Chronic Decerebrate Rats Research Articles

Taste responses in the nucleus tractus solitarius of the chronic decerebrate rat

The ingestive behavior of decerebrate rats has been studied for some time, yet little is known of its neural substrates. While taste fibers in rats proceed from hindbrain to thalamus and ventral forebrain, these regions return centrifugal fibers to the hindbrain by which lower-order taste activity may be influenced. We examined the functional characteristics of taste neurons in the nucleus tractus solitarii (NTS) of chronic decerebrate rats in which this reciprocal communication was disrupted and compared them with those of intact controls. Nine Wistar rats were decerebrated at the supracollicular level. After a minimum of one week recovery, they were immobilized with Flaxedil, anesthetized locally and prepared for recording. The responses of 50 taste cells were isolated bilaterally from the NTS of these animals, while the activity of 50 additional neurons was recorded from 12 intact rats under the same conditions. Taste stimuli included 7 NaLi salts, 3 sugars, HCl and citric acids, quinine HCl and NaSaccharin. Mean spontaneous activity in decerebrates was 6.5 spikes/s, 36.0% lower than the level in intact animals. Mean evoked activity was reduced by 32.6%. Analyses of the effects of stimulus quality, intensity and time course of the responses all indicated that the decrease in activity was attributable to the inability of taste cells in decerebrate rats to respond to demands for high discharge rates. This deficit could be responsible for the failure of these animals to develop conditioned taste aversions. Neurons from decerebrate preparations did, however, retain the broad sensitivity across stimuli that characterized taste cells in intact preparations. It was also typical that most neuron response profiles from decerebrates could be grouped into 3 loose clusters with peak sensitivities to acid-salt, salt or sugar. An analysis of similarities among stimulus activity profiles indicated that NaLi salts, sugars and an acid-quinine complex represented 3 groups of stimulus quality; in intact animals, the primary distinction was between sweet and non-sweet stimuli. Moreover, the response to sodium saccharin lost its bitter component in decerebrates. These findings were in general agreement with those derived from acute decerebrate rats.

Intraoral intake and taste reactivity responses elicited by sucrose and sodium chloride in chronic decerebrate rats.

The oral stimulating effects of sucrose and sodium chloride (NaCl) were assessed in chronic decerebrate and pair-fed intact control rats by measuring both oral motor taste-reactivity responses and intraoral intake volume. Taste-reactivity responses were videotaped during the first minute of the intraoral taste infusion. The infusion continued until the taste solution was rejected from the mouth, and the intake volume was computed accordingly. The number of ingestive taste-reactivity responses and the volume of intraoral intake consumed by pair-fed control and decerebrate rats increased with increasing sucrose concentration. Sucrose intake increased as concentration increased to 0.1 M, then plateaued between 0.3, 1.3, and 2.0 M sucrose for both groups. For control rats, intraoral NaCl elicited an inverted U-shaped function for both taste-reactivity responses and intake. Taste-reactivity responses of chronic decerebrate rats varied with NaCl concentration. In contrast to control rats, intake of NaCl did not differ from that of water for decerebrate rats. These data indicate that caudal brain-stem mechanisms are sufficient to control sucrose intake but are not adequate for the concentration dependent intake of NaCl. Second, these data also indicate that it is possible for taste-elicited oral motor responses to be dissociated from intake. The different roles of taste and postingestive factors in sucrose and NaCl intake are discussed.

Intraoral intake and taste reactivity responses elicited by sucrose and sodium chloride in chronic decerebrate rats.

Intraoral intake and taste reactivity responses elicited by sucrose and sodium chloride in chronic decerebrate rats.

Gustatory Activity in the NTS of Chronic Decerebrate Rats

Annals of the New York Academy of SciencesVolume 510, Issue 1 p. 458-461 Gustatory Activity in the NTS of Chronic Decerebrate Rats GREGORY P. MARK, GREGORY P. MARK Department of Psychology and Institute for Neuroscience University of Delaware Newark, Delaware 19716Search for more papers by this authorTHOMAS R. SCOTT, THOMAS R. SCOTT Department of Psychology and Institute for Neuroscience University of Delaware Newark, Delaware 19716Search for more papers by this author GREGORY P. MARK, GREGORY P. MARK Department of Psychology and Institute for Neuroscience University of Delaware Newark, Delaware 19716Search for more papers by this authorTHOMAS R. SCOTT, THOMAS R. SCOTT Department of Psychology and Institute for Neuroscience University of Delaware Newark, Delaware 19716Search for more papers by this author First published: November 1987 https://doi.org/10.1111/j.1749-6632.1987.tb43590.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume510, Issue1Olfaction and Taste IXNovember 1987Pages 458-461 RelatedInformation

