Biomedical subjects

B K Giza

Publications and source records attributed to B K Giza.

9 recordsLinked to original sources

PubMed1992

Administration of satiety factors and gustatory responsiveness in the nucleus tractus solitarius of the rat.

The administration of certain factors associated with postprandial satiety decreases gustatory responsiveness. We compared the effects of intravenous injections of glucose, insulin, pancreatic glucagon (PG), and cholecystokinin (CCK) on multiunit activity evoked from taste responsive neurons in the nucleus tractus solitarius of rats. Glucose, insulin, and PG reliably suppressed evoked responses to lingual application of 1.0M glucose, whereas responses that followed CCK remained unchanged. A common physiological consequence of glucose, insulin, and glucagon is increased glucose availability which may impact directly on gustatory neurons or indirectly through modifications in ventral forebrain or vagal afferent activity.

Animals↗

PubMed1991

Polysaccharides as taste stimuli: their effect in the nucleus tractus solitarius of the rat.

Rats show a pronounced preference for the tastes of starch-derived polysaccharides. Three of these compounds--Polycose, maltotriose and amylopectin--were used along with a standard array of chemicals in a study of their effectiveness as taste stimuli, as monitored by evoked single unit activity in the nucleus tractus solitarii (NTS). Maltotriose and amylopectin elicited very few spikes and no clear quality-related pattern of neural activity. Polycose, however, was an effective taste stimulus. It evoked an activity profile across neurons and over time that was poorly correlated with that of the prototypical sugar (sucrose) and only moderately related to those of the non-sugar prototypes (NaCl, HCl and quinine-HCl). The 14 cells (23%) that responded particularly well to Polycose were all members of neuronal subgroups that emphasized salt, acid and quinine sensitivity. Thus, despite the strong behavioral preference shown to Polycose, its neural profile is unlike those of other preferred stimuli. Polycose may represent a unique taste stimulus whose quality cannot be readily associated with those of the traditional 4 basic tastes.

Amylopectin↗

PubMed1991

The effect of amiloride on taste-evoked activity in the nucleus tractus solitarius of the rat.

Amiloride is an inhibitor of passive sodium transport. Its application to taste receptors blocks inward sodium current, suppresses sodium-induced neural activity and reduces the perceived intensity of NaCl. We recorded taste-evoked responses of single neurons in the nucleus tractus solitarius (NTS) of the rat before and after the lingual application of amiloride to determine which neurons would be affected, the degree of the effect and the subsequent form of the neural code for sodium. Responses to all 7 stimuli that contained Na+ or Li+ were suppressed by amiloride. Activity evoked by the 8 other stimuli was unaltered. NTS neurons could be divided into 4 subsets according to their response profiles: Group 1 (salt-sugar), Group 2 (salt), Group 3 (salt-acid) and Group 4 (acid-salt-bitter). The entire effect of amiloride was discharged on cells in Groups 1 and 2; those in Groups 3 and 4 were unaffected. Following amiloride application, the neural code for sodium and lithium salts was highly similar to those for acids, bitter salts and quinine. Thus the activity of neurons in Groups 1 and 2 may be responsible for the distinction between 'saltiness' and sour-bitter tastes. The results imply that specific receptors are responsible for the recognition and transduction of sodium salts and that this specificity is maintained in the peripheral taste nerves to be manifested in the NTS.

Amiloride↗

PubMed1991

Gustatory neural coding in the monkey cortex: stimulus intensity.

1. We analyzed the activity of single neurons in gustatory cortex of alert cynomolgus monkeys in response to a range of stimulus intensities. Chemicals were deionized water, fruit juice, and several concentrations of the four prototypical taste stimuli: 10(-3)-1.0 M glucose, 10(-3)-1.0 M NaCl, 10(-4)-3 x 10(-2) M HCl, and 10(-5)-3 x 10(-3) M quinine HCl. 2. Taste-evoked responses could be recorded from a cortical gustatory area that measured 2.5 mm in its anteroposterior extent, 6.0 mm dorsoventrally, and 3.0 mm mediolaterally. Taste-responsive cells constituted 62 (3.7%) of the 1,661 neurons tested. Nongustatory cells gave responses associated with mouth movement (10.1%), somatosensory stimulation (2.2%), and approach or anticipation (0.9%). 3. Intensity-response functions were determined across 62 gustatory neurons. Neural thresholds for each stimulus quality conformed well to human psychophysical thresholds. Mean discharge rate was a direct function of stimulus concentration for glucose, NaCl, and quinine HCl. The most effective of the basic stimuli was glucose. 4. Power function exponents were calculated from the responses of neural subgroups most responsive to each basic stimulus. Those for glucose, NaCl, and quinine were within the range of psychophysically derived values. Thus the perceived intensity of each basic quality is presumably based on the activity of the appropriate neural subgroup rather than on the mean activity of all taste cells. 5. The mean breadth-of-tuning (entropy) coefficient for 62 gustatory neurons was 0.65 (range, 0.00-0.98). 6. There was no clear evidence of chemotopic organization in the gustatory cortex. 7. An analysis of taste quality indicated that sweet stimuli evoked patterns of activity that were clearly distinct from those of the nonsweet chemicals. Among the latter group, NaCl was differentiable from HCl and quinine HCl, whose patterns were closely related. 8. The response characteristics of cortical taste cells imply gustatory thresholds and intensity-response functions for the nonhuman primate that conform well to those reported in psychophysical studies of humans, reinforcing the value of this neural model for human taste intensity perception.

