Enhanced Rate of Expression and Biosynthesis of Neuropeptide Y After Kainic Acid‐Induced Seizures

Bellmann, Romuald; Widmann, Rudolf; Olenik, Claudia; Meyer, Dieter; Maas, Dagmar; Marksteiner, Josef; Sperk, Günther

doi:10.1111/j.1471-4159.1991.tb08181.x

Cited by 116 publications

(37 citation statements)

References 24 publications

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“…NPY expression was found markedly increased in hilar GABAergic interneurons, granule cells and sprouted mossy fibers (Bellmann et al, 1991;Chafetz et al, 1995;Lurton and Cavalheiro, 1997;Scharfman et al, 1999Scharfman et al, , 2002Sperk et al, 1992;Takahashi et al, 2000;Vezzani et al, 1996). NPY in the dentate gyrus can influence synaptic transmission and neurogenesis, demonstrates remarkable plasticity after seizures (Scharfman and Gray, 2006), and may have an anticonvulsive action (Furtinger et al, 2001;Klapstein and Colmers, 1997;Vezzani et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Kharlamov

Kelly

2007

Brain Research

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This study characterized morphological changes in the cortex and hippocampus of Sprague-Dawley rats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neuropeptide Y (NPY) expression. Animals were lesioned in the left sensorimotor cortex and compared with age-matched naïve and sham-operated controls by immunohistochemical techniques at 1, 3, 7, and 180 days post-lesioning (DPL). NPY immunostaining was assessed by light microscopy and quantified by the optical fractionator technique using unbiased stereological methods. At 1, 3, and 7 DPL, the number of NPY-positive somata in the lesioned cortex was increased significantly compared to controls and the contralateral cortex. At 180 DPL, lesioned epileptic animals with frequent seizure activity demonstrated significant increases of NPY expression in the cortex, CA1, CA3, hilar interneurons, and granule cells of the dentate gyrus. In addition to NPY immunostaining, neuronal degeneration, cell death/cell loss, and astroglial response were assessed with cell-specific markers. Nissl and NeuN staining showed reproducible infarctions at each investigated time point. FJB-positive somata were most abundant in the infarct core at 1 DPL, decreased markedly at 3 DPL, and virtually absent by 7 DPL. Activated astroglia were detected in the cortex and hippocampus following lesioning and the development of seizure activity. In summary, NPY protein expression and morphological changes following cortical photothrombosis were time-, region-and pathologic state-dependent. Alterations in NPY expression may reflect reactive or compensatory responses of the rat brain to acute infarction and to the development and expression of epileptic seizures.

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Section: Discussionmentioning

confidence: 99%

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Kharlamov

Kelly

2007

Brain Research

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“…It is likely that a major part of transduced prepro-NPY is processed in a conventional way through the regulated secretory pathway into synaptic vesicles by prohormone convertases (Bellmann et al, 1991;Day et al, 1992). Expression of prohormone convertases is indeed upregulated in the brain after kainic acidinduced seizures (Marcinkiewicz et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Anticonvulsant and Antiepileptogenic Effects Mediated by Adeno-Associated Virus Vector Neuropeptide Y Expression in the Rat Hippocampus

Richichi¹,

Lin²,

Stefanin³

et al. 2004

J. Neurosci.

212

170

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Neuropeptide Y (NPY) inhibits seizures in experimental models and reduces excitability in human epileptic tissue. We studied the effect of long-lasting NPY overexpression in the rat hippocampus with local application of recombinant adeno-associated viral (AAV) vectors on acute kainate seizures and kindling epileptogenesis.Transgene expression was significantly increased by 7 d, reached maximal expression by 2 weeks, and persisted for at least 3 months. Serotype 2 AAV vector increased NPY expression in hilar interneurons, whereas the chimeric serotype 1/2 vector caused far more widespread expression, also including mossy fibers, pyramidal cells, and the subiculum. EEG seizures induced by intrahippocampal kainate were reduced by 50 -75%, depending on the vector serotype, and seizure onset was markedly delayed.In rats injected with the chimeric serotype 1/2 vector, status epilepticus was abolished, and kindling acquisition was significantly delayed. Thus, targeted NPY gene transfer provides a potential therapeutic principle for the treatment of drug-resistant partial epilepsies.

