Neuropeptide Y: emerging evidence for a functional role in seizure modulation

Vezzani, Annamaria; Sperk, Günther; Colmers, William F.

doi:10.1016/s0166-2236(98)01284-3

Cited by 446 publications

(336 citation statements)

References 61 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). In the present study, epileptic animals demonstrated alterations in NPY IR in both cortex and hippocampus; however, the significance of these changes is not known at present.…”

Section: Discussioncontrasting

confidence: 47%

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: Discussioncontrasting

confidence: 47%

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

Kharlamov

Kelly

2007

Brain Research

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“…hDG-hilus of the dentate gyrus, g-granular layer of DG. Śmiałowska et al, 1996;Vezzani et al, 1999). Thus, the increase in NPY mRNA observed in our study after L-SOP and L-CCG-I seems to be the consequence of the enhanced activation of NPY neurons by Glu.…”

Section: Anxiolytic Effect Of Intrahippocampal Mglur Ligands and Npy supporting

confidence: 53%

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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“…Intracerebroventricular (ICV) administration of NPY stimulates food intake (Clark et al 1985;Levine and Morley 1984;Stanley and Leibowitz 1984), modulates cognition (Flood et al 1987;Redrobe et al 1999), inhibits neuronal excitability (Colmers and Bleakman 1994) and has anticonvulsant effects (Vezzani et al 1999). NPY modulates the secretion of various hypothalamic neuropeptides, stimulates the corticotrophic axis (Krysiak et al 1999;Small et al 1997) and has potent inhibitory effects on gonadotrophic and somatotrophic axes (Catzeflis et al 1993).…”

Section: The Present Study Was Undertaken To Investigate the Possiblementioning

confidence: 99%

The Neuropeptide Y (NPY) Y1 Receptor Subtype Mediates NPY-induced Antidepressant-like Activity in the Mouse Forced Swimming Test

Redrobe

Dumont

Fournier

et al. 2002

Neuropsychopharmacology

184

123

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The present study was undertaken to investigate the possible antidepressant-like effects of neuropeptide Y (NPY)inNeuropeptide Y (NPY) is a 36-amino acid peptide that is widely distributed in the central nervous system (CNS). Intracerebroventricular (ICV) administration of NPY stimulates food intake (Clark et al. 1985;Levine and Morley 1984;Stanley and Leibowitz 1984), modulates cognition (Flood et al. 1987;Redrobe et al. 1999), inhibits neuronal excitability (Colmers and Bleakman 1994) and has anticonvulsant effects (Vezzani et al. 1999). NPY modulates the secretion of various hypothalamic neuropeptides, stimulates the corticotrophic axis (Krysiak et al. 1999;Small et al. 1997) and has potent inhibitory effects on gonadotrophic and somatotrophic axes (Catzeflis et al. 1993). In addition, NPY is thought to play a role in the pathophysiology of certain mood disorders and in the mechanism of action of antidepressant drugs (Heilig et al. 1988;Caberlotto et al. 1998 (Michel et al. 1998).Clinical studies have demonstrated decreased NPY levels in the cerebrospinal fluid (CSF) (Heilig and Widerlov 1990) and plasma (Nilsson et al. 1996) of depressed patients, when compared with healthy control subjects. In addition, NPY levels have been shown to be negatively correlated to scores of anxiety in clinically depressed patients (Heilig and Widerlov 1990), suggesting a possible link between low levels of NPY and predisposition to anxiety-related or stress-induced depression.Moreover, pre-clinical studies have shown that electroconvulsive shock stimulation increased NPY gene expression (Heilig et al. 1988), as well as the expression of NPY mRNA in distinct brain regions in rats (Caberlotto et al. 1998;Mikkelsen et al. 1994). In addition, chronic antidepressant treatment has been shown to alter NPY and NPY Y 1 -type receptor mRNA levels (Caberlotto et al. 1998), and to reduce NPY Y 2 -type receptor densities in certain brain regions (Widdowson and Halaris 1991). Interestingly, NPY-like immunoreactivity and NPY Y 1 -type receptor binding sites were shown to be decreased or increased, depending on the brain region studied, in the recently developed Flinders Sensitive Line (FSL) rats (Caberlotto et al. 1999), a purported genetic animal model of depression (Overstreet 1993;Overstreet et al. 1995).Additional evidence of a role for NPY in depressive disorders is found in studies using the olfactory bulbectomized (OB) rat model of depression. Sub-chronic ICV administration of NPY attenuated the increase in ambulation, rearing, grooming and defecation scores consistently found when OB animals are tested in the open field (Song et al. 1996). Treatment with NPY also increased noradrenaline (NA) and serotonin (5-HT) levels in the amygdala and hypothalamus (Song et al. 1996). In addition, NPY reversed the supression of lymphocyte proliferation seen following OB (Song et al. 1994). A decrease in lymphocyte proliferation has also been reported in depressed patients (Kronfol and House 1989). Another study demonstrated that OB caused long term...

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Neuropeptide Y: emerging evidence for a functional role in seizure modulation

Cited by 446 publications

References 61 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

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

The Neuropeptide Y (NPY) Y1 Receptor Subtype Mediates NPY-induced Antidepressant-like Activity in the Mouse Forced Swimming Test

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