Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Slices of the rat substantia nigra and striatum were superfused in vitro to measure release of tachykinins (TKs). Potassium (30 and 60 mM) infusion caused a 3- to 10-fold outflow of both substance P-like immunoreactivity (SP-LI) and neurokinin A-like immunoreactivity (NKA-LI) in the substantia nigra as well as in the striatum as measured by radioimmunoassay. The potassium-evoked release of SP-LI and NKA-LI was significantly, but not completely (by 25-70%) inhibited by simultaneous perfusion with L-glutamic acid (50 microM) and gamma-aminobutyric acid (GABA, 50 microM) in the substantia nigra. No significant inhibition was, however, observed in the striatum. The present data indicate a differential regulation of tachykinins in the striatum and substantia nigra by L-glutamic acid and GABA. The presynaptic regulation of TK release may therefore differ in the dendritic and terminal region of the striatonigral pathway.
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PMID:Effects of GABA and L-glutamic acid on the potassium-evoked in vitro release of substance P- and neurokinin A-like immunoreactivities are different in the rat striatum and substantia nigra. 248 28

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

During ontogeny, the central nervous system undergoes neuronal growth, regression, and remodeling. The development of neurotransmitter and modulator systems is a plastic process with individual temporal characteristics for each system. These characteristics include the synthesis, degradation, or uptake of neurochemicals and, largely independently, the appearance of their receptors. Message transmission during ontogeny is compounded by the variable development of these systems and by the coexistence and cofunction among these chemicals. Nine neurochemical systems are discussed: adenosine, gamma-aminobutyric acid, opioids, prostaglandins, serotonin, progesterone, substance P, thyrotropin-releasing hormone, and the catecholamines. The possible role of each of these in natural perinatal respiratory control is evaluated according to predetermined criteria. These include the presence of a substance system in respiratory-related regions, physiologically appropriate changes in its concentration in these regions, elicitation of respiratory effects by agonists and antagonists, and abolition with an antagonist of the effect of a substance during its presumed activation by a physiological process. It is suggested that excessive levels of suppressant neuromodulators or an imbalance among neurochemicals can partly explain the special features of respiratory control in the perinatal period.
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PMID:Neurochemicals and respiratory control during development. 256 52

The immunohistochemical localization of neuronal cell bodies and axons reactive for substance P (SP) and methionine-enkephalin (ME) was investigated in the corpus striatum of the adult cat brain and compared with that of glutamate decarboxylase (GAD), synthetic enzyme for gamma-aminobutyric acid. Striatal cell bodies reactive for ME could be identified only in colchicine treated cats, are medium size, ovoid striatal cells, and are found in large numbers in a more or less even distribution throughout the caudate nucleus, putamen, and nucleus accumbens. The striatal region most densely occupied by ME-immunoreactive cells is the ventral and central part of the caudate head. Modest numbers of larger ME-reactive neurons are dispersed throughout the entopeduncular nucleus and the pars reticulata of the substantia nigra. Striatal cells of medium size reactive for SP could be identified, with or without colchicine, in largest numbers in the medial half of the caudal three-fourths of the putamen and in clusters of irregular size and shape in the head of the caudate nucleus. Cells reactive for SP are also common in layer II and the islands of Calleja of the olfactory tubercle. We could not reliably visualize GAD-positive cell bodies in the striatum, even with colchicine treatment; however, they could be seen readily in all pallidal structures such as the globus pallidus, ventral pallidum, entopeduncular nucleus, and substantia nigra. Axons reactive for ME are found mainly in the globus pallidus where they form a dense and even network throughout the nucleus. The globus pallidus is almost devoid of SP reactivity except near its extreme caudal pole. Conversely, SP-immunoreactive axons form dense meshworks in the entopeduncular nucleus and substantia nigra where ME immunoreactivity is minimal. Fewer, but still ample numbers, of SP-reactive axons are present also in the ventral tegmental and retrorubral areas of the midbrain tegmentum and in the ventral pallidum of the basal forebrain, but only sparse ME-reactive axons are present in these areas. This differential distribution of SP- and ME-containing axons in the pallidal and nigral structures stands in contrast to the relatively homogeneous and dense distribution of GAD-containing axons throughout the dorsal and ventral pallidum, entopeduncular nucleus, and substantia nigra.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunohistochemical demonstration of differential substance P-, met-enkephalin-, and glutamic-acid-decarboxylase-containing cell body and axon distributions in the corpus striatum of the cat. 257 80

