Decerebrate Rats Research Articles

Medioventral medulla-induced locomotion

Previous anatomical studies demonstrated the presence of descending projections from the physiologically identified mesencephalic locomotor region (MLR) to the medioventral medulla (MED) in the cat. The present experiments were designed to determine if a similar low threshold locomotion-inducing area is present in the rat medulla. In addition, the nature of the neurochemical control of this area of the brain was explored using localized injections of neurochemical agents in the decerebrate rat during locomotion on a treadmill. A region virtually identical to that reported in the cat was found to lead to controlled locomotion on a treadmill following stimulation at low amplitude currents (≤60 μA). Injections of cholinergic agonists into the MED of the rat induced locomotion which could be blocked by injections of cholinergic antagonists. In addition, injections of GABA antagonists were found to induce stepping which could be blocked by injections of GABA or GABA agonists. Substance P (SP) also was found to induce walking following injection into the MED of the rat. Injections of an excitatory amino acid agonist (NMDA) also were found to induce locomotion in the rat. These effects were blocked by injections of an excitatory amino acid antagonist (APV). Since these results had not been reported for the cat MED, a short series of experiments revealed that the MED in the cat also responded to NMDA.

Role of supraspinal systems in environmentally induced antinociception: Effect of spinalization and decerebration on brief shock-induced and long shock-induced antinociception.

Prior research suggests that afferent nociceptive information can directly activate the opioid and nonopioid brainstem antinociceptive systems. Grau (1987a) has hypothesized that direct activation occurs when an organism is exposed to severe aversive stimuli and that forebrain systems mediate the activation of the antinociception systems when mild aversive stimuli are used. The present experiments tested this hypothesis by examining the impact of spinalization and decerebration on the antinociception observed after mild (3 0.75-s 1.0-mA shocks) and vs. severe (3 25-s 1.0-mA shocks) tailshocks. It was found that spinal transection eliminated the antinociception observed after both shock schedules, whereas decerebration blocked mild shock-induced, but not severe shock-induced, antinociception. Surprisingly, decerebration potentiated severe shock-induced antinociception. The opioid antagonist naltrexone had no effect on the antinociception observed after severe shock in sham or decerebrate rats.

Modulatory effects of endothelin-1 on central cardiovascular control in rats.

In urethane-anesthetized and immobilized rats, modulatory effects of endothelin-1 (ET-1) on central cardiovascular control were examined. An injection of 0.1 pmol of ET-1 into the cisterna magna caused immediate increases in arterial pressure (AP), renal sympathetic nerve activity (RSNA), and heart rate (HR) that lasted for 5-45 min. At doses of 1 and 10 pmol, intracisternal ET-1 elicited initial increases (phase I) followed by decreases in these variables below the pre-injection level (phase II). At the dose of 1 or 10 pmol, the arterial baroreceptor reflex was suppressed during the latter part of phase I and during phase II. The three variables subsequently returned to, or often exceeded, pre-injection levels in 30 to 60 min and reflex activity recovered (phase III). However, AP often remained below control throughout the 2-h observation period. Essentially identical responses to intracisternal ET-1 were observed in unanesthetized precollicular decerebrated or urethane-anesthetized rats. Application of a piece of filter paper soaked with 1 pmol of ET-1 to the ventral surface of the medulla (VSM) caused the pattern of changes similar to the following intracisternal injection. A microinjection of 4 pmol of ET-1 into the nucleus tractus solitarius (NTS) caused a moderate increase in RSNA with a minute fall in AP. Intrathecal administration of ET-1 resulted in moderate changes in AP and RSNA at the dose as high as 100 pmol. We conclude that intracisternally administered ET-1 modulates tonic and reflex control of AP and sympathetic vasomotor activity and that the VSM appears to be involved critically in this modulation.

Modulatory effects of rat endothelin on central cardiovascular control in rats.