A model for the study of visceral pain states: chronic inflammation of the chronic decerebrate rat urinary bladder by irritant chemicals

Normal healthy visceral tissue is largely insensitive to many kinds of tissue damaging stimuli, such as cutting, crushing or burning. When inflamed, however, visceral tissue frequently and easily elicits pain. Here we have produced inflammatory responses in urinary bladders of chronically decerebrated rats with irritant chemicals, as a model of a visceral pain state. The irritants used were 25% turpentine, 2.5% mustard oil, 2% croton oil. All produced a strong inflammatory response, as judged by protein extravasation and oedema, and invasion of the tissue with leucocytes, which started within hours of treatment. The inflammatory states were associated with hyperexcitable bladder reflexes; baseline pressures were larger at given volumes, and large micturition contractions occurred at lower volumes. These changes persisted for up to 48 h after a single treatment. The behaviour of the animals and their responsiveness to noxious stimulation were also assessed. In general animals were hypersensitive to noxious stimuli applied to the tail or caudal abdomen, with small or no changes in responses to hind limb or rostral abdominal stimulation. These irritants, particularly turpentine, applied to chronic decerebrate rats may thus provide useful models for studies of the neuronal processes which contribute to visceral nociception.

Pre- and postabsorptive insulin secretion in chronic decerebrate rats.

Basal, taste-stimulated (preabsorptive), and postabsorptive insulin secretion and plasma glucose responses were studied in chronic decerebrate rats and their pair-fed neurologically intact controls. In experiment 1, preabsorptive insulin responses (PIR) elicited by oral infusions of glucose solution was measured in chronic decerebrate rats. Oral glucose was ingested and led to a significant short-latency elevation in plasma insulin levels. Plasma glucose levels remained constant during this time. These data show that caudal brain stem mechanisms, in isolation of the forebrain, are sufficient for the neurally mediated PIR elicited by oral glucose stimulation. In experiment 2, effects of decerebration on postabsorptive insulin secretion were measured. During the 3 h immediately after transection there was no effect of decerebration on peripheral plasma insulin or glucose levels. Thereafter, however, basal plasma insulin levels of decerebrate rats were at least twice that of control rats. Plasma glucose levels of both groups remained identical despite the hyperinsulinemia in decerebrate rats. Atropine treatment decreased, and phentolamine administration elicited a greater absolute and percent change increase in insulin levels of decerebrate rats. These data indicate that altered autonomic tone contributes to maintaining the basal hyperinsulinemia in the decerebrate rat. In response to intragastric meals and glucose and intravenous glucose administration, insulin secretion was greater in decerebrate than in control rats. Percent change in insulin levels from base line was similar in both groups after intragastric meals and intravenous glucose. In response to intragastric glucose, however, percent increase in insulin levels was greater in decerebrate rats. Decerebrate rats demonstrated mild glucose intolerance after intragastric and intravenous treatments. These results are contrasted with the known effects of ventromedial hypothalamic lesions on insulin secretion and glucose homeostasis.

Sodium homeostasis in chronic decerebrate rats.

Physiological and behavioral concomitants of sodium need were studied in supracollicularly transected and pair-fed intact rats. Chronic decerebrate rats, like intact rats, reduced their urine sodium output when placed on a sodium-deficient diet. Similarly, 24 hr after sodium loading, decerebrate and intact rats excreted comparable levels of the excess sodium. In the 2 hr immediately following the loading, decerebrate rats excreted less sodium. In contrast, behavioral aspects of sodium homeostasis were completely absent in chronic decerebrate rats. In separate experiments, intraoral intake, and taste-reactivity responses, elicited by intraoral infusions of NaCl were measured during sodium-replete and sodium-deficient conditions. In response to oral infusions of NaCl, intact rats consumed significantly more and produced greater numbers of ingestive taste-reactivity responses when they were sodium deficient than when they were sodium replete. The same sodium-depletion treatments in chronic decerebrate rats, however, altered neither the intraoral intake of NaCl nor the frequency of NaCl-elicited ingestive taste-reactivity responses. These results suggest that the behavioral compensatory responses that follow changes in the internal sodium state are dependent upon forebrain mechanisms.

Sodium homeostasis in chronic decerebrate rats.

Sodium homeostasis in chronic decerebrate rats.

