Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurons containing the calcium-binding proteins, calbindin or parvalbumin, were studied by immunohistochemistry in the superficial dorsal horn of the rat spinal cord. Calbindin-containing cells were found in laminae I, II and III, being more abundant in laminae I and II. Some of the neurons in lamina I containing calbindin projected to the supraspinal area. Parvalbumin-containing neurons were mainly distributed in laminae IIi and III. Calbindin and parvalbumin were not detected in the same cells. Some 75% of the neurotensin-like immunoreactive neurons contained calbindin, which corresponded to 13% of the calbindin-containing neurons. Calbindin was sometimes found in the same cells with substance P, enkephalin or somatostatin but less frequently (44-46% of the peptide-containing neurons). Parvalbumin was not found together with these peptides. Electron microscopy showed that the immunoreactive products of calbindin or parvalbumin were mostly in the dendrites or cell bodies. Immunoreactive axon terminals were relatively few. In rhizotomized animals, neurons containing one of these proteins in laminae II and III were found to receive direct inputs of primary afferent fibers. These findings indicate that neurons containing these two proteins belong to different subpopulations of dorsal horn neurons. They may be important in primary afferent processing.
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PMID:Calcium-binding proteins calbindin and parvalbumin in the superficial dorsal horn of the rat spinal cord. 224 26

Calcium-binding protein (CaBP) and parvalbumin are two proteins that are expressed in brain and bind calcium in the micromolar range. The immunohistochemical distribution of these two proteins was examined in the basal ganglia of rats and rhesus monkeys. In the striatum, CaBP immunoreactivity is localized to a subset of striatonigral projection neurons; CaBP-positive neurons are distributed in areas containing somatostatin-immunoreactive fibers and not in the complementary areas containing dense mu opiate-receptor binding. These biochemical labels mark, respectively, the matrix and patch compartments of the striatum. Previous studies have shown that striatal matrix neurons project to the substantia nigra pars reticulata, whereas striatal patch neurons project to the substantia nigra pars compacta. Consistent with the restricted localization of CaBP in the matrix projection neurons is the confinement of CaBP-immunoreactive afferent fibers to the pars reticulata. CaBP is also localized to a portion of dopaminergic and a few nondopaminergic neurons in the substantia nigra pars compacta and in most dopaminergic neurons in the ventral tegmental area. Parvalbumin immunoreactivity is localized to a subset of substantia nigra pars reticulata neurons and their axons. In the lateral striatum, some medium-sized aspiny interneurons are also parvalbumin immunoreactive. The distinct distributions of CaBP and parvalbumin in the basal ganglia are discussed in terms of their possible roles as intracellular calcium buffer systems related to the physiologic response properties of the neurons in which they are contained.
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PMID:The neostriatal mosaic: compartmental distribution of calcium-binding protein and parvalbumin in the basal ganglia of the rat and monkey. 390 55

Different subpopulations of GABA neurons containing the neuropeptides somatostatin and neuropeptide Y, and the calcium binding protein parvalbumin were studied by immunocytochemistry using light and electron microscopy in the dorsomedial cortex of the lizard Psammodromus algirus to investigate the connectivity of different subsets of GABA neurons in the lizard dorsomedial cortical circuitry and to compare cortical regions of reptiles and mammals. GABA neurons were classified into different subsets by using the peroxidase anti-peroxidase immunohistochemical method on adjacent Araldite-embedded semithin sections. GABA neurons in the dorsomedial cortex fall into three major subsets: 1) neurons with somatostatin (and neuropeptide Y), which accounted for about 44% of the GABA population; 2) neurons with parvalbumin, which accounted for about 13% of the GABA neurons; and 3) neurons without parvalbumin or neuropeptides, which represented 40% of all GABA cells. This division of GABA neurons in non-overlapping subpopulations of neuropeptide- and parvalbumin-containing cells is similar to that found in the mammalian hippocampal formation. On the basis of the nerve terminal fields, somatostatin- and parvalbumin-immunoreactive neuronal populations appear to be functionally different, acting on different portions of the projection neurons. Parvalbumin-immunoreactive neurons inhibit the pyramidal neurons at the cell body level, whereas somatostatin-immunoreactive neurons inhibit them on distal dendrites. The results of the present study add more similarities between the lizard dorsomedial cortex and parts of the mammalian hippocampus.
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PMID:Subpopulations of GABA neurons containing somatostatin, neuropeptide Y, and parvalbumin in the dorsomedial cortex of the lizard Psammodromus algirus. 790 63