To characterize the modulatory action of rat endothelin (endothelin-3 or ET-3) on the cardiovascular control by the central nervous system (CNS), ET-3 was injected into the cisterna magna of urethane-anesthetized and immobilized rats. An injection of 100 pmol of ET-3 caused immediate rises in arterial pressure (AP), renal nerve activity (RNA), and heart rate (HR). These variables subsequently decreased and, in 5-20 min, fell below the pre-injection level. Simultaneously, the arterial baroreceptor reflex was almost totally suppressed. Although RNA and HR subsequently returned to, or often exceeded, pre-injection levels in 20 to 60 min and reflex activity recovered, AP sometimes remained below control for at least 2 h. A similar pattern of changes was elicited in unanesthetized precollicular decerebrated rats. The responses to ET-3 were abolished by hexamethonium chloride, but were not conspicuously altered by arginine vasopressin antagonist or angiotensin II antagonist. The CNS sites responsible for ET-induced changes were subsequently searched. Topical application of ET-3 to the ventral surface of the medulla (VSM) caused the pattern of changes in AP, RNA, and HR similar to that following intracisternal injection. Microinjection of ET-3 into the nucl. tractus solitarius (NTS) increased AP and RNA, whereas intrathecal administration of it decreased them. We conclude that intracisternally administered ET-3 centrally modulates both tonic and reflex control of AP by the sympathetic nervous system and that the VSM appears to be primarily responsible for the modulation, although NTS and spinal cord may also be involved in it.

Differential effects of morphine and clonidine on visceral and cutaneous spinal nociceptive transmission in the rat

1. The effect of morphine or clonidine administered systemically on visceral and cutaneous spinal nociceptive transmission was examined in 45 dorsal horn neurons in spinalized, decerebrate rats: 17 "cutaneous" dorsal horn neurons located in the L3-L5 spinal segments were excited by heating the glabrous skin of the hindpaw (48 degrees C, 15 s) and 28 "visceral" dorsal horn neurons located in the T13-L2 spinal segments were excited by colorectal distension (80 mmHg, 20 s). The 28 visceral dorsal horn neurons were subclassified as 18 short-latency abrupt neurons (SL-A), which were excited by colorectal distension at short latency (less than 1 s) and whose activity abruptly returned to base line following termination of the distending stimulus, and as 10 short-latency-sustained (SL-S) neurons, which also were excited at short latency (less than 1 s) by colorectal distension, but whose activity was sustained above base line for 4-31 s following termination of the distending stimulus. 2. Morphine produced a dose-dependent, naloxone-reversible inhibition of both spontaneous activity and/or neuronal responses during heating or colorectal distension of 8 SL-A, 7 SL-S, and 11 cutaneous dorsal horn neurons. Comparison of the effective doses of morphine to produce a 50% reduction in the response of the neurons (ED50s) during colorectal distension or heating demonstrated that, at the intensities of distension and heating employed, SL-S neurons were affected at the least dosage (ED50 = 0.46 mumol/kg), followed by SL-A neurons (ED50 = 1.95 mumol/kg) and cutaneous neurons (ED50 = 6.12 mumol/kg). Effects on spontaneous activity were variable: at low doses morphine produced an increase in the spontaneous activity of 2 SL-A and 5 cutaneous neurons; greater doses (up to 42 mumol/kg) inhibited in all of the SL-A and SL-S neurons, but not three cutaneous neurons studied. With the exclusion of these three neurons, the ED50s for inhibition of spontaneous activity were comparable to the ED50s for inhibition of neuronal responses during colorectal distension or heating of the hindpaw in all three neuronal groups. 3. Clonidine produced a dose-dependent, yohimbine- or phentolamine-reversible inhibition of both spontaneous activity and neuronal responses during heating or colorectal distension of 10 SL-A, 3 SL-S, and 6 cutaneous dorsal horn neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Characterization of superficial T 13-L 2 dorsal horn neurons encoding for colorectal distension in the rat: comparison with neurons in deep laminae

Fifty-five neurons responsive to colorectal distension located in the superficial spinal dorsal horn (0.0–0.3 mm ventral to the cord dorsum) of the T 13-L 2 spinal segments of pentobarbital-anesthetized, physiologically intact or spinalized (C 1 transection), decerebrate rats were characterized. These neurons could be separated into three groups based upon their response to an 80 mm Hg, 20 s colorectal distension: (1) short latency-abrupt (SL-A) neurons ( n = 22) that were excited by colorectal distension at a short latency (<1s) and abruptly terminated responses following the termination of the distending stimulus; (2) short latency-sustained (SL-S) neurons ( n = 26) that were excited by colorectal distension at a short latency (<1s) and demonstrated sustained responses (<4s) following termination of the distending stimulus; and (3) INHIB neurons ( n = 7) that were spontaneously active and were inhibited by colorectal distension. All 55 neurons had convergent cutaneous receptive fields (i.e. were ‘viscerosomatic’), exhibiting excitatory responses to noxious (pinch/heat) and/or non-noxious (brush) stimuli. Neurons excited by colorectal distension also demonstrated monotonic, accelerating responses to graded colorectal distension, were excited by the intraarterial administration of bradykinin, could be antidromically activated by electrical stimulation in the caudal ventrolateral medulla and were subject to tonic descending inhibitory modulation as evidenced by more vigorous responses to distension when rats were reversibly spinalized using a cold block. A comparison of these 55 superficial dorsal horn neurons with 90 neurons located in the deep spinal dorsal horn (0.4–1.3 mm ventral to the cord dorsum) demonstrated quantitative differences between SL-A neurons located superficially and those located at deeper sites; no quantitative differences between respective groups of SL-S and INHIB neurons were apparent.

