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)

The effects of leukemia inhibitory factor (LIF) on the expression of neurotransmitter synthetase and neuropeptide mRNAs in cultured rat cortical neurons were examined by reverse transcription-polymerase chain reaction. Nociceptin mRNA expression was increased by treatment with 20 or 80 ng/ml LIF for 24 h, but choline acetyl transferase, glutamic acid decarboxylase, enkephalin, dynorphin, substance P, somatostatin and galanin mRNA expression were not altered by LIF. These observations indicated a specific effect of LIF on nociceptin gene regulation in cultured cortical neurons.
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PMID:Leukemia inhibitory factor induces nociceptin mRNA in cultured rat cortical neurons. 1158 57

We have previously demonstrated a 60-80% ischemic loss of somatostatinergic neurons in the dorsal dentate hilus of the rat. However, several studies have failed to demonstrate ischemic loss of GABAergic neurons in hilus, although one study reports that 96% of the somatostatinergic neurons in the dorsal hilus colocalize GABA. In order to understand this paradox, we have now estimated, using unbiased stereology, the total number of neurons immunohistochemically stained against glutamic acid decarboxylase-65 (GAD65) and GAD67 in the dorsal dentate hilus. Rats were divided into groups subjected to either sham operation (n=8) or 8 min of transient global ischemia during systemic hypotension (n=8) and allowed to survive for 7-9 days. Results from cell counts (mean +/- SD) in sham rats demonstrated that the dorsal hilus contains 9,189+/-3,957 GAD65 neurons and 6,991+/-2,784 GAD67 neurons. After ischemia, corresponding cell counts demonstrated 10,216+/-4,866 GAD65 neurons and 10,119+/-5,906 GAD67 neurons, and these results were not significantly different (P>0.05) from results in sham rats. Power analysis of the t-test informs that losses less than 80% are not significant and reflects the excessive variance in our material. For comparison, we estimated a total of 21% ischemic neuron death in the dorsal hilus on cresyl violet-stained sections from other corresponding sham (n=7) and ischemic rats (n=7). This explains why ischemic loss of hilar GABAergic neurons can only be detected by counts of the vulnerable subpopulation colocalizing somatostatin. Our investigation has demonstrated a surprisingly high variation between rats in a number of GAD-immunopositive neurons located in the dorsal dentate hilus, which is related to variations between the individual rats and neurons in their endogenous GAD expression.
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PMID:Stereological cell counts of GABAergic neurons in rat dentate hilus following transient cerebral ischemia. 1171 83

The neurochemical contents of hippocamposeptal projecting nonprincipal neurons were examined in the mouse brain by using retrograde labeling techniques. We used the immunofluorescent multiple labeling method with a confocal laser-scanning microscope. First of all, the hippocamposeptal projecting nonprincipal neurons were glutamic acid decarboxylase 67-immunoreactive (IR), i.e., these hippocamposeptal projecting nonprincipal neurons were immunocytochemically GABAergic in the mouse brain. Next, most (93.0%) of the hippocamposeptal projecting GABAergic neurons were somatostatin-like immunoreactive (SS-LIR). The SS-LIR hippocamposeptal projecting neurons were frequently found in the stratum oriens of the CA1 and CA3 regions, and were also occasionally found in the stratum radiatum, stratum lucidum, and stratum pyramidale of the CA3 region. They were also frequently found in the dentate hilus. On the other hand, at least 40.6% of SS-LIR neurons in the hippocampus projected to the medial septum. Next, 38.0% of hippocamposeptal projecting GABAergic neurons were calbindin D28K (CB)-IR. Although the distribution of the CB-IR hippocamposeptal projecting neurons was generally similar to that of the SS-LIR projecting neurons in Ammon's horn, they were never seen in the dentate hilus. At least 22.1% of CB-IR GABAergic neurons in the hippocampus projected to the medial septum. Furthermore, 5.8% of hippocamposeptal projecting GABAergic neurons were parvalbumin-IR, which were most always found in Ammon's horn. Finally, no hippocamposeptal projecting GABAergic neurons were neuronal nitric oxide synthase-IR nor calretinin-IR. These results indicate that the SS-LIR neurons play a crucial role in the hippocamposeptal projection of the mouse brain, and they are also assumed to be involved in the theta oscillation of the mouse hippocampus.
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PMID:Immunocytochemical characterization of hippocamposeptal projecting GABAergic nonprincipal neurons in the mouse brain: a retrograde labeling study. 1212 84

