The relationship between specific gustatory nerve activity and central patterns of taste-evoked neuronal activation is poorly understood. To address this issue within the first central synaptic relay in the gustatory system, we examined the distribution of neurons in the nucleus of the solitary tract (NST) activated by the intraoral infusion of quinine using Fos immunohistochemistry in rats with bilateral transection of the chorda tympani (CTX), bilateral transection of the glossopharyngeal nerve (GLX), or combined neurotomy (DBLX). Compared with nonstimulated and water-stimulated controls, quinine evoked significantly more Fos-like-immunoreactive (FLI) neurons across the rostrocaudal extent of the gustatory NST (gNST), especially within its dorsomedial portion (subfield 5). Although the somatosensory aspects of fluid stimulation contributed to the observed increase in FLI neurons, the elevated number and spatial distribution of FLI neurons in response to quinine were remarkably distinguishable from those in response to water. GLX and DBLX produced a dramatic attenuation of quinine-evoked FLI neurons and a shift in their spatial distribution such that their number and pattern were indiscernable from those observed in water-stimulated controls. Although CTX had no effect on the number of quinine-evoked FLI neurons within subfield 5 at intermediate levels of the gNST, it produced intermediate effects elsewhere; yet, the spatial distribution of the quinine-evoked FLI neurons was not altered by CTX. These findings suggest that the GL provides input to all FLI neurons responsive to quinine, however, some degree of convergence with CT input apparently occurs in this subpopulation of neurons. Although the role of these FLI neurons in taste-guided behavioral responses to quinine remains speculative, their possible function in oromotor reflex control is considered.
The peripheral, central, and behavioral consequences of glossopharyngeal nerve transection (GLX), regeneration, and the prevention of regeneration on the quinine-elicited responses of adult rats were concurrently examined. Oromotor taste reactivity (TR) was videotaped during intraoral infusion of 7 ml of either quinine (3 mm) or distilled water at 17, 52, or 94 d after surgery. We confirmed previous findings by showing that 17 d after neurotomy, (1) the number of circumvallate (CV) and foliate taste buds, (2) gapes (a characteristic aversive TR response), and (3) the number of Fos-like immunoreactive (FLI) neurons in the gustatory NST (gNST), particularly in the medial portion (subfield 5) of the rostral central subdivision (RC), were all severely attenuated in GLX rats. We extended these findings by showing that these lesion-induced effects were enduring when the GL did not regenerate (up to 94 d). In contrast, when the GL regenerated, as few as 52 d were sufficient to re-establish quinine-elicited TR, especially gaping, and FLI expression in RC, particularly within subfield 5, to values comparable with quinine-stimulated sham-operated rats. Evidently, the gNST maintains its potential to restore accurately the organization of neural activity that is disrupted by nerve injury, as assessed by FLI, ultimately leading to the return of normal protective oromotor responses, provided the nerve regenerates. This recovery was complete despite the reappearance of a reduced population of CV taste buds ( approximately 75% control values) and may relate to peripheral and/or central changes that occur in tandem with regeneration of the GL.
The capacity of aging rats to defend body fluid homeostasis in response to a variety of dipsogenic and natriorexigenic stimuli was assessed. Male and female rats of both the Fischer 344 (FR) and Sprague-Dawley (SD) strains were used and tested at target ages of ∼5, 10, 15, and 20 mo in both longitudinal and cross-sectional studies. There were no consistent age-related declines in water intake in response to water deprivation or acute administration of hypertonic NaCl; angiotensin (ANG) I, II, III; or isoproterenol. Likewise, there were no major impairments in either urinary excretion of the hypertonic NaCl load or excretion of water or hypotonic NaCl loads, although the latter were excreted more slowly in the older cohorts. The preference/aversion functions for NaCl solutions differed between SD and FR rats, but did not change with age except in male FR rats that lost their aversion to dilute NaCl at 20 mo of age. Intake of hypotonic NaCl solution after acute sodium depletion (furosemide treatment) showed a partial decline with age, and the older rats sustained larger estimated sodium deficits after a 6-h repletion period. A more complete age-related decline was observed in the intake of hypertonic NaCl stimulated by chronic dietary administration of a kininase II inhibitor (ramipril). Male rats of 15–20 mo of age showed no ramipril-induced sodium appetite. Brain ANG II receptor density, determined by autoradiography, declined by almost 50% in the paraventricular nucleus at 20 mo of age and declined slightly in the organum vasculosum laminae terminalis but did not decline in either the supraoptic nucleus or subfornical organ. Thus the major deficits in fluid intake in aging rats are related to salt appetite; the mechanism was not identified definitively.
