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 major input and output pathways of the mammalian striatum have been well established. Recent studies have identified a number of neurotransmitters used by these pathways as well as by striatal interneurons, and have begun to unravel their synaptic connections. The major output neurons have been identified as medium spiny neurons which contain gamma-aminobutyric acid (GABA), endogeneous opioids, and substance P. These neurons project to the pallidum and substantia nigra in a topographic and probably chemically organized manner. The major striatal afferents from the cerebral cortex, thalamus, and substantia nigra terminate, at least in part, on these striatal projection neurons. Striatal interneurons contain acetylcholine, GABA, and somatostatin plus neuropeptide Y, and appear to synapse on striatal projection neurons. In recent years, much activity has been directed to the neurochemical and hodological heterogeneities which occur at a macroscopic level in the striatum. This has led to the concept of a patch-matrix organization in the striatum.
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PMID:Neurotransmitters in the mammalian striatum: neuronal circuits and heterogeneity. 244 56

An increasing number of messengers have recently been found to coexist with growth hormone (GH)-releasing factor (GRF) in hypothalamic neurons. In view of a possible cosecretion of these substances with GRF into the portal circulation, the effect of synthetic rat hypothalamic GRF(1-43) alone, or together with dopamine (DA), L-dopa, gamma-aminobutyric acid (GABA), neurotensin (NT) or galanin (GAL) on GH release was investigated by using dispersed rat anterior pituitary cells in monolayer culture. GRF in concentrations of 10(-16)-10(-7) M stimulated GH release from somatotrophs in a dose-related manner. DA (10(-5) M), L-dopa (10(-8) and 10(-5) M) and GABA (10(-9) and 10(-5) M) did not affect basal GH release, whereas DA, but not L-dopa or GABA, significantly suppressed GRF-induced GH secretion. However, the inhibitory effect of DA on GRF-stimulated GH secretion was not observed in the presence of somatostatin (10(-6) M). NT (10(-6) M) and GAL (10(-6) M) did not change basal GH release. GAL, but not NT, inhibited GRF-stimulated GH release, but the addition of NT abolished the inhibitory actions of both GAL and DA. These results indicate that substances, probably coreleased with GRF from the same nerve endings, interact in the regulation of GH secretion at the pituitary level.
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PMID:Influence of coexisting hypothalamic messengers on growth hormone secretion from rat anterior pituitary cells in vitro. 244 97

The developing fetal monkey visual cortex was studied immunocytochemically from 110-155 days post-conception in order to localize cell populations immunoreactive (ir) for gamma-aminobutyric acid, Substance P, cholecystokinin-octapeptide, somatostatin, neuropeptide Y, and proenkephalin A peptide (BAM-18). The area 17/18 border and all cortical laminae identified in the adult visual cortex were discernible from the youngest age examined. All ir-cell populations studied were present at each fetal age. However, despite a relatively adult-like cytoarchitecture, all ir-cell populations studied displayed patterns of immunostaining which were unlike those described in adult visual cortex, and showed significant changes in laminar distribution, morphology, and numbers over the time course of gestation examined. Despite the differences in the patterns of immunostaining between the fetal and adult visual cortex, ir-cell populations intrinsic to the developing visual cortex exhibited adult-like combinations of co-localized transmitters and peptides. The developing monkey cortex also contains ir-cell populations, particularly BAM-18-ir cells, which have not been detected immunocytochemically in the adult monkey cortex. Differences between the fetal and the adult ir-cell populations might be accounted for by cell death, morphological transformation, secondary migration or changes in gene expression for neurotransmitters and neuropeptides.
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PMID:Temporal sequence of neurotransmitter expression by developing neurons of fetal monkey visual cortex. 246 14

1. An isolated spinal cord-peripheral nerve preparation of the newborn rat was developed. In this preparation it is possible to record spinal reflexes from a lumbar ventral root in response to stimulation of the ipsilateral saphenous or obturator nerve. 2. Single shock, weak intensity stimulation of the saphenous nerve induced a fast conducted compound action potential in the L3 dorsal root and a fast depolarizing response in the ipsilateral L3 ventral root. As a stronger stimulus was applied to the saphenous nerve, a slowly conducted compound action potential appeared in the dorsal root and a slow depolarizing ventral root potential (v.r.p.) in the L3 ventral root. 3. Single shock stimulation of the obturator nerve induced a rapidly conducted compound action potential in the L3 dorsal root and monosynaptic and polysynaptic reflexes, with a fast time course, in the ipsilateral L3 ventral root. 4. The slow v.r.p. evoked by saphenous nerve stimulation was depressed by the tachykinin antagonist, [D-Arg1, D-Trp7,9, Leu11] substance P (spantide), 4-16 microM. The response recovered its original shape and size 30-60 min after the removal of this antagonist. 5. The saphenous nerve-evoked slow v.r.p. was depressed by [Met5] enkephalin (0.1-1 microM), dynorphin (1-13)(0.2 microM) and morphine (1-2 microM), and these effects were reversed by naloxone (1 microM). 6. Two endogenous peptides, galanin (1-2 microM) and somatostatin (1-2.5 microM), inhibited the slow v.r.p. evoked by saphenous nerve stimulation, whereas another endogenous peptide, calcitonin gene-related peptide (0.1-0.5 microM), potentiated the slow v.r.p. The slow v.r.p. was also inhibited by gamma-aminobutyric acid (GABA, 20 microM) and muscimol (0.2 microM), and their effects were antagonized by bicuculline (1 microM). 7. The present results suggest that substance P and neurokinin A are involved in the saphenous nerve-evoked C-fibre response in the spinal cord of the newborn rat.
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PMID:Pharmacological properties of a C-fibre response evoked by saphenous nerve stimulation in an isolated spinal cord-nerve preparation of the newborn rat. 247 38