We previously reported that the pharmacological properties of the hippocampal GABAA receptor and the expression of several subunits are modified during normal ageing. However, correlation between these post-synaptic modifications and pre-synaptic deficits were not determined. To address this issue, we have analysed the mRNA levels of several GABAergic molecular markers in young and old rat hippocampus, including glutamic acid decarboxylase enzymes, parvalbumin, calretinin, somatostatin, neuropeptide Y and vasoactive intestinal peptide (VIP). There was a differential age-related decrease in these interneuronal mRNAs that was inversely correlated with up-regulation of the alpha1 GABA receptor subunit. Somatostatin and neuropeptide Y mRNAs were most frequently affected (75% of the animals), then calretinin and VIP mRNAs (50% of the animals), and parvalbumin mRNA (25% of the animals) in the aged hippocampus. This selective vulnerability was well correlated at the protein/cellular level as analysed by immunocytochemistry. Somatostatin interneurones, which mostly innervate principal cell distal dendrites, were more vulnerable than calretinin interneurones, which target other interneurones. Parvalbumin interneurones, which mostly innervate perisomatic domains of principal cells, were preserved. This age-dependent differential reduction of specific hippocampal inteneuronal subpopulations might produce functional alterations in the GABAergic tone which might be compensated, at the post-synaptic level, by up-regulation of the expression of the alpha1 GABAA receptor subunit.
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PMID:Rat hippocampal GABAergic molecular markers are differentially affected by ageing. 1267 13

Rats treated with iminodipropionitrile develop a neurobehaviour syndrome with dyskinesia. Searching for the molecular correlates, we have examined the expression of selected genes involved in neurotransmission in motor regions using hybridization histochemistry. Frontal cortical and thalamic vasoactive intestinal peptide (VIP) expression, and striatal dynorphin, enkephalin (ENK) and substance P expression were increased. No change in cortical cholecystokinin (CCK), ENK, glutamic acid decarboxylase (GAD) and somatostatin (SRIF) expression, in striatal GAD, SRIF, nitric oxide synthase (NOS) and guanylate cyclase expression, and in thalamic CCK, GAD and thyrotropin-releasing hormone expression was found. NOS expression in the subthalamic nucleus as well as tyrosine hydroxylase, GAD and CCK expression in the substantia nigra were unchanged. These results confirm the involvement of striatal projection neurons in dyskinesia and suggest a novel role for VIP.
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PMID:Expression of neurotransmitter genes in motor regions of the dyskinetic rat after iminodipropionitrile. 1286 38

Gamma-aminobutyric acid (GABA)ergic neurons in the central nervous system regulate the activity of other neurons and play a crucial role in information processing. To assist an advance in the research of GABAergic neurons, here we produced two lines of glutamic acid decarboxylase-green fluorescence protein (GAD67-GFP) knock-in mouse. The distribution pattern of GFP-positive somata was the same as that of the GAD67 in situ hybridization signal in the central nervous system. We encountered neither any apparent ectopic GFP expression in GAD67-negative cells nor any apparent lack of GFP expression in GAD67-positive neurons in the two GAD67-GFP knock-in mouse lines. The timing of GFP expression also paralleled that of GAD67 expression. Hence, we constructed a map of GFP distribution in the knock-in mouse brain. Moreover, we used the knock-in mice to investigate the colocalization of GFP with NeuN, calretinin (CR), parvalbumin (PV), and somatostatin (SS) in the frontal motor cortex. The proportion of GFP-positive cells among NeuN-positive cells (neocortical neurons) was approximately 19.5%. All the CR-, PV-, and SS-positive cells appeared positive for GFP. The CR-, PV, and SS-positive cells emitted GFP fluorescence at various intensities characteristics to them. The proportions of CR-, PV-, and SS-positive cells among GFP-positive cells were 13.9%, 40.1%, and 23.4%, respectively. Thus, the three subtypes of GABAergic neurons accounted for 77.4% of the GFP-positive cells. They accounted for 6.5% in layer I. In accord with unidentified GFP-positive cells, many medium-sized spherical somata emitting intense GFP fluorescence were observed in layer I.
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PMID:Green fluorescent protein expression and colocalization with calretinin, parvalbumin, and somatostatin in the GAD67-GFP knock-in mouse. 1457 80

