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Biomedical subjects

W A Hunt

Publications and source records attributed to W A Hunt.

At least 73 records · Page 4Linked to original sources
PubMed1982

A characterization of beta-adrenergic receptors on cellular and perigranular membranes of rat peritoneal mast cells.

Beta-adrenergic receptors were characterized by measuring the specific binding of 3H-dihydroalprenolol (DHA) on intact isolated rat peritoneal mast cells (RPMC) and on perigranular membranes derived from purified RPMC granules. The specific binding of 3H-DHA reaches an equilibrium within 30 min at 5 degrees C and is linear with cell number. Scatchard analysis reveals two populations of binding sites on intact cells: with KD = 10.6 +/- 2.6 and 129 +/- 4.7 nM and Bmax of 186 +/- 38 and 1200 +/- 415 fmol/10(6) cells, respectively. Each cell contains 120 X 10(3) high-affinity binding sites and 720 X 10(3) low-affinity binding sites. There appears to be neither alpha-adrenergic nor muscarinic cholinergic receptors on the RPMC. Specific binding of 3H-DHA also occurred to isolated granules with perigranular membranes. The binding was saturable with a single population of binding sites with an affinity (KD) of 7.0 +/- 0.45 nM. Maximum binding (Bmax) was calculated at 56.6 +/- 1.9 fmol/10(9) granules. Subfractionation of granule components demonstrated that the specific binding sites appear to be localized exclusively on the perigranular membrane.

Animals↗
PubMed1981

Neurotransmitter function in the basal ganglia after acute and chronic ethanol treatment.

Acute and chronic administration of ethanol has multiple effects on several neurotransmitters in the basal ganglia. Dopamine is the transmitter predominantly affected. Acceleration of dopaminergic activity is observed at low doses of ethanol. However, at high doses the reverse is observed. During the ethanol withdrawal syndrome that develops after chronic treatment, dopaminergic responses are reduced, whether from presynaptic or postsynaptic origins. Evidence also indicates that cholinergic and GABAergic processes may be implicated in these actions of ethanol. Ethanol apparently induces a variety of alterations in neurotransmitter function as a result of its disruption of membrane structure and associated electric properties.

Animals↗
PubMed1981

Neurotransmitter-receptor binding in various brain regions in ethanol-dependent rats.

Since chronic ethanol administration has been demonstrated to induce a number of alterations in neurotransmitter utilization, the possibility was investigated that the receptors, on which these transmitters act, are altered because of a modified synaptic input. Male Sprague-Dawley rats were rendered physically-dependent on ethanol by the oral administration of 9-13 g/kg of ethanol each day over a 4 day period. The binding of radioligands specific for alpha-adrenergic, beta-adrenergic, dopaminergic, serotonergic, muscarinic cholinergic, and GABAergic receptors was assessed at various intervals after withdrawal in several areas of the brain. No alteration in receptor binding was observed at any point under the conditions studied. The data suggest that the signs of an ethanol withdrawal syndrome are not mediated through changes in the ability of neurotransmitters to interact with their receptors.

Alcoholism↗
PubMed1980

Suppression of the ethanol withdrawal syndrome by aliphatic diols.

Considerable evidence both in vitro and in vivo suggests that alcohols exert their intoxicating properties through an interaction with membranes. A wide range of alcohols and diols with divergent structures induce a virtually identical spectrum of intoxication signs. Because of their pharmacological similarities to ethanol, a number of aliphatic diols were tested to determine whether this class of compounds may have efficacy in suppressing the ethanol withdrawal syndrome in rats. All of the diols tested, when administered intragastrically, were effective without inducing intoxication. Furthermore, the withdrawal-suppressing potencies of these drugs were related to their ability to partition into membranes, the same property that determines their potency as depressants. Two halogenated hydrocarbons, which are amphiphiles like alcohols and diols, were both able to suppress the withdrawal syndrome, although several aliphatic hydrocarbons could not. The data suggest that short-chain aliphatic alcohols and diols may have a common site of action, possibly in a region in membranes near the aqueous membrane interphase.

Alcoholism↗
PubMed1979

Associative learning, habit, and health behavior.

Habit is defined as a firmly established behavior pattern marked by increasing automaticity, decreasing awareness, and partial independence from reinforcement. Reinforcement is viewed as of primary importance in the acquisition of behavior, whereas principles of associative learning enter to complement reinforcement in the maintenance of behavior. Habit is seen as a mechanism for short-circuiting the reinforcement process to avoid its overload and for providing the organism with speed and stability of response instead of the variability offered by reinforcement. The implications of this definition of habit for acquisition and alteration of health behavior are discussed; examples include smoking, obesity, alcoholism, and coronary-prone (type A) behavior.

Alcoholism↗
PubMed1979

Alterations in neurotransmitter activity after acute and chronic ethanol treatment: studies of transmitter interactions.

Acute and chronic ethanol treatment has multiple effects on the neurotransmitter systems in the nigrostriatal complex. A single dose of ethanol increases striatal dopamine release at low doses, but depresses it at high doses. In ethanol-dependent rats, dopamine release is accelerated during intoxication, but is reduced during a withdrawal syndrome. Concomitantly, high-affinity choline uptake, an index of cholinergic activity, is elevated at times when dopamine release is depressed. Changes in dopaminergic or cholinergic receptor activity do not induce or result from these effects. Neither has a role for GABA or substance P yet been implicated. The data suggest that interactions between at least two trasmitters in the caudate nucleus may occur after acute and chronic ethanol treatment.

Acetylcholine↗
PubMed1977

The metabolism of biogenic amines in experimental animals and in human subjects during acute and chronic administration of ethanol.

Ethanol has been shown to induce a shift in catecholamine metabolism peripherally from normally oxidative pathways to reductive pathways. The mechanisms of this effect may result from competitive inhibition of aldehyde dehydrogenase by acetaldehyde. The shift in metabolism cannot be found in brain and alterations in catecholamine function may reflect changes in the turnover of these amines.

Acetaldehyde↗