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H Bittiger

Publications and source records attributed to H Bittiger.

47 records · Page 3Linked to original sources
PubMed1982

Characterization of neurotransmitter receptors in the rat hippocampal formation.

The hippocampal formation has been extensively research in terms of its putative neurotransmitters, anatomical connections, and behavioral relevance. An aspect of importance is the assessment of apparent neurotransmitter receptors by using receptor binding assays. In the present study, such assays were done in vitro to investigate alpha 1-adrenergic, alpha 2-adrenergic, beta-adrenergic, muscarinic cholinergic, benzodiazepine, and opiate receptors in the rat hippocampal formation. The corresponding radioligands for these receptors were [3H]prazosin, [3H]p-aminoclonidine, [3H]dihydroalprenolol, [3H]quinuclidinyl benzilate, [3H]flunitrazepam, and [3H]naloxone. An analysis of the binding parameters for the ligands indicated saturable binding of a high affinity and the following rank order of maximal binding capacities: [3H]flunitrazepam greater than [3H]quinuclidinyl benzilate greater than [3H]naloxone greater than [3H]p-aminoclonidine greater than [3H]prazosin greater than [3H]dihydroalprenolol. Competition experiments with pharmacologic agonists and antagonists confirmed the specificity of each ligand. The results are integrated with information on other types of receptors and with neurotransmitter concentrations, and discussed in terms of hippocampal function.

Adrenergic alpha-Agonists↗
PubMed1980

In vivo [3H]spiperone binding to the rat hippocampal formation: involvement of dopamine receptors.

The existence of DA receptors in the rat hippocampus was demonstrated with an in vivo [3H]spiperone radioreceptor assay. Kinetic studies revealed that maximum binding of [3H]spiperone in hippocampus was much smaller than in striatum and frontal cortex but much higher than in cerebellum. In inhibition studies of [3H]spiperone binding, all neuroleptics tested were active in hippocampus as well as in striatum. In contrast, 5HT antagonists were definitely less potent in these two brain regions than in frontal cortex. Finally, even when 5HT receptors were blocked, dipropyl-ATN and haloperidol remained fully effective in hippocampus, striatum, but also in frontal cortex although to a lesser degree. From these results it was concluded that [3H]spiperone binds mainly to DA receptors in hippocampus as well as in striatum, whereas both 5HT and DA receptors are present in frontal cortex.

Animals↗
PubMed1980

Are only alpha 2-adrenergic receptors present in bovine retina?

The retina represents a part of the central nervous system (CNS) with a well studied, geometrically defined structure and a specialized function--the processing of light signals. Neurotransmitters such as glutamate, aspartate, glycine, gamma-aminobutyric acid (GABA), dopamine and acetylcholine are considered to be involved in the neuronal activity of the retina. Receptors for acetylcholine, GABA, dopamine and benzodiazepines have also been demonstrated. Thus, the retina can be considered as a model for the study of neuronal processing in general, in which the input, light signals, can be selected and regulated in a defined way. We report here that alpha-adrenergic receptors in the bovine retina have been characterized using radioreceptor assays. 3H-phentolamine (an alpha 1- and alpha 2-antagonist), 3H-clonidine (a preferential alpha 2-agonist) and 3H-WB 4101 [(2,6-dimethoxyphenoxyethyl)aminomethyl-1,4-benzodioxane, an alpha 1-antagonist] were used as radioligands, and WB 4101 and prazosin (alpha 1-antagonists), tolazine (an alpha 2-antagonist), yohimbine and its stereoisomers rauwolscine (preference for alpha 2-receptors) and corynanthine (preference for alpha 1-receptors), were used as inhibitors of radioaligand binding. Only alpha 2-adrenergic receptors were found.

Adrenergic alpha-Agonists↗
PubMed1980

Central actions of somatostatin.

