PubMed HealthSearch

SEARCH · PubMed Health

Results for “Receptors, Cholinergic”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

The rabbit cornea lacks cholinergic receptors.

Cholinergic receptors were studied in membranes prepared from rabbit cornea, iris-ciliary body, and retina, using 3H-quinuclidinyl benzilate (3H-QNB) to identify muscarinic receptors and 125I-alpha-bungarotoxin (125I-BGT) to identify nicotinic receptors. Muscarinic cholinergic receptors were not found in the cornea. As a positive control, muscarinic cholinergic receptors were characterized in preparations of the iris-ciliary body. Specific binding of 3H-QNB to iris-ciliary body membrane preparations was saturable, with a Kd of 1.3 nM QNB. Specificity of the assay for muscarinic receptors was confirmed by the relative abilities of the following compounds to displace 3H-QNB: atropine greater than pilocarpine greater than hexamethonium. Nicotinic cholinergic receptors were not found in the cornea. As a positive control, nicotinic cholinergic receptors were characterized in preparations of the retina. Specific binding of 1252-BGT to retinal membrane preparations was saturable with both high and low affinity receptors (Kd values of 1.0 nM and 93 nM BGT, respectively). Specificity of the assay for nicotinic receptors was confirmed by the relative abilities of the following compounds to prevent 125I-BGT binding: curare greater than or equal to nicotine greater than hexamethonium greater than atropine. The lack of cholinergic receptors in the cornea, which has high levels of acetylcholine and related enzymes, suggests either an extraordinary use or a lack of function for acetylcholine in this tissue.

Animals

Immunologic similarities between the hypothalamic alpha-bungarotoxin receptor and the Torpedo californica nicotinic cholinergic receptor.

The solubilized rat central nervous system (hypothalamic) nicotinic cholinergic receptor and the Torpedo nicotinic cholinergic receptors are immunologically similar and show greater than 60% immunologic cross-reactivity using a double-antibody technique. Antibodies to the Electrophorus and Torpedo receptors also decrease the rate of alpha-bungarotoxin binding to these membraneous receptors. It is concluded that the Torpedo and hypothalamic nicotinic receptors are immunologically similar and that receptor binding sites for alpha-bungarotoxin and antibodies are physically close. These studies indicate that alpha-bungarotoxin can be used to study the nicotinic cholinergic receptor of the rat hypothalamus.

Animals

Inhibition of drinking in water-deprived rats by combined central angiotensin II and cholinergic receptor blockade.

The effect of blockade of central angiotensin II (AII) receptors and cholinergic receptors on thirst induced by water deprivation was studied in Sprague-Dawley rats and rats with hereditary hypothalamic diabetes insipidus (DI). Neither central AII nor cholinergic blockade alone affected drinking. Antagonism of both receptors simultaneously, however, significantly inhibited water intake of both Sprague-Dawley and DI rats. This inhibitory effect was not observed in water-deprived, nephrectomized rats. The combined antagonism on water intake was specific, since milk intake in hungry rats was not affected by simultaneous AII and cholinergic blockade. Isorenin concentrations in brain tissue were at control levels in water-deprived, nephrectomized, and non-nephrectomized Sprague-Dawley rats but were increased in water-deprived DI rats. The results suggest that angiotensin and cholinergic receptors in the brain have a physiological role in thirst. Thirst is maintained when either receptor is intact, but reduced when both receptors are inhibited by antagonists. They are independently capable of maintaining thirst.

Animals

Biochemical indentification of the mammalian muscarinic cholinergic receptor.

The muscarinic cholinergic antagonist 3-quinuclidinyl benzilate (QNB) binds avidly but reversibly to the muscarinic cholinergic recptor of mammalian brain and peripheral tissues. [3H]QNB binding provides a simple, sensitive, specific assay for the muscarinic cholinergic receptor binding. Inhibition of [3H]QNB binding to homogenates of brain and guinea pig ileum by muscarinic drugs correlates with their pharmacologic potencies, while nicotinic agents and noncholinergic drugs have neglibible affinity. The regional distribution of [3H]QNB binding throughout rat and monkey brain parallels to a major extent other cholinergic markers, suggesting that the majority of cholinergic synapses in the brain are muscarinic. [3H]QNB accumulation in various brain regions after intravenous injection provides a means of labeling the muscarinic receptor in vivo. By labeling the receptor in vivo; autoradiographic studies under the light microscope have been performed to visualize the muscarinic receptor.

