatum (30%), and septum (30%). No significant change was found in the frontal cortex or the neurointermediate lobe of the pituitary. In contrast, 10 ECS treatments depleted DN-LI in hippocampal mossy fibers by 64%. A detailed time-course study revealed that a single shock caused a small but significant increase in hippocampal DN-LI, whereas three consecutive shocks depleted DN-LI by 30%. The maximal decrease in DN-LI was reached after six daily ECSs. The level of DN-LI in the hippocampus partly recovered, but remained lower than the control value 4, 7, and 14 d after the cessation of six daily ECSs (50, 77, and 83% of control value, respectively). In contrast with the ECS-induced depletion of hippocampal dynorphin, 10 daily ECSs caused a significant increase (40%) in (Met5)-enkephalin-LI in the hippocampus, as well as in other limbic-basal ganglia structures. Immunocytochemistry revealed that enkephalin-LI was increased in the perforant pathway, which is presynaptic to the dynorphin-containing mossy fiber pathway in the hippocampus. These observations suggest that different mechanisms may regulate these two opioid peptide systems in the hippocampus.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…There are various reports of changes in neuropeptides such as TRH (Walczak et al, 1983), somatostatin (Kato et al, 1983), opioid peptides (Vindrola et al, 1981;Przewlocki et al, 1983), and cholecystokinin (Iadarola et al, 1986) after AM-kindled seizures. In our previous report, we showed that i.c.v.…”

Section: Discussionmentioning

confidence: 99%

Long‐Term Increase in Striatal Thyrotropin‐Releasing Hormone Receptor Binding Caused by Amygdaloid Kindling

Kajita¹,

Ogawa²,

Sato³

1987

Epilepsia

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Our previous finding that intracerebroventricular (i.c.v.) administration of both thyrotropin-releasing hormone (TRH) and its analogue, gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide citrate (DN-1417), suppressed seizure development of amygdaloid (AM) kindling and kindled AM seizures leads to a new hypothesis that endogenous TRH may be an antiepileptic substance in the brain. In this study, we examined postictal chronological changes in both immunoreactive TRH (IR-TRH) and TRH receptor binding activity in discrete brain regions of AM-kindled rats to study the relationship of the brain TRH system to kindling-induced seizure susceptibility. AM-kindled rats were decapitated 30 min, 24 h, 48 h, 7 days, and 21 days after the last kindled convulsion. IR-TRH increased markedly in the AM/pyriform cortex and hippocampus 24 and 48 h after the last convulsion, and returned to the control (unstimulated, sham-operated) value within 3 weeks after the convulsions ended. In contrast, a significant increase in the striatal TRH binding sites was evident 24 h after the cessation of convulsions which lasted 21 days. A lasting change in the striatal TRH neural system may be related to kindling-induced seizure susceptibility.

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Opioid peptides, particularly dynorphin, after amygdaloid-kindled seizures

Cited by 28 publications

References 19 publications

Altered patterns of dynorphin immunoreactivity suggest mossy fiber reorganization in human hippocampal epilepsy

Altered patterns of dynorphin immunoreactivity suggest mossy fiber reorganization in human hippocampal epilepsy

Dynorphin- and enkephalin-like immunoreactivity is altered in limbic- basal ganglia regions of rat brain after repeated electroconvulsive shock

Long‐Term Increase in Striatal Thyrotropin‐Releasing Hormone Receptor Binding Caused by Amygdaloid Kindling

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