Somatostatin (SRIF) was applied microiontophoretically to neurons in the frontal and parietal neocortex, the hippocampus and the striatum of rats anaesthetized with either urethane or chloral hydrate. Qualitatively identical results were obtained under both anaesthetic conditions. In urethane-treated rats SRIF elicited a dose-dependent increase of the firing rate of 74% of the neurons studied in the frontal cortex and of 46% of the neurons studied in the parietal cortex. All cortical cells identified as pyramidal cells were excited. In the hippocampus SRIF provoked excitatory responses in two thirds of all neurons. Six out of the nine cells identified as pyramidal cells were excited by SRIF. In the striatum 80% of all neurons were excited. Following repeated exposure of central neurons to SRIF, the magnitude of the excitatory response gradually diminished, indicating desensitisation. SRIF in concentrations ranging from 10(-8) to 10(-4) M did not interfere with the binding of (3H)-muscimol to GABA receptor sites. The release of GABA from synapses preloaded with (3H-GABA) was not influenced by SRIF in the concentration range from 10(-6) to 10(-4) M. These results indicated that SRIF does not evoke the excitatory responses through attenuation of GABA-mediated inhibition. In conclusion, the findings support the hypothesis that somatostatin may function as a neurotransmitter in the central nervous system.

Action Potentials↗
PubMed1978

Sensory denervation of the plantar lumbrical muscle spindles in pyridoxine neuropathy.

Male albino rats treated with excessive amounts of pyridoxine developed an impairment of neuromuscular function. The equatorial region of the plantar lumbrical intrafusal muscle fibres was studied in the electron microscope and the calibre of the nerve fibres was determined in semi-thin sections of the posterior tibial nerves. Degeneration of the primary sensory endings coincided with the onset of ataxia, and in more advanced stages of the neuropathy as well as after a 2-month treatment-free period the equatorial region was denervated. There was a corresponding decrease in the number of large nerve fibres. It is considered essential that primary sensory endings of lumbrical muscle spindles should be included in studies of distally accentuated sensory neuropathies.

Animals↗
PubMed1977

A study of long-term effects of guanethidine on peripheral noradrenergic neurones of the rat.

In long-term experiments in rats the effects of guanethidine sulphate on peripheral adrenergic neurons in the heart, the vas deferens, the superior cervical ganglion and the ganglion innervating the vas deferens were studied in relation to the dosage and route of administration of the drug by biochemical, histofluorimetric and electron-microscopic methods. When administered daily in very high doses, i.e. 180 mg/kg orally or 25 mg/kg intraperitoneally, for several weeks guanethidine was found to induce toxic effects which appeared to be a result of mitochondrial changes in the ganglion cells. These changes were not directly related to the decrease in catecholamine content and the capacity of the neurones to retain exogeneous transmitter. The short neurones innervating the vas deferens appeared to be the structures most sensitive to guanethidine. As in the other tissues, however, the changes in these structures proved reversible to a considerable extent upon cessation of high-dose treatment. The structural changes induced in the animal by toxic doses of guanethidine are considered to have no bearing upon the pharmacological action of the drug under practical conditions.

Administration, Oral↗
PubMedDate not supplied

Ligands for expression cloning and isolation of GABA(B) receptors.

Outlined is the rationale behind the syntheses of radioligands [125I]CGP64213 and [125I]CGP71872, which led to the identification of cloned GABA(B) receptors 1a and 1b 17 years after the first pharmacological characterisation of native GABA(B) receptors by Bowery et al. [Nature 283 (1980) 92-94]. More recently it was shown that the N-terminal extracellular domains of GABA(B) receptors 1a and 1b contain the binding sites for agonists and antagonists [B. Malitschek et al., Mol. Pharmacol. 56 (1999) 448-454]. In order to isolate the extracellular domain(s) of GABA(B) receptors 1a (or 1b) and to purify and crystallise these proteins a third ligand [125I]CGP84963 was designed, which combines, in one molecule, a GABA(B) receptor binding part, an azidosalicylic acid as photoaffinity moiety and 2-iminobiotin, which binds to avidin in a reversible, pH-dependent fashion [W. Froestl et al., Neuropharmacology 38 (1999) 1641-1646].

Animals↗