The morphology, fine structure, and degree of colocalization with GABA, somatostatin, and neuropeptide Y of parvalbumin-containing cells were studied with immunocytochemistry in the cerebral cortex of the lizard Podarcis hispanica. Parvalbumin-containing cells make up a morphologically heterogeneous population of spine-free neurons, displaying the morphological features of nonprincipal cells previously described in Golgi studies. Electron microscopically, parvalbumin-immunoreactive cell bodies are similar in all cortical areas and layers. The perisomatic input is moderate in number, and boutons with either round clear vesicles or flattened vesicles were observed making asymmetric or symmetric synaptic contacts, respectively. Parvalbumin-immunoreactive dendrites are smooth and almost completely covered with synaptic boutons of different types, most of which establish asymmetric contacts. Parvalbumin-immunoreactive boutons are concentrated around cell bodies of principal cells. They are large, containing abundant mitochondria and small pleomorphic vesicles, and establishing symmetric synaptic contacts with somata, proximal dendritic shafts, and axon initial segments of principal cells. Colocalization studies revealed that all the parvalbumin-containing cells are GABA-immunoreactive, representing only a fraction of the GABA-immunopositive cell population, and that parvalbumin- and peptide- (somatostatin and neuropeptide Y) containing cells show a negligible overlap. These results demonstrate that in the cerebral cortex of the lizard Podarcis hispanica, parvalbumin-containing cells represent a subset of nonprincipal GABAergic neurons largely involved in perisomatic inhibition, which are different from the peptide-containing cells, and suggest that they may include both axosomatic and axoaxonic cells.
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PMID:Parvalbumin-containing neurons in the cerebral cortex of the lizard Podarcis hispanica: morphology, ultrastructure, and coexistence with GABA, somatostatin, and neuropeptide Y. 790 22

Physiological and morphological properties of large non-pyramidal cells immunoreactive for cholecystokinin, parvalbumin or somatostatin were investigated in vitro in the frontal cortex of 18-22-day-old rats. These three peptides were expressed in separate populations including large cells. Cholecystokinin cells and parvalbumin cells made boutons apposed to other cell bodies, but differed in their firing patterns in response to depolarizing current pulses. Parvalbumin cells belonged to fast-spiking cells. Parvalbumin fast-spiking cells also included chandelier cells. In contrast, cholecystokinin cells were found to be regular-spiking non-pyramidal cells or burst-spiking non-pyramidal cells with bursting activity from hyperpolarized potentials (two or more spikes on slow depolarizing humps). Large somatostatin cells belonged to the regular-spiking non-pyramidal category and featured wide or ascending axonal arbors (wide arbor cells and Martinotti cells) which did not seem to be apposed to the somata so frequently as large cholecystokinin and parvalbumin cells. For electron microscopic observations, another population of eight immunohistochemically-uncharacterized non-pyramidal cells were selected: (i) five fast spiking cells including one chandelier cell which are supposed to contain parvalbumin, and (ii) three large regular-spiking non-pyramidal cells with terminals apposed to somata, which are not considered to include somatostatin cells, but some of which may belong to cholecystokinin cells. The fast-spiking cells other than a chandelier cell and the large regular-spiking non-pyramidal cells made GABA-positive synapses on somata (4% and 12% of the synapses in two small to medium fast-spiking cells, 22% and 35% of the synapses in two large fast-spiking cells, and 10%, 18% and 37% of the synapses in three large regular-spiking non-pyramidal cells). A few terminals of the fast-spiking and regular-spiking non-pyramidal cells innervated GABAergic cells. About 30% of the fast-spiking cell terminals innervated spines, but few of the regular-spiking non-pyramidal cell terminals did. A fast-spiking chandelier cell made GABA-positive synapses on GABA-negative axon initial segments. These results suggest that large GABAergic cells are heterogeneous in neuroactive substances, firing patterns and synaptic connections, and that cortical cells receive heterogeneous GABAergic somatic inputs.
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PMID:Neurochemical features and synaptic connections of large physiologically-identified GABAergic cells in the rat frontal cortex. 963 65