Action Potentials↗

PubMed1990

Coding channels in the taste system of the rat.

Basic taste qualities are thought to be perceived independently, yet discrete neural coding channels have not been demonstrated in the central nervous system. The response profiles of taste cells in the nucleus tractus solitarius (NTS) of the rat were categorized into four groups, and the effects of amiloride, a passive sodium channel blocker, on each were determined. NTS neurons that responded specifically to sodium chloride (NaCl) or to NaCl and sugars were suppressed by amiloride; those broadly sensitive to salts, acids, and bitter stimuli were unaffected. Moreover, the response profile evoked by NaCl lost its distinctiveness after treatment with amiloride, becoming similar to those evoked by acids and quinine. Receptors that respond to sodium must relay their information through independent coding channels to identifiable subgroups of NTS neurons, the activity of which is responsible for the perception of saltiness.

Amiloride↗

PubMed1990

Effect of cholecystokinin on taste responsiveness in rats.

Alterations in taste responsiveness have been suggested to mediate the suppression of feeding that accompanies exogenous administration of cholecystokinin (CCK). We tested this possibility in electrophysiological and behavioral experiments. First we monitored taste-evoked activity in the nucleus tractus solitarii of anesthetized rats during intravenous injection of 2 or 6 micrograms/kg of CCK or vehicle. We found no significant effects on taste activity during the 30-min period after CCK administration. Then we employed a conditioned taste-aversion paradigm to measure the rat's perceived intensity of a series of glucose concentrations under the same three experimental conditions. At 2 micrograms/kg, CCK had no effect; at 6 micrograms/kg there was a significant increase in the perceived intensity of 2 of the 15 test solutions, which we attribute to elevated vagal tone. The potential contribution of gastric distension was eliminated in the electrophysiological study and was minimized by brief exposures to stimuli in the behavioral experiment. Thus CCK administration, in the absence of significant gastric distension, does not appear to alter taste responsiveness.

Animals↗

PubMed1987

Blood glucose level affects perceived sweetness intensity in rats.

Electrophysiological data indicate that hyperglycemia is associated with decreased neural taste responsiveness to 1.0 M glucose, but not to 0.01 M quinine HCl, in the rat's hindbrain. The present behavioral experiment was conducted to determine whether this suppression of neural activity is manifested in a reduced intensity perception to glucose, but not quinine. Each rat learned to avoid 1.0 M glucose through development of a conditioned taste aversion. Perceived intensity was then measured in control and in hyperglycemic rats by the extent to which they generalized to each test concentration of glucose. Experimental subjects treated moderate glucose concentrations (0.6-2.0 M) as if their intensity perceptions were reduced by 47%. This is consistent with the mean reduction of 43% in taste-evoked neural activity associated with hyperglycemia. A corresponding experiment gave no indication of a change in intensity perception to quinine as a function of hyperglycemia, again in accord with earlier electrophysiological results. We conclude that nutritional state may selectively affect gustatory sensitivity in the rat.

Animals↗

PubMed1987

A measure of taste intensity discrimination in the rat through conditioned taste aversions.

The ability of rats to make intensity discriminations was determined by forming a conditioned taste aversion to a moderate concentration of each of four basic taste stimuli, and then measuring the level of acceptance (number of licks during a 15 sec exposure) shown to a range of concentrations of the same chemical. Rats (N = 66) could discriminate between glucose concentrations that were separated by as little as 0.074 M, between NaCl concentrations that differed by 0.029 M, between HCl concentrations that were 9 X 10(-4) M apart, and between quinine HCl concentrations that differed by as little as 2.4 X 10(-6) M.

Animals↗

PubMed1987

Intravenous insulin infusions in rats decrease gustatory-evoked responses to sugars.

Physiological factors that affect food intake have been shown to influence taste-evoked activity in the rat's central nervous system. Insulin appears to have a bimodal effect on feeding, inhibiting intake when its rise is within the normal physiological range, but, with further increases, causing hyperphagia. We studied the effect of low intravenous doses (0.5 U/kg) of regular insulin on taste-evoked responses in the nucleus tractus solitarius. Taste activity was elicited by application to the tongue of glucose, fructose, NaCl, HCl, and quinine. We monitored responses before and after intrajugular injections of insulin or a control vehicle. Taste responsiveness to glucose and fructose was significantly reduced for the period 7-22 min following the injection. Activity representing NaCl, HCl, and quinine was unaffected. The suppression of responsiveness to sweet stimuli could decrease the hedonic appeal of tastants and so serve as a mechanism by which physiological doses of insulin could contribute to a reduction in feeding.

Animals↗