The effect of gamma-aminobutyric acid (GABA) on basal and bombesin (BBS)-stimulated release of somatostatin (SLI) and gastrin from isolated perfused rat stomach was examined. In the control study, BBS at a dose of 10 nM significantly stimulated release of SLI and gastrin. Infusion of GABA (1-1000 nM) caused a depression of SLI release induced by BBS (10 nM) in a dose-dependent fashion. However, at doses used in this study GABA had no effect on either basal level of SLI and gastrin or BBS-elicited gastrin release. These results indicate that GABA can specifically modulate BBS-induced SLI release from rat stomach.
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PMID:Effect of gamma-aminobutyric acid on bombesin-evoked release of somatostatin and gastrin from isolated rat stomach. 256 10

omega-Conotoxin GVIA (omega-CT) diminished the potassium-induced in vitro release of 3H-gamma-aminobutyric acid (3H-GABA) from slices of rat neostriatum in a manner which depended on the concentration of potassium. omega-CT (0.1 mmol/l) decreased the release of 3H-GABA induced by 25 mmol/l K+ from 11.6% to 6.1% of tissue content, ie. by 48%, while it did not affect the release of 3H-GABA caused by 20 mmol/l K+, which was 4.8% of tissue content. However, in the presence of a polyclonal antiserum or cysteamine (600 mumol/l), both of which diminish the effects of endogenous somatostatin, 0.1-10 nmol/l omega-CT decreased the release of 3H-GABA induced by 20 mmoles/l K+ by 40%. It is concluded that omega-CT did not only inhibit GABA-neurones, but had an additional inhibitory effect on somatostatin neurones which are known to depress the release of 3H-GABA. It is further concluded that neuronal interactions, which are possible in brain slice preparations, may impede the interpretation of effects of drugs, especially if agents are used which affect basic mechanisms of transmitter release and thus the release of various transmitters from neurones.
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PMID:Effect of omega-conotoxin GVIA on release of 3H-gamma-aminobutyric acid from slices of rat neostriatum. 256 33

The objective of this study was to identify neurons in layer IV of the monkey primary auditory cortex (area KA) that are postsynaptic to thalamocortical axon terminals. Thalamocortical axon terminals were labeled by lesion-induced degeneration; neurons postsynaptic to these afferents were labeled by the Golgi/EM method followed by postembedding immunocytochemistry. Five of the six non-pyramidal neurons examined received synapses from thalamocortical axon terminals. All of these cells were immunoreactive for gamma-aminobutyric acid (GABA). One of the cells stained also with an antiserum to somatostatin, and another for cholecystokinin. None of the cells examined were immunoreactive to substance P, and in no instance were two different peptides co-localized within the same GABA-positive neuron.
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PMID:Thalamocortical synapses with identified neurons in monkey primary auditory cortex: a combined Golgi/EM and GABA/peptide immunocytochemistry study. 256 76

Colocalization of gamma-aminobutyric acid (GABA) immunoreactivity with somatostatin (SOM), neuropeptide Y (NPY), cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP) immunoreactivity was demonstrated in non-pyramidal neurons of the basolateral amygdala using a two-color immunoperoxidase procedure. Approximately 80-90% of SOM- and NPY-positive neurons in the basolateral amygdala were also immunoreactive for GABA. Virtually all large CCK-positive neurons also exhibited GABA-like immunoreactivity. About one-half of VIP-positive neurons and small CCK-positive cells were also immunoreactive for GABA.
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PMID:Coexistence of GABA and peptide immunoreactivity in non-pyramidal neurons of the basolateral amygdala. 256 3

In area CA1 of hippocampus, a subpopulation of gamma-aminobutyric acid (GABA)-containing interneurons that make synaptic contacts on pyramidal cells also contains the neuropeptide, somatostatin. The effects of GABA and somatostatin on hippocampal pyramidal cells have been investigated separately, but it is not known whether an interaction occurs between these co-localized substances. We demonstrate that somatostatin has a potent inhibitory effect on GABA-mediated synaptic potentials which hyperpolarize pyramidal cells. This effect may be relevant to the well-documented epileptogenicity of the hippocampus, as well as the phenomenon of long-term potentiation, which is a well-studied example of synaptic plasticity.
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PMID:Selective depression of GABA-mediated IPSPs by somatostatin in area CA1 of rabbit hippocampal slices. 256 13

The mechanism of action of somatostatin on the motility of intestine was examined in the entire preparation and the longitudinal muscle attached with Auerbach's plexus (LA) preparation of guinea pig ileum, in relation to the cholinergic neuron and gamma-aminobutyric acid (GABA)ergic neuron. Somatostatin produced a transient potentiation of electrical stimulation-induced twitch contractions followed by an inhibition. The excitatory effect of somatostatin was associated with an increase in the release of [3H]acetylcholine (ACh) from the preparations preloaded with [3H]choline. Bicuculline, a GABAA antagonist, inhibited the somatostatin-induced excitatory effect. Somatostatin inhibited the electrical stimulation-induced twitch contraction and release of [3H]ACh, and the inhibition was greater in the entire preparation than in the LA. Phaclofen, a GABAB antagonist, prevented the inhibitory effects of somatostatin. Somatostatin induced a Ca2+ -dependent, tetrodotoxin-sensitive release of [3H]GABA from the preparations preloaded with [3H]GABA. Therefore somatostatin exerts excitatory and inhibitory effects on the cholinergic neuron due to the stimulation of the GABAergic neuron, and the motility of the intestine is regulated.
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PMID:Putative mechanisms involved in excitatory and inhibitory effects of somatostatin on intestinal motility. 257 73


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