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Biomedical subjects

A H Mulder

Publications and source records attributed to A H Mulder.

At least 217 records · Page 12Linked to original sources
PubMed1976

Potassium-induced release of tritiated histamine from rat brain tissue slices.

The release of exogenous histamine was studied by superfusing brain slices following incubation with the radiolabeled amine. Histamine was released in a calcium-dependent way by 40 mM potassium. This release was high in hypothalamus and striatum and low in hippocampus and cortex. Compound 48/80, a mast cell histamine releasing agent, also induced histamine release, but only from hypothalamic tissue slices. It is suggested that the potassium-induced release of accumulated exogenous histamine is mainly from glial cells.

Animals↗
PubMed1976

Release and receptor stimulating properties of p-tyramine in rat brain.

Radiolabeled p-tyramine could be released from rat striatal slices, which were previously allowed to accumulate this amine, upon depolarization with media containing 40 mM potassium. This depolarization-induced release did not occur in the absence of calcium ions in the medium and over 75% of the labeled material released was identified chromatographically as tyramine. The possible existence of a direct receptor-stimulating activity of p-tyramine was examined by injecting this amine intraventricularly into rats, after pretreatment with various drugs, which inhibit catecholaminergic function, and measuring their motor activity. If injected into rats, which were pretreated with reserpine or alpha-methyl-p-tyrosine, p-tyramine induced a marked increase in the motor activity, which was not accompanied by a significant decrease in brain catecholamines, ruling out the possibility of indirect receptor stimulation. Since the presence of endogenous p-tyramine in the brain has been reported, these data may indicate a specific synaptic role for this amine, perhaps as a neurotransmitter.

Animals↗
PubMed1975

On the presence of a MSH-release inhibiting system in the rat neurointermediate lobe.

Rat neurointermediate lobes were superfused in vitro and showed a stable secretion rate of MSH after 30 min. MSH secretion from lobes of untreated rats was reversibly inhibited during superfusion with medium containing 45 mM K+. This inhibition could not be induced using lobes from median eminence lesioned or reserpinized rats. Superfusion with 45 mM K+ also induced release of dopamine from lobes preincubated with the labeled transmitter. It is concluded that the MSH-release inhibiting system present in the rat neurointermediate lobe may be identical to the dopaminergic arcuate-intermediate lobe system.

Animals↗
PubMedDate not supplied

Selectivity of various opioid peptides towards delta-, kappa; and mu-opioid receptors mediating presynaptic inhibition of neurotransmitter release in the brain.

The selectivity of a series of opioid peptides towards the mu-, delta- and kappa-opioid receptors mediating differential inhibition of electrically-induced neurotransmitter release from rat brain slices was studied, viz. cortical [3H]noradrenaline release (inhibited via mu-receptors), striatal [3H]dopamine release (inhibited via kappa-receptors) and striatal [14C] acetylcholine release (inhibited via delta-receptors). The highest affinity pD2 7.4) and selectivity towards mu-receptors was exhibited by Tyr-D-Ala-Gly-(NMe)Phe-Gly-ol (DAGO), whereas [D-Pen2, D-Pen5]enkephalin (DPDPE) was found to be the most selective delta-receptor agonist (pD2 7.3). Also the hexapeptides [D-Ser2]Leu-enkephalin-Thr (DSLET) and [D-Thr2]Leu-enkephalin-Thr (DTLET) showed a relatively high selectivity and, in addition, a high affinity (pD2 8.2-8.4) for delta-opioid receptors. Both dynorphin(1-13) and dynorphin(1-8) exhibited a high affinity for kappa-receptors (pD2 resp. 8.3 and 8.0), but the latter was far less selective. Both of the dynorphin A-related peptides showed affinity to mu-receptors (pD2 6.7-6.8), but dynorphin(1-8), in contrast to dynorphin(1-13), also displayed a high affinity to delta-receptors (pD2 7.6).

Adrenocorticotropic Hormone↗