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Biomedical subjects

M C Beinfeld

Publications and source records attributed to M C Beinfeld.

At least 109 records · Page 6Linked to original sources
PubMed1983

The distribution of cholecystokinin and vasoactive intestinal peptide in rhesus monkey brain as determined by radioimmunoassay.

The concentration of cholecystokinin (CCK) and vasoactive intestinal peptide (VIP) in dissected cortical and subcortical areas of four rhesus monkeys' brains was determined by radioimmunoassay (RIA). Cerebral cortical samples from one human brain are included for comparison. Preliminary data from two baboon brains are described. The results are similar to previous studies on rat (1-7), human (7-12), porcine (12,13), bovine (3) and guinea pig brains (14) and indicate that: 1) both CCK and VIP are widely distributed in cortical and subcortical areas in these species, 2) CCK is generally more abundant than VIP in primate brain, and 3) the distribution of CCK and VIP in the rat brain parallel those in infrahuman primate and human brain.

Animals↗
PubMed1983

Cholecystokinin in the central nervous system: a minireview.

This review focuses on the structure, distribution, neuronal pathways, receptor binding, release, biosynthesis and degradation of CCK in the central nervous system. Other aspects of the isolation and chemistry of CCK (1), its role in satiety (2), as a hormone or neurotransmitter (3,4), and its evolution (5) have been reviewed recently.

Animals↗
PubMed1983

The development of motilin, cholecystokinin and vasoactive intestinal peptide immunoreactivity in the forebrain and hindbrain of the rat, as determined by radioimmunoassay.

Forebrain and brainstem motilin, cholecystokinin (CCK) and vasoactive intestinal peptide (VIP) were determined in rats from 4 days before to birth to 180 days after. CCK and VIP develop postnatally, as previously reported. Motillin concentrations in both areas, however, were highest 4 days before birth, decreasing after birth. In the oldest animals, motilin, CCK and VIP levels were decreased. The presence of substantial motilin immunoreactivity in the brain before birth is suggestive of a possible role for motillin in the regulation of development.

Animals↗
PubMed1983

Cholecystokinin-immunoreactive neurons in rat and monkey cerebral cortex make symmetric synapses and have intimate associations with blood vessels.

Neurons displaying cholecystokinin-like immunoreactivity (CCK neurons) in rat and monkey cerebral cortex were examined by light and electron microscopic immunocytochemistry. CCK neurons were found to be mainly bipolar cells present in all layers and in all areas of the rat cerebral cortex. CCK neurons were also found in all regions examined in monkey cortex (pre- and post-central gyri and superior parietal lobule). The somata and the dendritic processes of CCK neurons receive relatively few synapses but both symmetric and asymmetric axosomatic and axodendritic synapses were found. The majority of axon terminals displaying CCK-like immunoreactivity formed symmetric synapses, most frequently with the somata and proximal dendrites of pyramidal and nonpyramidal neurons. The somata and processes of CCK neurons were also found to establish very close nonsynaptic associations with blood vessels and with other neurons, suggesting possible roles for the peptide in the maintenance of neuronal excitability and cerebral blood flow.

Animals↗
PubMed1982

Cholecystokinin in the nucleus of the solitary tract of the rat: evidence for its vagal origin.

Nerve fibers and terminals immunoreactive for cholecystokinin (CCK) were demonstrated in the nucleus of the solitary tract (NTS) of the rat using light and electron microscopic immunocytochemistry. The following morphological and biochemical evidence suggests that CCK in the NTS seems to be of extrinsic, most probably vagal, origin: (1) axon fragments of the intracranial vagus were identified by immunostaining on their way to the solitary tract: (2) CCK-immunostaining could be localized in nerve terminals in the nucleus of the solitary tract, where only a very few immunopositive dendrites or cell bodies were present; and (3) transecting the major neuronal afferents (via solitary tract and/or more laterally) resulted in a complete disappearance of radioimmunoassayable CCK from the nucleus of the solitary tract.

Animals↗
PubMed1982

Distribution of cholecystokinin (CCK) in the rat lower brain stem nuclei.

The cholecystokinin (CCK) concentration in individual brain stem nuclei of rat was determined using the Palkovits punch method19 and the CCK RIA3, CCK has a unique distribution in the brain stem, unlike other neuropeptides and biogenic amines8,19. In general, the CCK levels in the brain stem are 5-20% of rat cerebral cortex. The colliculi, midbrain central gray, nucleus of the solitary tract, and the interpeduncular nucleus had the highest CCK content (2.7-1 ng CCK mg protein).

Animals↗
PubMed1982

Origin of the cholecystokinin-containing fibers in the rat caudatoputamen.

