Alterations in somatostatin and proenkephalin mRNA in response to a single amygdaloid stimulation versus kindling

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

doi:10.1016/0169-328x(91)90030-2

Cited by 41 publications

(21 citation statements)

References 19 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: 70%

“…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: 95%

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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: 70%

mentioning

confidence: 95%

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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“…We cannot exclude the possibility that functional evidence for additional GABAergic synapses would have eventually developed after longer periods of chronic epilepsy, but at the stage examined, glutamatergic axon sprouting and synaptogenesis by granule cells are well established (Mello et al, 1993;Mathern et al, 1998;Okazaki et al, 1999;Wuarin and Dudek, 2001), so one might expect that GABAergic synaptogenesis would have occurred. Perhaps surviving interneurons only appear to sprout axon collaterals, because seizure activity increases antigen expression (Feldblum et al, 1990;Wanscher et al, 1990;Shinoda et al, 1991;Schwarzer et al, 1995;Houser and Esclapez, 1996;Esclapez and Houser, 1999), making preexisting axon collaterals more visible by immunocytochemical methods. Stereological analysis of inhibitory synapse numbers at different stages of epileptogenesis would help resolve this issue.…”

Section: Potential Compensatory Mechanismsmentioning

confidence: 99%

Reduced Inhibition of Dentate Granule Cells in a Model of Temporal Lobe Epilepsy

2003

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Patients and models of temporal lobe epilepsy have fewer inhibitory interneurons in the dentate gyrus than controls, but it is unclear whether granule cell inhibition is reduced. We report the loss of GABAergic inhibition of granule cells in the temporal dentate gyrus of pilocarpine-induced epileptic rats. In situ hybridization for GAD65 mRNA and immunocytochemistry for parvalbumin and somatostatin confirmed the loss of inhibitory interneurons. In epileptic rats, granule cells had prolonged EPSPs, and they discharged more action potentials than controls. Although the conductances of evoked IPSPs recorded in normal ACSF were not significantly reduced and paired-pulse responses showed enhanced inhibition of granule cells from epileptic rats, more direct measures of granule cell inhibition revealed significant deficiencies. In granule cells from epileptic rats, evoked monosynaptic IPSP conductances were Ͻ40% of controls, and the frequency of GABA A receptor-mediated spontaneous and miniature IPSCs (mIPSCs) was Ͻ50% of controls. Within 3-7 d after pilocarpine-induced status epilepticus, miniature IPSC frequency had decreased, and it remained low, without functional evidence of compensatory synaptogenesis by GABAergic axons in chronically epileptic rats. Both parvalbumin-and somatostatin-immunoreactive interneuron numbers and the frequency of both fast-and slow-rising GABA A receptor-mediated mIPSCs were reduced, suggesting that loss of inhibitory synaptic input to granule cells occurred at both proximal/somatic and distal/dendritic sites. Reduced granule cell inhibition in the temporal dentate gyrus preceded the onset of spontaneous recurrent seizures by days to weeks, so it may contribute, but is insufficient, to cause epilepsy.

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“…Particular to neuropeptides, mRNA levels have been shown to increase at different rates and to be modulated by several effectors that interact in a given cell (second messengers, hormones, crosstalk among them, and so forth). Enhanced biosynthesis of several peptides, such as proenkephalin, somatostatin, and TRH, upon kindling stimulation has been demonstrated by the increased levels of their corresponding mRNAs (13,21,34). TRH mRNA increase was observed only after behavioral stage V by some investigators (22,23), whereas others detected it at earlier stages (21).…”

Section: P De Gortari Et Almentioning

confidence: 99%

“…Electrophysiological changes occur during kindling development, such as increases in the duration and frequency of local afterdischarges (AD) and of interictal spikes (2,3) and a progressive enhancement of cortical and subcortical AD propagation (4). Several chemical (5)(6)(7)(8)(9)(10)(11)(12)(13) and structural modifications (14)(15)(16) occur in brain regions reported to be particularly susceptible to seizures. Once kindling is established, the animal exhibits a long-lasting diminution of convulsive thresh-old and occasional spontaneous seizures.…”

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confidence: 99%

Brain Thyrotropin‐Releasing Hormone Content Varies Through Amygdaloid Kindling Development According to Afterdischarge Frequency and Propagation

et al. 1998

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Summary:Purpose: Thyrotropin-releasing hormone (TRH), present in extra hypothalamic brain areas, has been proposed to have neuromodulatory functions and to be susceptible to change by electrical stimulation paradigms. We measured TRH concentrations of several brain areas during kindling development before its establishment and determined whether the changes detected in TRH levels were related to the behavioral stages of kindling, the number of stimulations required to reach these stages and, with the electrophysiological parameters characteristic of this paradigm (amygdaloid afterdischarge (AD) frequency, duration, and propagation).Methods: Male Wistar rats were implanted stereotaxically with indwelling bipolar electrodes in the basolateral nucleus of the amygdala and with two stainless-steel electrodes epidurally in frontal cortex. Amygdaloid kindling was induced by daily electrical stimulation; AD frequency and duration were recorded and analyzed throughout the development of kindling. TRH was extracted from several regions and quantified by radioimmunoassay (RIA).Results: Modifications in TRH concentrations were detected, depending on the region assayed, from stage I1 of kindling. A positive correlation was noted between the levels of TRH and the frequency and propagation of AD, but not with the number of stimulations. The rate of change in TRH concentration in relation to AD frequency or duration was highest in frontal cortex followed by hippocampus and amygdala. Conclusions: A graded response was noted in the increase in TRH concentration dependent on the increase of AD frequency and propagation. The rate of response correlated with the region's epileptogenic susceptibility.

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Alterations in somatostatin and proenkephalin mRNA in response to a single amygdaloid stimulation versus kindling

Cited by 41 publications

References 19 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

Reduced Inhibition of Dentate Granule Cells in a Model of Temporal Lobe Epilepsy

Brain Thyrotropin‐Releasing Hormone Content Varies Through Amygdaloid Kindling Development According to Afterdischarge Frequency and Propagation

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