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“…Therefore, the antianxiety action of both these compounds is in line with the above-mentioned concept about the role of Glu transmission in anxiety. On the other hand, studies of the interdependence of glutamate and NPY in the hippocampus have shown that glutamatergic activation increases the synthesis and expression of NPY in hippocampal neurons (Schwarzer and Sperk, 1998;Schwarzer et al, 1996;Marksteiner et al, 1990;Bellmann et al, 1991;Bendotti et al, 1991) and that NPY inhibits Glu transmission in this structure (Silva et al, 2005;Tu et al, 2005; Klapstein and Colmers, 1997; Bijak and Śmiałowska, 1995; Figure 6 Photomicrographs showing NPYmRNA expression in emulsion-covered coronal sections from the region of dentate gyrus (DG) of the rat hippocampal formation. An increase in a number of labelled neurons and in grain density over individual neurons is seen after L-SOP (b) and L-CCG-I (c) microinjection in comparison with the control (a).…”

Section: Anxiolytic Effect Of Intrahippocampal Mglur Ligands and Npy mentioning

confidence: 99%

“…It contains numerous NPY interneurons and is rich in mGluRs (Kohler et al, 1986;Redrobe et al, 1999;Dumont et al, 1998). It was revealed that the enhancement of glutamatergic transmission strongly stimulated NPY synthesis and/or increased the content of that peptide in the hippocampus Bellmann et al, 1991;Schwarzer et al, 1996). Thus, it seemed of interest to find out whether anxiolytically active mGluR ligands could regulate NPY neurons in the hippocampal formation and whether such an interaction was engaged in their antianxiety effects.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Intrahippocampal Injection of Group II and III Metobotropic Glutamate Receptor Agonists on Anxiety; the Role of Neuropeptide Y

Śmiałowska

Wierońska

Domin

et al. 2006

Neuropsychopharmacol

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Earlier studies conducted by our group and by other authors indicated that metabotropic glutamatergic receptor (mGluR) ligands might have anxiolytic activity and that amygdalar neuropeptide Y (NPY) neurons were engaged in that effect. Apart from the amygdala, the hippocampus, another limbic structure, also seems to be engaged in regulation of anxiety. It is rich in mGluRs and contains numerous NPY interneurons. In the present study, we investigated the anxiolytic activity of group II and III mGluR agonists after injection into the hippocampus, and attempted to establish whether hippocampal NPY neurons and receptors were engaged in the observed effects. Male Wistar rats were bilaterally microinjected with the group II mGluR agonist (2S,, NPY, the Y1 receptor antagonist BIBO 3304, and the Y2 receptor antagonist BIIE 0246 into the CA1 or dentate area (DG). The effect of those compounds on anxiety was tested in the elevated plus-maze. Moreover, the effects of L-CCG-I and L-SOP on the expression of NPYmRNA in the hippocampus were studied using in situ hybridization method. It was found that a significant anxiolytic effect was induced by L-SOP injection into the CA1 region or by L-CCG-I injection into the DG. The former effect was inhibited by BIBO 3304, the latter by BIIE 0246. NPY itself showed antianxiety action after injection into both structures. In the CA1 area, the effect of NPY was prevented by BIBO 3304, whereas in the DG by BIIE 0246. Both the mGluR agonists L-CCG-I and L-SOP induced a potent increase in NPYmRNA expression in the DG region of the hippocampal formation. The obtained results indicate that group II and III mGluR agonists, L-CCG-I and L-SOP, as well as NPY display anxiolytic activity in the hippocampus, but act differently in the CA1 and DG. It was observed that group III mGluRs and Y1 receptors were engaged in the response in the CA1 area, whereas group II mGluRs and Y2 receptors played a pivotal role in the DG region.

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Enhanced Rate of Expression and Biosynthesis of Neuropeptide Y After Kainic Acid‐Induced Seizures

Cited by 116 publications

References 24 publications

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Anticonvulsant and Antiepileptogenic Effects Mediated by Adeno-Associated Virus Vector Neuropeptide Y Expression in the Rat Hippocampus

The Effect of Intrahippocampal Injection of Group II and III Metobotropic Glutamate Receptor Agonists on Anxiety; the Role of Neuropeptide Y

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