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Biomedical subjects

S Z Langer

Publications and source records attributed to S Z Langer.

At least 19 recordsLinked to original sources
PubMed1979

Release of radioactive purines from cat nictitating membrane labeled with 3H-adenine.

Cat nictitating membranes were incubated with 1-2 x 10(-7) M 3H-adenine or 3H-adenosine for 1 h. A tissuebath ratio of about 15 was found for both compounds in intact and denervated membranes. In intact nictitating membranes sympathetic nerve stimulation (4 Hz, 5 min) caused a net release of purines (0.66 +/- 17% of the tissue content), which was reduced by alpha-blockade. Noradrenaline (1-3 microM) or tyramine 60 microM), which produced the same contractile response as did nerve stimulation, increased purine release to the same extent as did nerve stimulation. The effect of either agent was reduced or abolished by phentolamine. Purine release could also be induced by acetylcholine and ATP. This release was not altered after surgical denervation. There was an excellent correlation between the contractile response and the purine release induced by nerve stimulation, noradrenaline, tyramine and acetylcholine. However, ATP caused a larger release of 3H-purines than expected from the contractile responses, possibly indicating displacement. The results indicate that most if not all of the 3H-purines released by nerve stimulation in the cat nictitating membrane are derived from postjunctional elements.

Acetylcholine↗
PubMed1979

Specific tricyclic antidepressant binding sites in rat brain.

The discovery of high-affinity binding sites for psychoactive drugs such as benzodiazepines, opiates and neuroleptics has opened up new approaches to the study of these drugs and their mechanisms of action. Although most tricyclic antidepressants inhibit neuronal uptake of noradrenaline and serotonin, their mechanism of action remains unclear. Changes in the sensitivity of the beta-receptor after chronic tricyclic antidepressant treatment suggest that they modulate noradrenergic neurotransmission. Tricyclic antidepressants also act directly on cholinergic, histaminergic, alpha-adrenergic and serotonergic receptors. It is not clear, however, which, if any, of these effects are related to the primary antidepressant effect or whether they are simply responsible for some of the side effects. We have thus investigated the possibility that specific binding sites for tricyclic antidepressants exist in the central nervous system. So far, binding studies using 3H-labelled tricyclic antidepressant drugs have only detected binding to histaminergic H2 and cholinergic muscarinic receptors and low-affinity binding. We demonstrate here a population of specific high-affinity binding sites for 3H-imipramine on brain membranes which may be responsible for the antidepressant effects of these drugs.

Animals↗
PubMed1979

The effects of chemical sympathectomy with 6-hydroxydopamine on alpha-adrenoceptor and muscarinic cholinoceptor binding in rat heart ventricle.

The specific binding of 3H-dihydroergocryptine to alpha-adrenoceptors in membranes from the heart ventricle of rats chemically denervated with 6-hydroxydopamine was significantly decreased in comparison with control animals. In contrast the muscarinic cholinoceptor binding of 3H-quinuclinidyl benzilate was unchanged after chemical sympathectomy. These results are interpreted as indicating that the muscarinic receptors are principally postsynaptic but that a significant proportion of the alpha-adrenoceptors are located on noradrenergic nerve terminals.

Animals↗
PubMed1979

Presynaptic GABA autoreceptors on GABAergic nerve endings of the rat substantia nigra.

The release of 3H-GABA evoked by exposure to 30 mM potassium during 1 min was found to calcium independent in the rat occipital cortex and calcium dependent in the substantia nigra. Exposure to either muscimol 1 microM or GABA 1 microM inhibited the potassium-evoked release of 3H-GABA from the substantia nigra but not from the occipital cortex. The inhibitory effect of muscimol 1 microM on the potassium-evoked release of 3H-GABA from the substantia nigra was significantly antagonized by picrotoxin 10 microM. Exposure to either 10 or 100 microM pricrotoxin alone did not affect the potassium-evoked release of 3H-GABA. These results are compatible with the presence of a negative feedback mechanism in bagaergic nerve terminals of the rat substantia nigra which is mediated by presynaptic GABA autoreceptors. In addition, these results emphasize the importance of the calcium-dependent nature of the release of the neurotransmitter for demonstrating the modulation of transmitter release through presynaptic receptors.

Animals↗
PubMed1979

Specific labelling of postsynaptic alpha 1 adrenoceptors in rat heart ventricle by 3H-WB 4101.

The alpha-adrenoceptor ligand, 3H-WB 4101 binds to a single population of independent sites in the rat heart ventricle. These sites are not affected by chemical sympathectomy with 6-hydroxydopamine and thus appear to be located postsynaptically. The relative order of potencies for displacement of 3H-WB 4101 binding:prazosin greater than phentolamine greater than yohimbine, is characteristic of that of the alpha 1 type of adrenoceptors. In heart ventricle 3H WB-4101 thus seems to label specifically postsynaptically located alpha 1-adrenoceptors. The significance of the specificity of this ligand is discussed with relevance to its use in the central nervous system.

Adrenergic alpha-Antagonists↗
PubMed1979

Angiotensin II facilitates the potassium-evoked release of 3H-noradrenaline from the rabbit hypothalamus.

Antiotensin II facilitated in a concentration-dependent manner the potassium-evoked 3H-noradrenaline over-flow from the rabbit hypothalamus. This effect which is probably mediated through presynaptic angiotensin facilitatory receptors on noradrenergic nerve terminals was blocked by the specific angiotensin receptor antagonist, saralasin. These results demonstrate that angiotensin II also facilitates the stimulation-evoked release of noradrenaline in the central nervous system.

Angiotensin II↗