Large Amounts of cholecystokinin-octapeptide (CCK) are present in the rat caudatoputamen. The peptide occurs in axons and nerve endings but not in perikarya. The origin of CCK in the caudatoputamen was investigated with the use of immunocytochemistry and a radioimmunoassay specific for CCK. Although a small amount of CCK (approximately 30 percent) originates in the amygdaloid complex, the bulk of the peptide (approximately 70 percent) occurs in processes of neurons located ventral to the caudatoputamen, that is, the claustrum or the piriform cortex. The claustrum and piriform cortex receive inputs from various cortical areas and the olfactory system, respectively, and may process information and relay it to the caudatoputamen. Thus CCK may by the transmitter in the final common pathway linking various cortical areas and the olfactory system to the caudatoputamen.

Amygdala↗
PubMed1982

Cyclic nucleotide antagonists of cholecystokinin: structural requirements for interaction with the cholecystokinin receptor.

Previously, we have found that, in pancreatic acini, butyryl derivatives of cGMP antagonize the action of cholecystokinin by inhibiting binding of the peptide to its membrane receptors. In the present study, we found that derivatives of cAMP and cIMP can also inhibit binding of cholecystokinin as well as its actions on acinar cell function. Moreover, the inhibition caused by cyclic nucleotide derivatives did not require the presence of a butyryl moiety, because certain 8-bromo-cyclic nucleotides also inhibited the interaction of cholecystokinin with its receptors. Cyclic nucleotide derivatives can also increase pancreatic enzyme secretion; however, for the various cyclic nucleotides tested, there was no apparent correlation between their abilities to stimulate enzyme secretion and their abilities to antagonize the actions of cholecystokinin. Finally, cyclic nucleotide derivatives also inhibited binding of 125I-cholecystokinin to antibodies that were specific for the biologically active, C-terminal region of cholecystokinin. Thus, certain cyclic nucleotide derivatives possess a conformational structural which resembles that of the biologically active portion of cholecystokinin, and this structural similarity accounts for the abilities of these nucleotide derivatives to interact with cholecystokinin receptors and, by so doing, to inhibit the action of cholecystokinin on its target tissues.

Animals↗
PubMed1981

Postnatal ontogeny of cholecystokinin receptors in rat brain.

The postnatal ontogeny of cholecystokinin receptors and cholecystokinin was determined in rat brain. The binding of cholecystokinin (CCK) to rat forebrain receptors was very low at 1-2 days of age, rose to a maximum at 12 days (Bmax = 31 fmol/mg protein, Kd = 1.47 nM), and declined to adult levels by 26 days (Bmax = 17 fmol/mg protein, Kd = 1.39 nM). In contrast, forebrain concentrations of CCK measured by radioimmunoassay rose monotonically through day 27. Possible implications of the transient developmental peak of CCK receptors are discussed.

Aging↗
PubMed1981

The distribution of cholecystokinin immunoreactivity in the central nervous system of the rat as determined by radioimmunoassay.

The regional distribution of cholecystokinin (CCK) in the rat brain was determined utilizing a radioimmunoassay which detects both gastrin and CCK. CCK concentration is highest in the caudate nucleus (10-14 ng CCK 8 equivalents/mg protein), followed by the cerebral cortex. Within the cerebral cortex, CCK is highest in the cingulate, pyriform, and entorhinal areas. There are substantial CCK concentrations in all other brain regions except pons, medulla and cerebellum. CCK is widely distributed in the hypothalamus, where it is highest in the median eminence and ventromedial nucleus. Considerable CCK-like immunoreactivity is also present in the posterior lobe of the pituitary gland, but is not detectable in anterior and intermediate lobes. Though the antisera used in this study cross-react with gastrin the dominant CCK-like material found in rat brain co-elutes with sulfated CCK 8 and separates from gastrin on Sephadex G-25 and HPLC chromatography.

Animals↗
PubMed1981

Cholecystokinin in the central nervous system.

We have used high performance liquid chromatography and radioimmunoassay to characterize the CCK-like molecules in the central nervous system. The major form of CCK is the sulfated octapeptide. This molecule is distributed unevenly among various brain regions; the highest levels are found in the cortex and striatum. We have focused our attention on three areas in particular, the posterior pituitary, the caudate nucleus, and the hippocampus. The first of these receives its CCK-containing fibers from the hypothalamic magnocellular nuclei, the second appears to be innervated by the claustrum (or piriform cortex). The CCK in the hippocampus, on the other hand, is in intrinsic neurons. These structures and others in the brain have CCK binding sites.

Animals↗