Animals

Regional and subcellular distribution of myocardial muscarinic cholinergic receptors.

Regional and subcellular distributions of muscarinic cholinergic receptors were investigated in the myocardium of commonly used laboratory animals. The density of receptor sites (expressed in terms of either pmol/g protein or pmol/g tissue), amongst the regions examined, was found much higher in right and left atrium in the case of rat and rabbit whereas for the guinea pig and dog, the distribution was diffuse. However, irrespective of the species and/or region studies, the microsomal fraction, amongst the subcellular fractions, showed the highest enrichment or receptors.

Animals

Development of muscarinic cholinergic receptors in inbred strains of mice: identification of receptor heterogeneity and relation to audiogenic seizure susceptibility.

The concentrations and biochemical properties of muscarinic acetylcholine receptors in the brains of two highly inbred strains of mice, DBA/2J and C57BL/6J, have been studied using [3H]quinuclidinyl benzilate (QNB), a potent and specific receptor antagonist. As is the case with rat brain, murine muscarinic receptors exist in at least two forms, which differ in their affinities for receptor agonists but which have the same high affinity for receptor antagonists. Carbamylcholine binding to mouse neural membranes can be resolved into two components with KDs of 5.2 times 10(-7) and 7.9 times 10(-5) M. There is a regional heterogeneity of brain receptors with respect to their distribution between these high and low agonist affinity forms. Brain stem and hypothalamus receptors display binding properties that would be expected if over 60% of their receptors were in the high affinity state, while only 30-40% of cortex, striatum and thalamus receptors appear to be in the high affinity form. Hippocampal receptors display the least amount of high agonist affinity character. Saturation curves and Scatchard plots of QNB binding at 2, 14, 21 and 42 days postnatal age in both strains indicate no differences or changes in the affinity or nature of the binding with age. Significant increases in QNB binding per mg membrane protein were observed between 14 and 42 days in the cortex, hippocampus, striatum, thalamus and hypothalamus, but not in the midbrain-pons-medulla region. In the hippocampus the DBA mice had significantly more QNB binding. In the hypothalamus decreases with age in total binding were noted in DBA, while slight increases were noted in C57. Compared to C57, hippocampal receptors in DBA displayed lower agonist affinity at 14 and 21 days, a trait which was not apparent when DBA had outgrown their audiogenic seizure sensitivity at 42 days. The differences in receptor density and agonist state distribution between the two strains may be related to audiogenic seizure sensitivity.

Acoustic Stimulation

Rapid loss of nicotine-cholinergic receptor binding activity in the deafferented avian optic lobe.

The levels of alpha-bungarotoxin (alpha-BuTX) sensitive receptor sites were investigated in the optic lobe after optic deafferentation in the neonatal and adult chicken. Within two days a 30% loss of alpha-BuTX binding sites per optic lobe is observed in the neonatal chick after enucleation. The results are similar with the adult chicken in experiments where the receptor binding activity is measured in the optic lobe and in the optic tectum after enucleation. The possibility that acetylcholine is a neurotransmitter in the vertebrate retinotectal pathway is discussed.

Age Factors

On the ability of choline and its analogues to interact with muscarinic cholinergic receptors in the rat brain.

Choline displaced [3H]QNB binding from rat brain muscarinic receptors competitively, (Ki = 460 microM) but it was only 1/1000th as potent as ACh. Deanol was an extremely weak displacer of [3H]QNB binding while hemicholinium-3 was 50 times more potent than choline. Although brain levels of choline are well below its Ki value for muscarinic receptors, choline may directly interact with rat brain muscarinic receptors in some circumstances.

Animals