Neural substrates for reflex salivation induced by taste, mechanical, and thermal stimulation of the oral region in decerebrate rats.

In order to investigate the neural mechanisms of reflex salivary secretion, experiments were carried out on anesthetized, decerebrate rats from which the volumes of submandibular salivary secretion and the efferent discharges in the preganglionic parasymapathetic fibers innervating the submandibular gland were recorded. Salivary secretion was induced by either infusing a taste solution, or an aliquot of hot water (45-55 degrees C) into the oral cavity, or by pinching the frontal parts of the oral region with a pair of forceps. The reflex salivation induced by noxious thermal and mechanical stimuli was markedly reduced by lesioning either the caudal (VC), or the interpolar (VI) trigeminal sensory nuclei. Taste-elicited salivary secretion was significantly reduced by lesioning the nucleus of the tractus solitarius (NTS). Of 43 preganglionic parasympathetic fibers sampled, 27 responded to both noxious mechanical and thermal stimulation of the oral region, and to electrical stimulation of the VC. Ten fibers responded only to taste stimulation and to electrical stimulation of the NTS. The remaining 6 fibers responded to both taste and noxious thermal stimulation of the oral region. These fibers responded well to NTS stimulation, but gave only a slight response to VC stimulation. These results suggest that two distinct neural pathways exist which mediate reflex salivation in the lower brain stem of the rat, i.e., the taste pathway via the NTS and the nociceptive pathway via the trigeminal sensory nuclei.

Electrophysiological evidence for a tonic activity of the spinal cord intrinsic opioid systems in a chronic pain model

The aim of this electrophysiological investigation was to evaluate the activity of the spinal endogenous opioid systems in a chronic pain model, the arthritic rat. The activity of nociceptive non-specific dorsal horn neurons ( n = 23) were recorded in 23 spinal unanesthetized decerebrated rats. Naloxone (1 mg/kg i.v.) induced a highly significant increase in the spontaneous firing rate of these neurons. This observation is in favor of a tonic activity of spinal opioid endogenous systems in such a disease. In addition, the same dose of naloxone facilitates the transmission of noxious messages at the spinal level as revealed by the large enhancement of the responses of these neurons to C-fiber stimulation. These results are in good agreement with behavioral data showing that such a relatively high dose of naloxone induced well-reproducible hyperalgesia and with some biochemical observations showing an increase of levels and biosynthesis of endogenous opioids in the spinal cord of the arthritic rat.

HYDROSTATIC PRESSURE ENHANCES BARORECEPTOR REFLEXES IN THE RAT

The effects of increased hydrostatic pressure on baroreceptor reflexes in the decerebrate rat have been investigated. Baroreceptor 'sensitivity' was assessed from the relationship between cardiac interval and systolic blood pressure following infusion of phenylephrine to animals exposed to increases in hydrostatic pressure (1-30 bar) with helium. Resting heart rate and systolic blood pressure were reduced and the 'sensitivity' of the baroreflex heart rate response was significantly increased by exposure to pressure. This enhancement of cardiovascular reflex function, elicited by moderate increases in hydrostatic pressure may, in part, be centrally mediated.

Patterns of activity in sympathetic postganglionic nerves to skeletal muscle, skin and kidney during stimulation of the medullary raphe area of the rat

In chloralose/urethane anaesthetised rats multi and single fibre activity was recorded in renal sympathetic nerves and in sympathetic nerves to skeletal muscle and to the skin of the hind limb. The activity was pulse-modulated and inhibited by stimulating baroreceptors with an increase in blood pressure following i.v. phenylephrine. The study investigated the effect of stimulating medial regions of the lower brainstem on activity in these sympathetic nerves. Comparing renal nerve and skin sympathetic nerve activity two main patterns of response were seen, either an inhibition of both or excitation of both. In contrast when comparing renal nerve activity with muscle sympathetic nerve activity a third pattern was evoked from a few sites located in nucleus raphe obscurus, an inhibition of renal nerve activity and excitation of muscle sympathetic activity. The latter is the same pattern as that evoked in the cat. Unlike the cat, however, the decerebrate rat was not observed to generate this differential pattern of activity either spontaneously or following the administration of physostigmine. It is argued that the activation of cell bodies located in raphe obscurus is responsible for inducing a pattern of sympathetic activity similar to that occurring during paradoxical sleep in other animals.