Substance P (SP) and serotonin are contained in ventral medullary projections to the intermediolateral cell column (IML) of the spinal cord, and both neurotransmitters excite sympathetic preganglionic neurons upon injection into the IML. Since gamma-aminobutyric acid (GABA) in the ventral medulla inhibits, and GABA-receptor antagonists excite sympathetic outflow to the cardiovascular system, experiments were done to determine if SP and serotonin in the spinal cord were responsible for mediating these GABAergic effects. Anesthetized rats were either given intrathecal injections of SP antagonists acutely, or pretreated with intrathecal injections of the serotonin neurotoxin, 5,7-dihydroxytryptamine. The effects of these drugs on mean arterial pressure (MAP) and heart rate (HR), as well as their ability to block the responses to topical application of GABA or the GABA antagonist, bicuculline, at the ventral medulla were assessed. Three SP antagonists (50 micrograms) decreased MAP to 2/3 baseline values, but did not change HR. They also blocked the characteristic increases in MAP and HR elicited by application of bicuculline to the ventral medulla. A lower dose (5 micrograms) of a SP antagonist also decreased MAP and blocked the bicuculline-induced increases in MAP and HR, an effect which was reversed in 1-2 h. Neonatal capsaicin treatment reduced the SP content in the dorsal horns of the thoracic spinal cord, but did not affect the cardiovascular responses to intrathecal injection of SP antagonist nor the blockade of bicuculline-induced responses. Intrathecal injection of 5,7-dihydroxytryptamine two weeks prior to the experiments resulted in 56% depletion of serotonin in the thoracic spinal cord, but did not change either basal MAP and HR, nor the responses to bicuculline and GABA applied to the ventral surface of the medulla. These data provide evidence for a role of spinal cord SP in cardiovascular regulation.
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PMID:Spinal cord substance P mediates bicuculline-induced activation of cardiovascular responses from the ventral medulla. 258 25

Geniculo-geniculate projections of immunoreactive neurons for gamma-aminobutyric acid (GABA), leucine-enkephalin (ENK), neuropeptide Y (NPY) and substance P (SP) in the intergeniculate leaflet (IGL) and ventral lateral geniculate nucleus (VLG) of the rat were examined by using a combination of retrograde tracing method and immunocytochemistry. After injection of the fast blue (FB) dye into the IGL and VLG, many ENK immunoreactive neurons, and some NPY immunoreactive neurons were labelled by FB dye in the contralateral IGL. However, GABA and SP immunoreactive neurons in the IGL and VLG were not labelled retrogradely by FB dye. A unilateral electrical lesion of the IGL and VLG caused a reduction of the ENK and NPY immunoreactive fibres in the contralateral IGL and VLG. These findings suggested that ENK is one major component of the neuroactive substances in the geniculo-geniculate projection, and NPY also contributes partly to this projection. Furthermore, the unilateral destruction of the IGL and VLG showed a marked loss of the NPY immunoreactive fibres and a slight loss of the ENK immunoreactive fibres in the bilateral suprachiasmatic nuclei.
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PMID:Geniculo-geniculate projection of enkephalin and neuropeptide Y containing neurons in the intergeniculate leaflet of the thalamus in the rat. 278 30

The effect of 5-(2-cyclohexylideneethyl)-5-ethyl barbituric acid (CHEB) on the isolated spinal cord of the immature rat was examined using extracellular recording. At concentrations less than 20 microM CHEB increased the monosynaptic reflex (MSR) but depressed the reflex at greater concentrations (30-100 microM). At concentrations which enhanced the monosynaptic reflex, CHEB reduced the responses of motoneurones to glycine and to a lesser extent to those of L-glutamate. In the presence of strychnine (5 microM), which enhanced both mono- and polysynaptic reflexes, CHEB produced only slight enhancement of the monosynaptic reflex. At concentrations of 30-100 microM the responses to gamma-aminobutyric acid (GABA), glycine, L-glutamate and eledoisin-related peptide (ERP a substance P and analogue) were all reduced. At these concentrations CHEB directly depolarised the motoneurone membrane. Increases in [Mg2+]0, which reduced spontaneous activity, blocked the enhancement, by CHEB, of the monosynaptic reflex. The actions of CHEB in small doses may be due therefore to its ability to block the action of glycine and thus block tonic inhibition.
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PMID:Strychnine-like action of the convulsant barbiturate, CHEB. 286

