Amygdaloid kindling of rats increases preprosomatostatin mRNA and somatostatin without affecting glutamic acid decarboxylase (GAD) mRNA or GAD

Shinoda, Hisaharu; Schwartz, Joan P.; Nadi, N. S.

doi:10.1016/0169-328x(89)90041-7

Cited by 47 publications

(12 citation statements)

References 24 publications

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“…However, only the cortical sections above the striatum and the dorsal hippocampus were immunocytochemically analyzed in this study, and therefore changes in other cortical areas cannot be excluded. In line with these data, literature reports show that (a) preprosomatostatin mRNA levels are increased in the cortex and striatum 1 and 3 days after the last kindling stimulation but are back to baseline at 7 and 21 days (Shinoda et al, 1989(Shinoda et al, , 1991; (b) somatostatin-LI levels in the striatum of kindled rats killed 7 or 60 days after the last stimulation are not significantly different from matostatin processing or in somatostatin transport to the terminals may explain this discrepancy. In fact, somatostatin-LI in brain tissue homogenates is identified as somatostatin-14, prosomatostatin, and, to a lower level, somatostatin-28 (Sperk and Widmann, 1984); in contrast, it is identified as somatostatin-14 by >95% in the isolated nerve terminals (Bonanno et al, 1991).…”

Section: Discussionsupporting

confidence: 73%

“…Once established, this latent hyperexcitability is essentially permanent. An increase in preprosomatostatin mRNA and in somatostatin levels has been found in the hippocampus, the cortex, and the striatum during and following kindling epileptogenesis (Shinoda et al, 1989(Shinoda et al, , 1991Schwarzer et a!., 1996). These events probably reflect augmented peptide synthesis.…”

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confidence: 92%

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Time‐ and Region‐Specific Variations in Somatostatin Release Following Amygdala Kindling in the Rat

Simonato

Bregola

Beani

et al. 1998

Journal of Neurochemistry

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Somatostatin biosynthesis is activated during and following kindling epileptogenesis. The aim of this study was to investigate whether this phenomenon translates into enhanced release of the peptide and whether it is involved in kindling maintenance. A marked increase in somatostatin-like immunoreactivity (somatostatin-LI) was observed in hilar interneurons of the hippocampus and in their presumed projections to the outer molecular layer 1 week, but not 1 month, after the last kindled seizure. No overt changes were observed in the striatum or in the cortex. Compared with sham-stimulated controls, (a) in the hippocampus, high-K~-evokedsomatostatin-LI release was unchanged in synaptosomes taken from rats killed 7 days after the last kindled seizure but was bilaterally reduced after 30 days; (b) in the striatum, it was increased (mainly ipsilaterally to stimulation) 7, but not 30, days after the last seizure; and (c) in the cortex, somatostatin-LI release was bilaterally increased in synaptosomes taken from kindled rats 30, but not 7, days after the last seizure. This study shows that distinct changes occur in synaptosomal somatostatin-LI release after kindling acquisition, depending on the brain area analyzed and on the time elapsed from the last generalized seizure.

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Section: Discussionsupporting

confidence: 73%

mentioning

confidence: 92%

Time‐ and Region‐Specific Variations in Somatostatin Release Following Amygdala Kindling in the Rat

Simonato

Bregola

Beani

et al. 1998

Journal of Neurochemistry

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“…1986;White et al, 1987;Gall, 1988;Morris et al, 1988;Shinoda et al, 1988;Olenik et al, 1989). The time course of peptide changes observed in our present PTZ kindling experiments was surprising.…”

Section: Discussioncontrasting

confidence: 47%

Neuropeptide Levels after Pentylenetetrazol Kindling in the Rat

Marksteiner

Lassmann

Saria

et al. 1990

Eur J of Neuroscience

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Levels of several neuropeptides were measured in the frontal cortex, dorsal hippocampus, striatum, and amygdala/pyriform cortex in rats kindled for 5 weeks by daily injection of pentylenetetrazol (30 mg/kg, i.p.). Significantly increased concentrations (by 30 - 140%) were found in all examined brain areas for neuropeptide Y, somatostatin (except hippocampus) and neurokinin-like immunoreactivity 10 days after the last kindling session. Similar but less pronounced changes were also found 24 h after the last seizure. The increase in total neurokinin-like immunoreactivity was due to a marked increase in neurokinin B as revealed by HPLC analysis. Increases in peptide levels, however, were restricted to fully kindled animals. At the same time no changes in levels of substance P, vasoactive intestinal polypeptide and calcitonin gene-regulated peptide were observed. Cholecystokinin octapeptide was enhanced only in the hippocampus (by 46%). The increases in neuropeptide Y, somatostatin, and neurokinin-like immunoreactivity subsided after 3 months. A markedly decreased seizure threshold was observed 10 days and 2 months after the final kindling session. No nerve cell degeneration was observed in kindled rats 24 h or 10 days after the last pentylenetetrazol injection. Some animals (2 of 4), however, exhibited signs of blood - brain barrier damage when examined 24 h after the last kindling session which may reflect the preceding convulsions. No such changes were detected after 10 days. The increases in peptide levels may suggest increased activity of respective neurons which, at least to some degree, may be associated with gamma-aminobutyric acid. The changes in peptide levels may be more closely related to the kindling procedure itself than to the decreased seizure threshold of the animals.

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“…Somatostatin and specific peptides or their mRNA are also affected by kindling (Naranjo et al 1986;Shinoda et al 1989). …”

Section: Heinz Rüthrich · Gisela Grecksch · Manfred Krugmentioning

confidence: 98%

Effects of piracetam on pentylenetetrazol-kindling development, hippocampal potentiation phenomena and kindling-induced learning deficit

Rüthrich

Grecksch

Krug

1999

Naunyn-Schmiedeberg's Arch Pharmacol

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Kindling is a generally accepted model for studying epilepsy development in the context of overexpression of processes of neuronal plasticity. In previous studies we have shown that establishment of kindling by repeated application of subconvulsive doses of pentylenetetrazol (PTZ) also led to marked changes in hippocampal excitability and an impairment in learning behaviour. With the intention of further investigating the relationship between kindling development, kindling-induced changes in excitability and learning deficits, rats were chemically kindled under pretreatment with the nootropic drug piracetam. Furthermore, we tested acute piracetam effects on developed kindling seizures, the learning deficit and potentiation effects. At the investigated dose piracetam did not influence the kindling development. The kindling-induced potentiation of hippocampal field potentials was significantly diminished in piracetam-pretreated rats. Piracetam acutely injected completely antagonized this potentiation effect. Piracetam brought about a significant improvement in impaired learning performance in rats pretreated during kindling induction and acutely injected before the learning experiment, respectively. Possible correlations between the suppressing of the kindling related potentiation in hippocampal structures by piracetam and its beneficial effect on learning impairment are discussed as antagonizing overexpression of potentiation in the course of kindling.

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Amygdaloid kindling of rats increases preprosomatostatin mRNA and somatostatin without affecting glutamic acid decarboxylase (GAD) mRNA or GAD

Cited by 47 publications

References 24 publications

Time‐ and Region‐Specific Variations in Somatostatin Release Following Amygdala Kindling in the Rat

Time‐ and Region‐Specific Variations in Somatostatin Release Following Amygdala Kindling in the Rat

Neuropeptide Levels after Pentylenetetrazol Kindling in the Rat

Effects of piracetam on pentylenetetrazol-kindling development, hippocampal potentiation phenomena and kindling-induced learning deficit

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