Neuropeptide-containing neurons in the endopiriform region of the rat: morphology and colocalization with calcium-binding proteins and nitric oxide synthase

Kowiański, Przemysław; Moryś, Janusz; Wójcik, Sławomir; Dziewíatkowski, J; Łuczyńska, Anna; Spodnik, Edyta; Timmermans, Jean‐Pierre

doi:10.1016/j.brainres.2003.10.020

Cited by 25 publications

(20 citation statements)

References 55 publications

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“…In the adult rodent claustrum, each calcium-binding protein appears mainly localized to a differ-ent cell population, and part of these cells are likely GABAergic interneurons (Druga et al, 1993;Real et al, 2003a;Kowianski et al, 2004). Our results indicate that each calcium-binding protein shows a different temporal and spatial pattern of development.…”

Section: Discussionmentioning

confidence: 63%

“…To correlate the core/ shell compartments identified in our previous study with the different histogenetic parts of the claustrum, we compare the expression of calcium-binding proteins with that of Cad8, a marker of the dorsolateral claustrum. Finally, because calcium-binding proteins are expressed in subsets of GABAergic neurons in the claustrum (Druga et al, 1993;Real et al, 2003a;Kowianski et al, 2004), we also analyzed the expression of the inhibitory neurotransmitter GABA during claustral development and discussed the possible subpallial origin of these cells. Considering that the claustral complex is involved in propagation of epileptiform activity from the amygdala (Kudo and Wada, 1990;Hoffman and Haberly, 1996;Wada and Kudo, 1997;Mohapel et al, 2001;Zhang et al, 2001), and that the severity of seizures is related to the inhibitory GABAergic activity (Stevens et al, 1988), we hope that our data will help for future studies on the role of each specific GABAergic subpopulation in the development of temporal lobe epilepsies.…”

Section: Indexing Terms: Calcium-binding Proteins; Dorsal Claustrum; mentioning

confidence: 99%

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Embryonic and postnatal development of GABA, calbindin, calretinin, and parvalbumin in the mouse claustral complex

et al. 2004

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We analyzed the development of immunoreactive expression patterns for the neurotransmitter gamma-aminobutyric acid (GABA) and the calcium-binding proteins calbindin, calretinin, and parvalbumin in the embryonic and postnatal mouse claustral complex. Each calcium-binding protein shows a different temporal and spatial pattern of development. Calbindin-positive cells start to be seen very early during embryogenesis and increase dramatically until birth, thus becoming the most abundant cell type during embryonic development, especially in the ventral pallial part of the claustrum. The distribution of calbindin neurons throughout the claustrum during embryonic development partly parallels that of GABA neurons, suggesting that at least part of the calbindin neurons of the claustral complex are GABAergic and originate in the subpallium. Parvalbumin cells, on the other hand, start to be seen only postnatally, and their number then increases while the density of calbindin neurons decreases. Based on calretinin expression in axons, the core/shell compartments of the dorsal claustrum start to be clearly seen at embryonic day 18.5 and may be related to the development of the thalamoclaustral input. Comparison with the expression of Cadherin 8, a marker of the developing dorsolateral claustrum, indicates that the core includes a central part of the dorsolateral claustrum, whereas the shell includes a peripheral area of the dorsolateral claustrum, plus the adjacent ventromedial claustrum. The present data on the spatiotemporal developmental patterns of several subtypes of GABAergic neurons in the claustral complex may help for future studies on temporal lobe epilepsies, which have been related to an alteration of the GABAergic activity.