1. Inhibitory postsynaptic currents (IPSCs) evoked in CA1 pyramidal cells (n = 46) by identified interneurones (n = 43) located in str. oriens were recorded in order to compare their functional properties and to determine the effect of synapse location on the apparent IPSC kinetics as recorded using somatic voltage clamp at -70 mV and nearly symmetrical [Cl-]. 2. Five types of visualised presynaptic interneurone, oriens-lacunosum moleculare (O-LMC), basket (BC), axo-axonic (AAC), bistratified (BiC) and oriens-bistratified (O-BiC) cells, were distinguished by immunocytochemistry and/or synapse location using light and electron microscopy. 3. Somatostatin immunoreactive O-LMCs, innervating the most distal dendritic shafts and spines, evoked the smallest amplitude (26 +/- 10 pA, s.e.m., n = 8) and slowest IPSCs (10-90 % rise time, 6.2 +/- 0.6 ms; decay, 20.8 +/- 1.7 ms, n = 8), with no paired-pulse modulation of the second IPSC (93 +/- 4 %) at 100 ms interspike interval. In contrast, parvalbumin-positive AACs evoked larger amplitude (308 +/- 103 pA, n = 7) and kinetically faster (rise time, 0.8 +/- 0.1 ms; decay 11.2 +/- 0.9 ms, n = 7) IPSCs showing paired-pulse depression (to 68 +/- 5 %, n = 6). Parvalbumin- or CCK-positive BCs (n = 9) terminating on soma/dendrites, BiCs (n = 4) and O-BiCs (n = 7) innervating dendrites evoked IPSCs with intermediate kinetic parameters. The properties of IPSCs and sensitivity to bicuculline indicated that they were mediated by GABAA receptors. 4. In three cases, kinetically complex, multiphasic IPSCs, evoked by an action potential in the recorded basket cells, suggested that coupled interneurones, possibly through electrotonic junctions, converged on the same postsynaptic neurone. 5. The population of O-BiCs (4 of 4 somatostatin positive) characterised in this study had horizontal dendrites restricted to str. oriens/alveus and innervated stratum radiatum and oriens. Other BiCs had radial dendrites as described earlier. The parameters of IPSCs evoked by BiCs and O-BiCs showed the largest cell to cell variation, and a single interneurone could evoke both small and slow as well as large and relatively fast IPSCs. 6. The kinetic properties of the somatically recorded postsynaptic current are correlated with the innervated cell surface domain. A significant correlation of rise and decay times for the overall population of unitary IPSCs suggests that electrotonic filtering of distal responses is a major factor for the location and cell type specific differences of unitary IPSCs, but molecular heterogeneity of postsynaptic GABAA receptors may also contribute to the observed kinetic differences. Furthermore, domain specific differences in the short-term plasticity of the postsynaptic response indicate a differentiation of interneurones in activity-dependent responses.
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PMID:Cell surface domain specific postsynaptic currents evoked by identified GABAergic neurones in rat hippocampus in vitro. 1074 79

The functional role of the calcium-binding proteins parvalbumin, calretinin, and calbindin D-28k for epileptogenesis and long-term seizure-related alterations of the hippocampal formation was assessed in single- and double-knockout mice, using a kainate model of mesial temporal lobe epilepsy. The effects of a unilateral intrahippocampal injection of kainic acid were assessed at one day, 30 days, and four months post-injection, using various markers of GABAergic interneurons (GABA-transporter type 1, GABA(A)-receptor alpha1 subunit, calretinin, calbindin D-28k, somatostatin, and neuropeptide Y). Parvalbumin-deficient, parvalbumin/calbindin-deficient, and parvalbumin/calretinin-deficient mice exhibited no difference in cytoarchitecture of the hippocampal formation and in the number, distribution, or morphology of interneurons compared to wild-type mice. Likewise, mutant mice were not more vulnerable to acute kainate-induced excitotoxicity or to long-term effects of recurrent focal seizures, and exhibited the same pattern of neurochemical alterations (e.g., bilateral induction of neuropeptide Y in granule cells) and morphogenic changes (enlargement and dispersion of dentate gyrus granule cells) as wild-type animals. Quantification of interneurons revealed no significant difference in neuronal vulnerability among the genotypes.These results indicate that the calcium-binding proteins investigated here are not essential for determining the neurochemical phenotype of interneurons. Furthermore, they are not protective against kainate-induced excitotoxicity in this model, and do not appear to modulate the overall level of excitability of the hippocampus. Finally, seizure-induced changes in gene expression in granule cells, which normally express high levels of calcium-binding proteins, apparently were not affected by the gene deletions analysed.
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PMID:Neurodegenerative and morphogenic changes in a mouse model of temporal lobe epilepsy do not depend on the expression of the calcium-binding proteins parvalbumin, calbindin, or calretinin. 1077 38