Injury-induced plasticity of the flexor reflex in chronic decerebrate rats

The hindlimb-flexor-withdrawal reflex elicited by stimulation of the skin of the hindpaw has been examined in chronic decerebrate rats. This flexor reflex manifests as a typical phasic avoidance response when measured either behaviourally in the decerebrate rat or electrophysiologically in the decerebrate-spinal preparation. Once the threshold of the cutaneous flexor-reflex afferents in the skin have been exceeded a brief burst of activity with only a short afterdischarge occurs in the flexor motoneurones. The response to sustained stimuli adapts rapidly. In the absence of any treatment to the hindlimb the threshold, duration and responsiveness of the reflex remains stable when tested repeatedly. Thermal or chemical stimuli of sufficient intensity to produce tissue injury and prolonged local inflammation in a hindpaw of the chronic decerebrate rat result in marked and long-lasting (several weeks) alterations in the ipsilateral withdrawal reflex. The mechanical threshold necessary to elicit the reflex by stimulation of the hindpaw falls so that light touch or brush can now elicit a response instead of the firm pressure or pinch required pre-injury. Suprathreshold stimuli to the inflamed skin generate a sustained oscillating pattern of flexion in contrast to the brief flicking movement found in control animals. Electromyographic recordings from the hamstring flexor muscles ipsilateral to the inflamed hindpaw show decreased mechanothresholds, increased spontaneous activity, prolonged afterdischarges to brief stimuli and a slowly adapting tonic response to sustained stimulation. Populations of single cutaneous mechanoreceptive C-primary afferents recorded both from untreated decerebrate rats and from rats with an inflamed hindpaw are indistinguishable in terms of their response properties. There is no difference in threshold, spontaneous activity or afterdischarge between the two populations. The possible mechanisms responsible for the conversion of the high threshold phasic flexor reflex into a low threshold tonic reflex are discussed as are the possible implications for sensory disorders that accompany chronic injury in man.

Short-term and long-term habituation of the acoustic startle response in chronic decerebrate rats.

Short-term and long-term habituation of the acoustic startle response in chronic decerebrate rats.

Short-term and long-term habituation of the acoustic startle response in chronic decerebrate rats.

Chronic decerebrate rats, maintained in good condition for 31-84 postoperative days, showed significant within-session habituation of the acoustic startle response. However, they showed no habituation over days under conditions that produced significant response deficits in controls. The decerebrates' stimulus-provoked response deficits may have endured for up to 40 min between sessions, and they were apparently more than normally susceptible to stimulus-provoked sensitization. The data are consistent with intrinsic models which assume that the mechanisms for short-term habituation are intrinsic to the stimulus-response (S-R) pathway in the lower brain stem. On the other hand, relatively permanent long-term habituation of the acoustic startle response must be mediated by extrinsic mechanisms rostral to the S-R pathway which superimpose an inhibitory influence on that pathway.

Long term alterations in the excitability of the flexion reflex produced by peripheral tissue injury in the chronic decerebrate rat

Chronic decerebrate rats have been prepared by the aspiration of all the cranial contents rostral to the mesencephalon. With careful nursing, body temperature control and orogastric tube feeding the rats survive for up to 4 months. The decerebrate rats have intact brain stem and spinal reflexes including locomotion, righting reflexes and grooming. Mild noxious cutaneous thermal and mechanical stimuli of an intensity which does not produce tissue damage evokes flexion withdrawal reflexes, vocalization, orientation to the site of the injury and generalized escape or attack responses, from the animals. These effects are transient and only occur during the application of the stimulus. The rats do not exhibit stress reactions, aggression or vocalization when handled before or after application of such noxious stimuli. The production of localized tissue injury by thermal or chemical means results in long term alterations (up to 6 weeks) in the thresholds and excitability of the flexor reflex, both ipsilateral and contralateral, to the site of the injury. It is proposed that the reduction in the flexor reflex threshold is analogous to the hyperalgesia and allodynia that follows tissue injury in man and that the long term alterations in the flexor reflex in the chronic decerebrate rat provide a model for the study of chronic pain, without the ethical problems associated with such studies in intact animals.

