Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biochemical assays on microdissected samples, denervation studies, subcellular fractionation, and light and electron microscopic autoradiography of high affinity uptake have been performed to study the cellular localization of transmitter candidates in the rat hippocampal formation. High affinity uptake of glutamate and aspartate is localized in the terminals of several excitatory systems, such as the entorhino-dentate fibres (perforant path), mossy fibres (from granular cells) and pyramidal cell axons. Thus, in stratum radiatum and oriens of CA1, 85% of glutamate and asparate uptake and 40% of glutamate and aspartate content are lost after lesions of ipsilateral plus commissural fibres from CA3/CA4. Hippocampal efferents also take up aspartate and glutamate, since these activities are heavily reduced in the lateral septum and mamillary bodies after transection of fimbria and the dorsal fornix. The synthesis (by glutamic acid decarboxylase), content and high affinity uptake of gamma-aminobutyrate (GABA) are not reduced after lesions of these or other projection fibre systems. A localization in intrinsic neurons is confirmed by a selective loss of glutamic acid decarboxylase after local injections of kainic acid. Peak concentrations of the enzyme occur near the pyramidal and granular cell bodies, corresponding to the site of the inhibitory basket cell terminals, and in the outer parts of the molecular layers. Some 85% of glutamic acid decarboxylase is situated in 'nerve ending particles'. Acetylcholine synthesis (by choline acetyltransferase) disappears after lesions of septo-hippocampal fibres. Since 80% of the hippocampal choline acetyltransferase is in 'nerve ending particles', the characteristic topographical distribution of this enzyme should reflect the distribution of cholinergic septo-hippocampal afferents. Serotonin, noradrenaline, dopamine and histamine are located/synthesized in afferent fibre systems. Some monoamine-containing afferents to the hippocampal formation pass via the septal area, others via the amygdala. The hippocampal formation also contains nerve elements reacting with antibodies against neuroactive peptides, such as enkephalin, substance P, somatostatin and gastrin/cholecystokinin.
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PMID:Localization of putative transmitters in the hippocampal formation: with a note on the connections to septum and hypothalamus. 3 19

Cholecystokinin (CCK) binding sites were localized by in vitro autoradiography in human postmortem brain materials from 12 patients without reported neurological diseases using [125I]Bolton-Hunter CCK octapeptide (BHCCK-8) as a ligand. The pharmacological characteristics of BHCCK-8 binding to mounted tissue sections were comparable to those previously reported in the rat. CCK-8 being the most potent displacer, followed by caerulein, CCK-4, and gastrin I. The distribution of BHCCK-8 binding sites was heterogeneous. These sites were highly concentrated in a limited number of gray matter areas and nuclei. The highest binding densities were seen in the glomerular and external plexiform layers of the olfactory bulb. BHCCK-8 binding sites were also enriched in the neocortex, where they presented a laminar distribution with low levels in lamina I, moderate concentration in laminae II to IV, high density in lamina V, and low levels in lamina VI. A different laminar distribution was seen in the visual cortex, where a low receptor density was observed in lamina IV but higher density in laminae II and VI. In the basal ganglia the nucleus accumbens, caudatus, and the putamen presented moderate to high densities of binding sites, while the globus pallidus lacked sites of BHCCK-8 binding. In the limbic system the only area presenting moderate to high density was the amygdaloid complex, particularly in the granular nucleus, while most of the thalamic nuclei were extremely poor or lacked BHCCK-8 binding. The hippocampal formation showed low (CA1-3) to moderate (subiculum) densities. Midbrain areas generally disclosed very low levels of BHCCK-8 binding sites. The pontine gray and the nucleus reticularis tegmenti pontis showed a relatively high density of CCK-8 receptor specific binding. Moderate to very high densities were found in few nuclei of the lower brainstem and spinal cord as the inferior olives and their accessory nuclei, the arcuate nuclei, the striae medullares, the efferent (motor) nucleus of the vagus, and the substantia gelatinosa of the cervical and thoracic spinal cord. These results are discussed in relation to the distribution of endogenous peptide and to the known physiological and pharmacological effects of substances acting on these receptors.
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PMID:On the distribution of cholecystokinin receptor binding sites in the human brain: an autoradiographic study. 350 67

The presence of cholecystokinin octapeptide (CCK-8) immunoreactivity in the vicinity of the pyramidal neurones of the mammalian hippocampus has allowed us to investigate the central postsynaptic actions of CCK-8 and a number of related peptides, at a site thought to be innervated by a peptidergic pathway. Intracellular records from pyramidal cells of the CA1 region of the hippocampal slice preparation were used to determine changes in excitability and associated changes in membrane potential and resistance evoked by the pressure application of peptides into the cell body layer, from an independently mounted multibarrelled micropipette. The tetra- and octa-peptide C-terminal fragments of cholecystokinin evoked abrupt and rapidly reversible depolarizations which were accompanied by marked increases in excitability and a decrease in membrane input resistance. A comparison was made of the actions of these peptides with those of glutamate, released by iontophoresis from an adjacent barrel of the same multibarrelled pipette. The rate of onset of the cholecystokinin-evoked response was similar to that of the response evoked by glutamate. C-terminal fragments of gastrin (G-13 and G-14) and bombesin were also found to be excitatory to pyramidal neurones in the CA1 region. However, the nonsulphated form of CCK-8 was inactive, as was substance P, a peptide not present in the hippocampus.
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PMID:The actions of cholecystokinin and related peptides on pyramidal neurones of the mammalian hippocampus. 616 16