Cholecystokinin decreases sucrose intake in chronic decerebrate rats.

The capacity of chronic decerebrate rats to reduce their intake of an orally infused sucrose solution in response to peripherally administered cholecystokinin octapeptide (CCK-8) was investigated. The sucrose intake of both 24-h food-deprived chronic decerebrate rats and pair-fed control rats was reduced by CCK-8 relative to the intake after desulfated CCK-8. The intake-reducing effect of CCK-8 in the chronic decerebrate rat provides compelling evidence that the caudal brain stem is of sufficient neural complexity to mediate this response. Although others have hypothesized that connections between the caudal brain stem and forebrain are required to mediate this effect(s) of CCK-8, our results demonstrate that these pathways are not necessary.

Brainstem systems mediate the enhancement of palatability by chlordiazepoxide

Previous studies have indicated that the benzodiazepine receptor complex is involved in enhancing taste palatability after chlordiazepoxide (CDP) administration. Positive, palatability-dependent ingestive reactions elicited by orally infused tastes are facilitated in rats by CDP (10 mg/kg), and this effect is reversible by benzodiazepine antagonists. In contrast, the rats' more neutral or aversive reactions are not facilitated by CDP. Because benzodiazepine receptors exist in highest density in the forebrain, it has seemed plausible to posit forebrain structures as the locus of CDP action. However, benzodiazepine receptors do exist in the caudal brainstem (albeit in lesser density), and the isolated decerebrate brainstem has been demonstrated to possess considerable taste processing and response capacity. The present study examined the effects of CDP on taste reactivity in chronic mesencephalic decerebrate rats. The results show that CDP can act on the subdiencephalic brainstem to enhance positive ingestive reactions even in the absence of communications with the forebrain. This indicates that both the relevant benzodiazepine receptors and the minimal neural circuit needed to modulate taste reactivity exist within or below the mesencephalon.

Opioid and nicotinic medullary hyperalgesic influences in the decerebrated rat

The effects of ethylketazocine (EKC) administered intraperitoneally and the nicotinic ligands (−)- and (+)-nicotine, (−)-cytisine, (−)-lobeline, and (+)-2-methylpiperidine administered into the 4th ventricle on the latency of the thermally evoked withdrawal reflex of the decerebrate rat were investigated. EKC administered intraperitoneally produced both hyperalgesia and analgesia. (−)-Nicotine administered into the 4th ventricle produced a biphasic dose related effect on the latency of the withdrawal reflex; low doses produced a dose related analgesia while higher doses produced hyperalgesia. (−)-Cytisine and (−)-lobeline administered into the 4th ventricle produced biphasic effects. (+)-2-Methylpiperidine administered into the 4th ventricle produced a significant degree of hyperalgesia. Both the analgesic and hyperalgesic effects of (−)-nicotine were antagonized by mecamylamine (1 mg/kg) and naltrexone (5 mg/kg). The hyperalgesic action of (+)-2-methylpiperidine was antagonized by naltrexone but not by mecamylamine. These observations suggest that there are both medullary opioidergic and nicotinic cholinergic mechanisms for modulating both analgesic and hyperalgesic processes and that nicotinic ligands have multiple mechanisms of action in the brain.

Effect of the forebrain on flexion reflexes in rats with ankle joint urate arthritis

Ankle joint urate arthritis in rats is associated with increased responses to ankle stimulation and decreased responses to stimulation of the distal foot. To determine the influence of the forebrain on flexion reflexes in this model, responses to ankle and foot stimulation were examined in chronic decerebrate rats, decerebrated either before or after the induction of the arthritis. The increased responsiveness to stimulation of the arthritic ankle which had been observed after 24 h of urate arthritis was equally apparent in animals decerebrated 24 h before the induction of the arthritis and in those decerebrated 24 h after the urate injection. However, the decreased responsiveness of the distal foot to pressure or temperature stimuli, which had been observed in arthritic animals with an intact forebrain, was still apparent in animals decerebrated 24 h after the induction of the arthritis but did not appear in animals who had been decerebrated before the arthritis induction. It is concluded that the forebrain is required for the production of the reduced responsiveness of the distal foot but is not required for its maintenance once the insensitive state has been acquired.

Descending excitation and inhibition of spinal cord lamina I projection neurons.

