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Stuart A McCaughey

Publications and source records attributed to Stuart A McCaughey.

4 recordsLinked to original sources

Taste-evoked responses to sweeteners in the nucleus of the solitary tract differ between C57BL/6ByJ and 129P3/J mice.

C57BL/6ByJ (B6) and 129P3/J (129) mice have different alleles of Tas1r3, which is thought to influence gustatory transduction of sweeteners, but studies have provided conflicting results regarding differences in sweetness perception between these strains. Single-unit taste-evoked activity was measured in the nucleus of the solitary tract (NST) in anesthetized B6 and 129 mice to address this controversy and to provide the first electrophysiological characterization of this nucleus in mice. Neurons had properties similar to those of NST cells in other species, including mean breadth-of-tuning of 0.8 +/- 0.0. There were no strain differences in neural responses at 600 or 900 ms after onset, but, with a 5 s evoked period, responses to the sweeteners sucrose, maltose, acesulfame-K, SC-45647, and D-phenylalanine were significantly larger in B6 relative to 129 mice. The strains did not differ in their mean response to NaSaccharin, but it evoked an across-neuron pattern of activity that was more similar to that of sucrose and less similar to that of NaCl in B6 mice compared with 129 mice. Neurons were classified as sucrose, NaCl, or HCl responsive, with the former more common in B6 than 129 mice. Relative to other neurons, sucrose-responsive cells had delayed but more sustained sweetener responses in both strains. The results suggest that B6 mice perceive some sweeteners as more intense, but NaSaccharin as sweeter and less salty, relative to 129 mice. Furthermore, activity evoked by sweeteners includes a phasic response sent to different NST cells than a later tonic response, and only the latter differs between B6 and 129 mice.

Animals↗

Calcium deprivation increases the palatability of calcium solutions in rats.

Calcium-deprived rats have elevated intakes of CaCl2, other calcium salts, and some non-calcium compounds. We used taste reactivity to examine the effects of calcium deprivation on the palatability of CaCl2 and other solutions. Nine male Sprague-Dawley rats were calcium-deprived by maintenance on a low-calcium diet, and eight replete rats were used as controls. All rats were videotaped during intraoral infusion of the following solutions: 30 and 300 mM CaCl2, 30 mM calcium lactate, 100 and 600 mM NaCl, 30 mM MgCl2, 1 mM quinine.HCl, 2.5 mM sodium saccharin, and deionized water. We counted individual orofacial and somatic movements elicited by the infusions and used them to calculate total ingestive and aversive scores. Relative to controls, calcium-deprived rats gave a significantly larger number of tongue protrusions and had higher total ingestive scores for CaCl2, calcium lactate, NaCl, and MgCl2. Our results suggest that CaCl2, calcium lactate, NaCl, and MgCl2 taste more palatable to rats when they are calcium-deprived than replete, and this may be responsible for the increased intake of these solutions following calcium deprivation.

Analysis of Variance↗

Lesions of the subfornical organ decrease the calcium appetite of calcium-deprived rats.

There are several indications that neurons in the rat's subfornical organ (SFO) are sensitive to internal calcium status. We investigated the role of the SFO in regulating calcium intake by comparing the consumption of 30 mM CaCl2 by rats with (a) lesions of >90% of the SFO, (b) lesions that left the SFO mostly intact but disconnected its rostroventral stalk, (c) misplaced lesions that spared most of the SFO, or (d) a sham lesion procedure. In one experiment involving calcium-replete rats, these four groups had similar CaCl2 intakes. In another experiment involving calcium-deprived rats, those with lesions of the SFO or its rostroventral stalk consumed less CaCl2 than did those with missed or sham lesions. The SFO therefore appears to play a role in the calcium appetite that accompanies calcium deprivation in rats, most likely through its rostroventral efferents, but it is not important for need-free calcium intake.

Animals↗

Magnesium appetite in the rat.

Rats modify their ingestive behaviour to correct deficiencies of minerals such as sodium and calcium. Here, we examined the effect of magnesium deprivation on the ingestion of MgCl2 and other solutions. Male Sprague-Dawley rats were fed a nutritionally complete or magnesium-deficient diet and were then given 3.2, 10, 32, or 100mM MgCl2, 32mM CaCl2, 32mM NaCl, 10mM HCl, or 2.5mM saccharin, and their intake was measured for 24h in a two-bottle choice test with water. Within the first 5 min, magnesium-deprived subjects given 3.2, 32, or 100mM MgCl2 or 32mM CaCl2 drank significantly more of these solutions than did replete rats. In a separate study, rats fed replete, magnesium-deficient, or calcium-deficient diets were given a three-bottle choice between water, 32mM MgCl2, and 32mM CaCl2. The deprived rats preferred the solution that ameliorated their deficiency; for example, during the first 1h, the magnesium-deprived rats drank 3.1 +/- 0.5ml MgCl2 and 1.1 +/- 0.4ml CaCl2, whereas the calcium-deprived rats drank 1.8 +/- 0.5ml MgCl2 and 3.9 +/- 0.4ml CaCl2. Thus, magnesium deprivation leads to a compensatory appetite for magnesium, and the appetites for magnesium and calcium are distinct and specific. The rapid expression of magnesium appetite suggests that it depends in part on innate, gustatory factors.

Analysis of Variance↗