Lack of ingestive compensation to osmotic stimuli in chronic decerebrate rats

Chronic decerebrate rats fitted with oral fistulas for remote injection of water or nutrient were tested for their capacity to behaviorally compensate for dehydration by increasing their ingestion of water. Decerebrates and their controls were given water for ingestion via the oral fistula in 50-microliter aliquots following various challenges. The rats' ejection of water from the mouth marked behavioral termination of the drinking. The volume of water was measured 1 and 24 h after an intragastric meal of regular diet; 0.5, 4, 8, and 24 h following subcutaneous isotonic or hypertonic NaCl injection; and 1, 4, 8, and 24 h following an intragastric meal of regular or 3% NaCl adulterated diet. Unlike controls, decerebrates failed to increase the amount of water ingested following intracellular dehydration regardless of the means of producing dehydration or the duration of time permitted for a response. However, both control and decerebrate rats increased their ingestion of a sweet solution (0.03 M sucrose) demonstrating their capacity to respond and confirming their ability to compensate for food deprivation. This lack of increased water intake in response to dehydration for decerebrate rats favors the existence of at least some aspects of the regulatory circuitry for this behavioral control of water balance to lie in the forebrain.

Production and regulation of ingestive consummatory behavior in the chronic decerebrate rat

A given taste does not always elicit the same response be it ingestion or rejection. Rather, the afferent-efferent relationships yielding these responses are regulated by neural signals deriving from the organism's physiological state and experience. By examining preparations with increasing degrees of ablation, it is not only possible to establish the neural boundary conditions for the production of ingestive consummatory behavior but also for its regulation. A comparison of the capacity of brain levels for regulating palatability provides an alternative approach to the prevalent single integrator hypothesis. Ablated preparations, like chronic decerebrate rats, do not spontaneously eat or drink. Nevertheless, we have developed methodologies for examining the topography of ingestion and rejection responses and fluid intakes of decerebrate rats. Using these methods we have shown that the discriminative responses to tastes of decerebrates do not differ from those of intact rats. The decerebrate rat can not only produce ingestive consummatory responses, but can also regulate these responses as a function of deprivation-repletion. This demonstration coupled with the evidence for sympathoadrenal function in the decerebrate rat leads us to conclude that neural mechanisms caudal to the forebrain are sufficient for production of ingestive consummatory responses as well as aspects for its regulation.

The taste reactivity test. II. Mimetic responses to gustatory stimuli in chronic thalamic and chronic decerebrate rats

The taste reactivity test described in the preceding paper was used to begin determining the capacity of brain stem structures to execute and regulate ingestive behavior. Both chronic thalamic and chronic decerebrate rat preparations were examined repeatedly, and their gustatory mimetic responses compared through frame-by-frame videotape analysis with the responses of neurologically normal controls. In response to orally injected taste stimuli, chronic decerebrate rats executed the same mimetic response components, and very similar response sequences observed in intact rats. In contrast, all taste stimuli elicited a quinine-like rejection sequence from chronic thalamic rats. In thalamic rats mimetic responses associated with ingestion were completely absent. Based on the similarities in the ingestion and rejection responses of decerebrate and intact rats, it appears that discriminative responses to taste result from integrative mechanisms complete within, or caudal to, the midbrain. Since decerebrate rats have the capacity to execute both ingestion and rejection response sequences, neural mechanisms rostral to the midbrain in some way suppress ingestion and/or releaser ejection responses in the thalamic preparation.

Neurological tests and behavioral deficits in chronic thalamic and chronic decerebrate rats

The taste reactivity of chronic decerebrate rats is very similar to intact rats although chronic thalamic rats display only the quinine-like rejection sequence. The performance of intact (n = 12), decerebrate (n = 10) and thalamic (n = 10) preparations was further compared across a set of simple behavior tests to more broadly assess the behavioral capacities of the rodent brain stem. Decerebrate rats were immobile. They exhibited no spontaneous activity other than grooming, but often overreacted with well-coordinated movements (i.e., running, jumping and climbing) to seemingly inappropriate activating stimuli such as tail pinch, handling or water squirted on the fur. Decerebrates had lower thresholds for elicited attack and grooming behaviors than thalamic or intact rats. The thalamic preparation exhibited a wider range of intact neurological responses than the decerebrate. Cage climbing, resistance to gravity, suspension and muscle tone reactions, rhythmic vibrissae movements and examination of object with snout and mandible were difficult to distinguish from controls. Decerebrates either did not perform these responses or did so in a clearly different manner. In contrast, grooming behavior in thalamics was much less effective than in decerebrates. Thalamic rats spontaneously executed grooming sequences, but the responses were misdirected and ineffective. Despite their relative immobility, decerebrates coordinated grooming sequences and maintained their fur. No single mechanism appears to account for the constellation of deficits and capacities observed in either chronic thalamic or chronic decerebrate rats.

Classical conditioning of the corneal reflex in the chronic decerebrate rat

Classical conditioning of the corneal reflex in the chronic decerebrate rat