Opioids are thought to control the excitability of hippocampal principal neurons indirectly by inhibiting GABAergic interneurons. However, direct inhibition of hippocampal principal neurons by opioids has also been reported. To understand better the neuromodulatory role of opioids in rat hippocampal circuits, we analyzed types of micro- and delta-opioid receptor (MOR, DOR)-expressing hippocampal neurons. Most MOR-immunoreactive neurons in the granular and pyramidal cell layers exhibited multipolar morphologies characteristic of GABAergic neurons. Virtually all neurons in the hippocampal formation expressing high MOR mRNA levels cocontained the mRNA for glutamic acid decarboxylase (GAD). Most parvalbumin-, several calretinin-, and several pre-proenkephalin-containing neurons expressed the MOR gene in the hippocampal formation. Expression of high DOR mRNA levels was restricted to GAD-positive neurons in the principal cell layers, oriens layer and hilus. More than 90% of the parvalbumin-positive neurons in the hippocampal formation strongly expressed the DOR gene. Granule cells expressing vesicular glutamate transporter 1 (VGLUT1) mRNA contained very low MOR and DOR transcript levels. In VGLUT1-positive pyramidal cells, weak DOR but no MOR gene expression was detected. Whereas most somatostatinergic hilar neurons were negative for MOR and DOR mRNA, somatostatinergic oriens layer neurons frequently expressed these receptors. Taken together, weak expression of MOR and DOR genes in hippocampal principal cells is in concordance with direct opioid-mediated inhibition of principal cells. However, strong expression of the MOR and DOR genes in the hippocampus is restricted to gamma-aminobutyric acid (GABA)ergic neurons, with DORs being selectively expressed in the parvalbumin- and somatostatin-containing subpopulations. Activation of MOR and/or DOR in parvalbumin- and somatostatin-containing neurons, which provide GABAergic inhibition to the perisomatic and distal dendritic regions of principal cells, respectively, is likely to facilitate principal cell excitation.
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PMID:Neuronal types expressing mu- and delta-opioid receptor mRNA in the rat hippocampal formation. 1468 76

In some brain regions, previous studies reported the frequent coexistence between neuronal nitric oxide synthase (nNOS) and somatostatin (SOM). In the hippocampus, nNOS and SOM were mainly expressed in GABAergic nonprincipal neurons. Here we estimated the immunocytochemical colocalization of nNOS and SOM in the mouse hippocampus using the optical disector. Both in the Ammon's horn and dentate gyrus, we encountered only a few nNOS-immunoreactive (IR)/SOM-like immunoreactive (LIR) neurons. They were mainly located in the stratum oriens of the Ammon's horn and in the dentate hilus. The nNOS-IR/SOM-LIR neurons usually showed characteristic large somata with thick dendrites, whereas the majority of nNOS-IR/SOM-negative neurons showed small somata with thin dendrites. Quantitative data revealed that the double-labeled cells represented only 4% and 7% of nNOS-IR neurons and SOM-LIR neurons, respectively, in the whole area of the hippocampus. We also found the laminar and dorsoventral differences in the degree of colocalization between nNOS and SOM. The percentages of nNOS-IR neurons containing SOM-like immunoreactivity were relatively high in the stratum oriens of the ventral CA1 region (24%), stratum lucidum of the dorsal CA3 region (29%) and dorsal dentate hilus (32%), but they were quite low in the other layers. On the other hand, the percentages of SOM-LIR neurons containing nNOS immunoreactivity were somewhat high in the stratum lucidum of the dorsal CA3 region (19%) and dorsal dentate hilus (28%), whereas they were very low in the other layers. Immunofluorescent triple labeling of axon terminals for nNOS, SOM and glutamic acid decarboxylase indicated that some nNOS-IR/SOM-LIR neurons might be dendritic inhibitory cells. The present results show the infrequent colocalization of nNOS and SOM in the mouse hippocampus, and also suggest that the double-labeled cells may be a particular subpopulation of hippocampal GABAergic nonprincipal neurons.
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PMID:Patterns of colocalization of neuronal nitric oxide synthase and somatostatin-like immunoreactivity in the mouse hippocampus: quantitative analysis with optical disector. 1502 20