The development of spontaneous limbic seizures was investigated in a rat model in which electrical tetanic stimulation of the angular bundle was applied for up to 90 min. This stimulation produced behavioural and electrographic seizures that led to a status epilepticus (SE) in most rats (71%). Long-term EEG monitoring showed that the majority of the rats (67%) that underwent SE, displayed a progressive increase of seizure activity once the first seizure was recorded after a latent period of about 1 week. The other SE rats (33%) did not show this progression of seizure activity. We investigated whether these different patterns of evolution of spontaneous seizures could be related to differences in cellular or structural changes in the hippocampus. This was the case regarding the following changes. (i) Cell loss in the hilar region: in progressive SE rats this was extensive and bilateral whereas in nonprogressive SE rats it was mainly unilateral. (ii) Parvalbumin and somatostatin-immunoreactive neurons: in the hilar region these were almost completely eliminated in progressive SE rats but were still largely present unilaterally in nonprogressive SE rats. (iii) Mossy fibre sprouting: in progressive SE rats, extensive mossy fibre sprouting was prominent in the inner molecular layer. In nonprogressive SE rats, mossy fibre sprouting was also present but less prominent than in progressive SE rats. Although mossy fibre sprouting has been proposed to be a prerequisite for chronic seizure activity in experimental temporal lobe epilepsy, the extent of hilar cell death also appears to be an important factor that differentiates between whether or not seizure progression will occur.
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PMID:Progression of spontaneous seizures after status epilepticus is associated with mossy fibre sprouting and extensive bilateral loss of hilar parvalbumin and somatostatin-immunoreactive neurons. 1120 1

Parvalbumin-containing fast-spiking interneurons in the cerebral cortex exhibit widespread electrical coupling, as do somatostatin-containing low-threshold spiking interneurons. Besides the classical neurotransmitter gamma-aminobutyric acid, these cortical interneurons may also release various neuropeptides including substance P (SP), as well as the freely diffusible messenger nitric oxide (NO). To investigate whether these two networks of interneurons might interact via these nonclassical messengers, we performed immunocytochemistry for SP and NO signaling pathways in rat somatic sensory cortex. SP was found in a subset of parvalbumin-positive cells concentrated in layers IV and V, whereas its receptor, NK1, was found in a subset of somatostatin-containing neurons (and also, at much lower levels, in a disjoint subset of parvalbumin-containing neurons). Only 4% of SP-containing axon terminals were apposed to NK1-positive dendrites, suggesting that in the cerebral cortex, SP may act predominantly as a paracrine neuromediator. Nitric oxide synthase-I (NOS-I), the synthetic enzyme for NO, was found almost exclusively in NK1-positive neurons; 95% of intensely somatostatin/NK1-positive neurons were also positive for NOS-I, and 94% of NOS-positive neurons were also positive for NK1. Immunoreactivity for soluble guanylyl cyclase (the NO receptor) was at high levels in the apical dendrites of layer V pyramidal neurons and in parvalbumin/SP-positive neurons. These data point to a novel reciprocal chemical interaction between two inhibitory networks in the rat neocortex.
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PMID:Substance P and nitric oxide signaling in cerebral cortex: anatomical evidence for reciprocal signaling between two classes of interneurons. 1174 51

The release of glutamate and GABA is modulated by presynaptic metabotropic glutamate receptors (mGluRs). We used immunocytochemical methods to define the location of the group III receptor mGluR7a in glutamatergic and GABAergic terminals innervating GABAergic interneurons and pyramidal cells. Immunoreactivity for mGluR7a was localized in the presynaptic active zone of both identified GABAergic and presumed glutamatergic terminals. Terminals innervating dendritic spines showed a variable level of receptor immunoreactivity, ranging from immunonegative to strongly immunopositive. The frequency of strongly mGluR7a positive terminals innervating the soma and dendrites of mGluR1 alpha/somatostatin-expressing interneurons was very high relative to other neurons. On dendrites that received mGluR7a-enriched glutamatergic innervation, at least 80% of GABAergic terminals were immunopositive for mGluR7a. On such dendrites virtually all (95%) vasoactive intestinal polypeptide (VIP) positive (GABAergic) terminals were enriched in mGluR7a. The targets of VIP/mGluR7a-expressing terminals were mainly (88%) mGluR1 alpha-expressing interneurons, which were mostly somatostatin immunopositive. Parvalbumin positive terminals were immunonegative for mGluR7a. Some parvalbumin immunoreactive dendrites received strongly mGluR7a positive terminals. The subcellular location, as well as the cell type and synapse-specific distribution of mGluR7a in isocortical neuronal circuits, is homologous to its distribution in the hippocampus. The specific location of mGluR7a in the presynaptic active zone of both glutamatergic and GABAergic synapses may be related to the proximity of calcium channels and the vesicle fusion machinery. The enrichment of mGluR7a in the main GABAergic, as well as in the glutamatergic, innervation of mGluR1 alpha/somatostatin-expressing interneurons suggests that their activation is under unique regulation by extracellular glutamate.
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PMID:Enrichment of mGluR7a in the presynaptic active zones of GABAergic and non-GABAergic terminals on interneurons in the rat somatosensory cortex. 1218 95


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