Various putative striatal transmitters and related compounds were studied for their effects on the release of gamma-aminobutyric acid (GABA) from slices of the head of the rabbit caudate nucleus. The slices were preincubated with [3H]GABA and then superfused and stimulated electrically at 5 or 20 Hz. Aminooxyacetic acid was present throughout. The main changes observed were the following. The basal and, less consistently, the electrically evoked overflow of [3H]GABA were enhanced by 3,4-dihydroxyphenylethylamine (dopamine), an effect not blocked by cis-flupentixol or domperidone and not mimicked by apomorphine and D1-selective agonists. The electrically evoked overflow was diminished by 5-hydroxytryptamine (serotonin); the inhibition was prevented by methiothepin. The basal but not the electrically evoked overflow was enhanced by carbachol; acetylcholine and nicotine also accelerated the basal outflow whereas oxotremorine caused no consistent change; the effect of carbachol and acetylcholine were blocked by hexamethonium but not by atropine or by tetrodotoxin. These findings indicate that the GABA neurons in the caudate nucleus may be stimulated by dopamine, although the receptor type involved remains unclear; inhibited by serotonin; and stimulated by acetylcholine acting via a nicotine receptor. However, all drug effects observed were relatively small. No evidence was obtained for autoreceptors, alpha 2-adrenoceptors or receptors for opioids, adenosine or substance P at the GABA neurons.
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PMID:A search for receptors modulating the release of gamma-[3H]aminobutyric acid in rabbit caudate nucleus slices. 286 5

By using a multibarrelled microelectrode, the possibility that putative transmitters may influence on the field potential evoked in the solitary tract nucleus by electrical stimulation of the carotid sinus nerve (the NTS response) was examined electrophysiologically in the cat. After iontophoretic application of a selective antagonist to the putative transmitter, it was determined whether or not the NTS response was influenced. Both substance P antagonist and naloxone altered the NTS response recorded in the depressor and apneic (or hypopneic) response zone as well as in the pressor and apneustic (or inspiratory) response zone throughout the rostral, intermediate and commissure regions, suggesting that substance P and opioid peptide may play the role of excitatory transmitters. Under the polarizing cathodal current which may activate inhibitory inputs to the site of the NTS response, bicuculline and prazosin strongly enhanced the NTS response recorded in the pressor and apneustic zone, while naloxone weakly enhanced the NTS response recorded in the depressor and apneic zone. These results suggest that gamma-aminobutyric acid, alpha-adrenergic agonist and opioid peptide may have an inhibitory influence on the NTS response.
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PMID:Study of possible transmitters in the solitary tract nucleus of the cat involved in the carotid sinus baro- and chemoreceptor reflex. 288 9

We performed a neurochemical study of the brain of two unrelated patients, living in different continents, with neuroacanthocytosis. The levels of monoamines and their metabolites, gamma-aminobutyric acid and substance P, were measured in several brain areas and the monoamine metabolites in cerebrospinal fluid. The binding of 3H-spiperone to striatal membranes and to lymphocytes was also measured. Both patients had a progressive neurological disorder with onset in the third decade of life and characterized by a complex movement disorder, epilepsy, muscular wasting, and changes in behavior. The movement disorder initially manifested with oromandibular dystonia and limb chorea, but at the time of death was characterized by a severe dystonic syndrome. The chemical changes were similar in the two patients. The most important neurochemical findings were a depletion of dopamine and its metabolites in most brain areas, most notably in the striatum, and elevation of norepinephrine levels in the putamen and globus pallidus. Substance P was markedly reduced in the striatum and substantia nigra. Our findings may provide clues to the neurochemical mechanisms underlying dystonia.
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PMID:Neurochemical findings in neuroacanthocytosis. 290 27


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