Brain 5-HT2A receptors have been implicated in various behavioural and physiological processes including hippocampus-dependent learning and memory. To clarify the cellular localization and chemical identity of 5-HT2A receptor-immunoreactive (-ir) neurons in the rat septal complex and dorsal hippocampus, an immunofluorescence histochemical study was performed using a monoclonal antibody to the 5-HT2A receptor. Pretreatment with colchicine increased the number of 5-HT2A receptor-ir cell bodies, indicating that the 5-HT2A receptor protein undergoes microtubule-dependent anterograde transport in axons and dendrites. 5-HT2A receptor immunoreactivity was detected in septal cholinergic neurons, identified with an antiserum to the vesicular acetylcholine transporter (VAChT), and in GABAergic cell bodies in the medial septum/diagonal band of Broca, identified with antisera to glutamic acid decarboxylase (GAD) and the calcium-binding protein parvalbumin. In the dorsal hippocampus, 5-HT2A receptor immunoreactivity was demonstrated in cells located in the pyramidal cell layer (CA1-3) throughout the Ammon's horn and in the granular cell layer of the dentate gyrus. Furthermore, 5-HT2A receptor immunoreactivity was present in most hippocampal interneurons identified by the presence of GAD65, parvalbumin, calbindin D-28k, somatostatin and neuropeptide Y. In contrast, 5-HT2A receptor immunoreactivity was present in only a few interneurons containing cholecystokinin and calretinin immunoreactivity. The results suggest that serotonin acting on 5-HT2A receptors can modulate hippocampal functions via direct actions on hippocampal glutamatergic principal cells and indirectly via actions on hippocampal interneurons with different phenotypes as well as GABAergic and cholinergic septohippocampal neurons.
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PMID:Chemical identity of 5-HT2A receptor immunoreactive neurons of the rat septal complex and dorsal hippocampus. 1512 29

Temporal lobe epilepsy is often associated with pathological changes in the dentate gyrus, and such changes may be more common in humans than in some nonprimate species. To examine species-specific characteristics that might predispose the dentate gyrus to epileptogenic damage, we evaluated recurrent excitation of granule cells with and without basal dendrites in macaque monkeys, measured miniature inhibitory postsynaptic currents (mIPSCs) of granule cells in macaque monkeys and compared them to rats, and estimated the granule cell-to-interneuron ratio in macaque monkeys and rats. In hippocampal slices from monkeys, whole-cell patch recording revealed antidromically evoked excitatory PSCs that were four times larger and inhibitory PSCs that were over two times larger in granule cells with basal dendrites than without. These findings suggest that granule cells with basal dendrites receive more recurrent excitation and, to a lesser degree, more recurrent inhibition. Miniature IPSC amplitude was slightly larger in monkey granule cells with basal dendrites than in those without, but mIPSC frequency was similar and only 26% of that reported for rats. In situ hybridization for glutamic acid decarboxylase and immunocytochemistry for somatostatin, parvalbumin, and neuronal nuclei revealed interneuron proportions and distributions in monkeys that were similar to those reported for rats. However, the interneuron-to-granule cell ratio was lower in monkeys (1:28) than in rats (1:11). These findings suggest that in the primate dentate gyrus, recurrent excitation is enhanced and inhibition is reduced compared with rodents. These primate characteristics may contribute to the susceptibility of the human dentate gyrus to epileptogenic injuries.
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PMID:Recurrent excitation of granule cells with basal dendrites and low interneuron density and inhibitory postsynaptic current frequency in the dentate gyrus of macaque monkeys. 1526 66


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