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Section: Discussionmentioning

confidence: 63%

Section: Indexing Terms: Calcium-binding Proteins; Dorsal Claustrum; mentioning

confidence: 99%

Embryonic and postnatal development of GABA, calbindin, calretinin, and parvalbumin in the mouse claustral complex

et al. 2004

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“…Conversely, calretinin immunoreactive neurons are present in the endopiriform nucleus where parvalbumin neurons are few or absent [Paxinos et al, 1999]. Colocalization of calcium-binding proteins with somatostatin, nitric oxide synthase, neuropeptide Y and vasoactive intestinal peptide has been found in the rodent endopiriform nucleus [Kowianski et al, 2004]. Claustral neurons have also been reported to share immunoreactivity to latexin with adjacent cortical regions [Arimatsu et al, 1999].…”

Section: Introductionmentioning

confidence: 99%

“…The insular claustrum and endopiriform nucleus contain populations of projection neurons with polymorphous perikarya and spiny dendrites [Brand, 1981;LeVay and Sherk, 1981] some of which may be NADPH-diaphorase positive [Hinova-Palova et al, 1997], as well as interneurons [Braak and Braak, 1982] which are immunoreactive for calcium binding proteins [Druga et al, 1993;Kowianski et al, 2004] and are characterized by round or ovoid perikarya and aspinous, beaded dendrites [Reynhout and Baizer, 1999]. In some species complementarity of immunoreactivity for parvalbumin (Pv) and calretinin (Cr) has been observed in the insular claustrum, with a strongly Pv immunoreactive region corresponding in position within the insular claustrum to a Cr immunonegative region [Druga et al, 1993;Paxinos et al, 1999;Real et al, 2003].…”

Section: Introductionmentioning

confidence: 99%

The Claustrum Is Not Missing from All Monotreme Brains

2004

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Many authors have reported that the claustrum, which comprises the insular claustrum and the endopiriform nucleus, is missing from the monotreme forebrain. We used Nissl and myelin staining in conjunction with enzyme histochemistry for acetylcholinesterase and immunohistochemistry for parvalbumin, calbindin, calretinin and tyrosine hydroxylase to examine the brains of two monotremes, the short-beaked echidna (Tachyglossus aculeatus) and the platypus (Ornithorhynchus anatinus). We found that although the insular claustrum is a small structure in the echidna brain, it is nevertheless clearly present as loosely clustered neurons embedded in the white matter ventrolateral to the putamen and deep to the piriform and entorhinal cortices. Neurons in this region share the chemical features of the adjacent cortex (presence of a similar proportion of parvalbumin immunoreactive neurons and minimal activity for acetylcholinesterase and tyrosine hydroxylase), unlike the adjacent putamen and ventral pallidum. A putative endopiriform nucleus can be identified in the interior of the piriform lobe of the echidna as calretinin immunoreactive neurons embedded within the white matter. The situation is much less clear in the platypus, but our data suggest that there may be an insular claustrum deep to frontal cortex, separated from layer VI by only a thin layer of white matter. We could not identify an endopiriform nucleus in our platypus material. Our findings indicate that presence of the claustrum cannot be considered a feature confined to therian mammals and lend weight to arguments that this structure was present in the ancestral mammalian brain.

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“…NPY colocalizes with somatostatin, gamma-aminobutric acid (GABA), and nitric oxide synthase (Bidmon et al, 2001a;Kowianski et al, 2004;Kubota et al, 1994), and can modulate neuronal excitability by multiple pre-and postsynaptic mechanisms under both physiological and pathophysiological conditions. In arterial occlusion models of ischemia, variable short-term alterations of NPY expression in perilesional cortex and subcortical structures have been reported (Allen et al, 1995;Cheung et al, 1995;Grimaldi et al, 1990).…”

Section: Introductionmentioning

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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Neuropeptide-containing neurons in the endopiriform region of the rat: morphology and colocalization with calcium-binding proteins and nitric oxide synthase

Cited by 25 publications

References 55 publications

Embryonic and postnatal development of GABA, calbindin, calretinin, and parvalbumin in the mouse claustral complex

Embryonic and postnatal development of GABA, calbindin, calretinin, and parvalbumin in the mouse claustral complex

The Claustrum Is Not Missing from All Monotreme Brains

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

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