1. Lamina I cells were recorded in the lumbar dorsal horn of decerebrate rats. Their projecting axons were mainly located in the contralateral dorsolateral funiculus (DLF) in the upper cervical cord. 2. The effect on these cells of short and long trains of stimuli applied to the upper cervical DLF was examined by measuring the ongoing activity of the cells, their response to peripheral stimuli, and the size of their receptive fields. 3. The presence of tonic descending influences from brain stem to spinal cord was investigated by measuring the properties of the lamina I cells before and during block of descending impulses. 4. The results of DLF stimulation and of cord block show that substantial and prolonged excitation affected many cells, whereas some were inhibited for shorter periods of time. 5. The experiments were repeated with stimulation of the DLF caudal to chronic section to eliminate descending fibers. The results suggest that the changes of excitability in intact animals were partly produced by stimulation of descending fibers and partly by the invasion of collaterals activated by the antidromic stimulation of the axons projecting from the lamina I cells. 6. Although long trains of DLF stimuli generally excited lamina I cells, only inhibitions were seen in the deep dorsal horn. Moreover, stimulation rostral to an acute unilateral DLF lesion was without effect on lamina I cells but inhibited deep cells. 7. It is proposed that the lamina I cells might activate brain stem circuits, which in turn influence deep dorsal horn cells.

Sciatic nerve blood flow response to carbon dioxide

Sciatic nerve blood flow (NBF) during hypercarbia was examined in unanesthetized decerebrate rats by means of laser Doppler flowmetry (LDF). During inspiration of gas mixtures containing no CO 2, followed by either 5, 10 or 20% CO 2, arterial pCO 2 increased by 13, 18 and 68 mm Hg, respectively. Blood pressure (BP) and the LDF signal, which were measured continuously, increased for 30–40 s following the start of inhalation of CO 2 and then decreased. Three min after the start of inhalation of 5 or 10% CO 2, BP had returned to the baseline and the LDF signal was increased by 14 and 15%, respectively, compared with preinhalation values. In rats inspiring 20% CO 2, systemic BP remained elevated 12% above the baseline and NBF was increased by 18%. The results indicate that dilatation of the vasa nervorum during hypercarbia is less than that at cerebral blood vessels. The nerve vasculature dilates maximally in response to 5% CO 2, with a rise in NBF of about 1.1% per mm Hg increase in p aCO 2.

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.

Role of muscle microvasculature during hyperdynamic and hypodynamic phases of endotoxin shock in decerebrate rats.

Microcirculatory derangements in skeletal muscle could act to change cardiac output during endotoxemia. To explore this idea, we measured arteriole and venule responses to low-dose and high-dose endotoxemia in the rat cremaster muscle by direct in vivo videomicroscopy. Our data indicate that cardiac output increased in the low-dose group and decreased in the high-dose group. In both animal groups, a differential arteriolar response occurred to give small arteriole dilation and large arteriole constriction while venous diameters did not change. We conclude that: 1) changes in cardiac output during endotoxemia are not related to microvascular responses in skeletal muscle, and 2) the microvascular responses in skeletal muscle could be responsible for the decreased systemic vascular resistance during high cardiac output endotoxemia, but not for the elevated systemic vascular resistance during low cardiac output endotoxemia.

The effect of dantrolene sodium on the discharge of alpha and gamma motoneurones to the soleus muscle in the decerebrate rat.

1. The effects of intravenous infusion of the direct acting muscle relaxant, dantrolene sodium (5 mg kg-1), on tension, integrated EMG, soleus muscle motor unit discharge frequency and gamma nerve fibre discharge were measured in the decerebrate rat. 2. Dantrolene sodium did not have any detectable direct effect upon the discharge of the gamma nerve fibres. 3. The soleus muscle of the decerebrate preparations exhibited spontaneous tension and reflex responses. 4. With the muscle held at constant length, dantrolene sodium caused an increase in the integrated EMG in 15 out of 18 experiments and a decrease in muscle tension in 15 out of 17. The results from these experiments showed great variability. 5. Dantrolene sodium caused a slight reduction in the tension response to tonic stretch; this was accompanied by an increase in the integrated EMG. 6. Dantrolene sodium also caused a shift in the relationship between tension and integrated EMG during the phasic component of the stretch reflex, with a greater integrated EMG being associated with a reduced tension. 7. Motor unit discharge frequencies were found to increase but not sufficiently to overcome the action of dantrolene sodium. It is concluded that motor unit recruitment must play an important role in the compensation for the muscle weakening action of dantrolene sodium.

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.