On the basis of electrophysiological studies, the glossopharyngeal nerve (GL) is far more responsive to quinine than the chorda tympani (CT) or greater superficial petrosal (GSP) nerves. The licking behavior of water-deprived rats to quinine (0.03-3.0 mM) and distilled water (10-s trails) was tested before and after various nerve transections. GL+CT section caused a substantial reduction in responsiveness. GSP+CT section had a moderate effect, and GL section alone produced only marginal impairments. Control, partially desalivated, and CT-sectioned rats were unaffected. Thus, the GL is not necessary for normal unconditioned taste-guided appetitive responsiveness to quinine, but the collective input from the GSP and CT is necessary and most likely sufficient. These data suggest that the quinine-evoked input of the GL and CT converge centrally.
Lick responses to sucrose and maltose (0.01-1.0 M) were measured in nondeprived rats during brief-access taste trials before and after histologically confirmed gustatory neurotomy. Pronounced decreases in sugar responsiveness occurred after combined section of the chorda tympani (CT) and greater superficial petrosal nerves. The additional section of the glossopharyngeal nerve (GL) flattened the sucrose concentration-response function. Extirpation of the sublingual and submaxillary salivary glands also attenuated sugar responsiveness. Section of the CT or GL alone or in combination caused less severe or no decreases in sugar licking. There were signs of licking impairments after some of these neurotomies, but the data suggest that changes in sugar responsiveness were not solely motor in origin. Thus the 7th nerve is necessary and most likely sufficient for the maintenance of normal unconditioned appetitive responsiveness to sucrose and maltose.
Studies examining the effects of transection and regeneration of the glossopharyngeal (GL) and chorda tympani (CT) nerves on various taste-elicited behaviors in rats have demonstrated that the GL (but not the CT) nerve is essential for the maintenance of both an unconditioned protective reflex (gaping) and the neural activity observed in central gustatory structures in response to lingual application of a bitter substance. An unresolved issue, however, is whether recovery depends more on the taste nerve and the central circuits that it supplies and/or on the tongue receptor cell field being innervated. To address this question, we experimentally cross-wired these taste nerves, which, remarkably, can regenerate into parts of the tongue they normally do not innervate. We report that quinine-stimulated gaping behavior was fully restored, and neuronal activity, as assessed by Fos immunohistochemistry in the nucleus of the solitary tract and the parabrachial nucleus, was partially restored only if the posterior tongue (PT) taste receptor cell field was reinnervated; the particular taste nerve supplying the input was inconsequential to the recovery of function. Thus, PT taste receptor cells appear to play a privileged role in triggering unconditioned gaping to bitter tasting stimuli, regardless of which lingual gustatory nerve innervates them. Our findings demonstrate that even when a lingual gustatory nerve (the CT) forms connections with taste cells in a non-native receptor field (the PT), unconditioned taste rejection reflexes to quinine can be maintained. These findings underscore the extraordinary ability of the gustatory system to adapt to peripherally reorganized input for particular behaviors.
Chorda tympani nerve (CT) transection in rats severely impairs NaCl taste detection. These rats can detect higher concentrations of NaCl, however, suggesting that remaining oral nerves maintain some salt sensibility. Rats were tested in a gustometer with a 2-response operant taste-detection task before and after sham surgery (n = 5), combined transection of the CT and the greater superficial petrosal nerves (GSP; 7x, n = 6), or transection of the glossopharyngeal nerve (GL; 9x, n = 4). Thresholds did not significantly change after sham surgery. Although the GL responds to NaCl and innervates nearly 60% of total taste buds, 9x surgery had no effect. However, 7x surgery increased NaCl detection threshold by approximately 2.5 log(10) units, greater than that reported for CT transection alone. These results suggest that the GSP contributes to NaCl sensitivity in rats and also demonstrate that the GL and perhaps the superior laryngeal and lingual nerve proper can maintain some NaCl detectability at high concentrations. These findings confirm the primacy of the 7th nerve relative to the 9th nerve in sensibility of NaCl in the rat model.
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