A performance comparison of communication links between rural hospitals and a digital health sciences library

CO2 laser pulses selectively excite A-delta and C mechano-thermal nociceptors in the superficial layers of the skin. To study the jaw-opening reflex elicited by a purely nociceptive input, we delivered laser pulses to the perioral region in 15 subjects. Sensory threshold was very low (9 mJ/mm2). High-intensity noxious laser pulses (more than 4 x sensory threshold) evoked a single phase of electromyogram suppression (laser silent period, LSP) at an onset latency of 70 ms in the contracted masseter and temporal muscles, bilaterally. Even maximum-intensity laser pulses failed to activate the suprahyoid muscles. The recovery curves to paired laser stimuli showed that at short interstimulus intervals the test LSP was strongly suppressed. At about 380 ms it recovered to 50%, i.e. its recovery curve resembled that of the masseter late silent period after electrical mental nerve stimulation (SP2). In experiments studying the interaction with heterotopic stimuli and non-nociceptive responses, chin-taps or electrical shocks delivered to the supraorbital, infraorbital or mental nerves before laser stimulation strongly suppressed the LSP. A preceding perioral laser pulse strongly suppressed the masseter SP evoked by supraorbital stimulation and the SP2 evoked by mental stimulation, but left SPI unaffected. We conclude that the perioral A-delta fibre input elicits a jaw-opening reflex simply by inhibiting the jaw-closers. The LSP response is mediated by a multisynaptic chain of brainstem interneurons and shares with the masseter SP2 part of the central circuit in the ponto-medullary region. We also propose that a common centre processes the various inputs for jaw opening.     

Histamine H3 receptors contribute to drinking elicited by eating in rats

A role for endogenous histamine and its H3 receptor subtype for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats. The i.p. injection of the H3 agonist R-alpha-methylhistamine (Ramh, 2.5 mg/kg) shortened the latency to initiate drinking and increased 1-h water intake in nondeprived rats freely eating pellets and drinking water. The ICV injection (through a surgically implanted chronic cannula) of 10 micrograms Ramh increased water intake; this Ramh-induced drinking was abolished by previous ICV injection of the H3 antagonist thioperamide (Th, 60 micrograms). For rats drinking and eating after 24-h food deprivation, s.c. Th inhibited drinking behavior: for example, 10 mg/kg Th s.c. delayed the latency to initiate drinking and inhibited 1-h water intake without inhibition of food intake. In contrast, 60 micrograms Th ICV failed to inhibit food-related drinking in rats eating after food deprivation. For nondeprived rats eating a small cracker, 10 mg/kg Th s.c. delayed the latency to initiate drinking and abolished water intake without effect of eating, and 60 micrograms Th ICV had similar effects upon drinking elicited by ingestion of cracker. The IG infusion (through a surgically implanted gastric catheter) of 2 ml 600 or 900 mOsm/kg NaCl, a treatment that is subthreshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was abolished by 10 mg/kg Th s.c. and attenuated by 60 micrograms Th ICV. The IG infusion of 2 ml 1800 mOsm/kg NaCl, a treatment that is above threshold for increase in systemic plasma osmolality, elicited drinking that was attenuated by 10 mg/kg s.c. or 60 micrograms Th ICV. These results demonstrate that peripheral and central H3 receptors for histamine have a role in drinking elicited by eating and the postprandial gastrointestinal osmotic consequences of eating. These findings extend the evidence demonstrating a histaminergic contribution to food-related drinking in rats.     

The relation of feeding and activity following septal lesions in rats.

The patterns of intake of liquid diet (Exp I) and water (Exp II) were recorded in 12 female Long-Evans diet-deprived rats with septal lesions and 13 neurologically intact controls during the 1st hr of diet access. The occurrences of grooming, resting/sleeping, and exploring were also recorded. Findings show that both groups consumed similar amounts of diet in 1 meal during the 1-hr diet access period. Controls consumed the meal in 1 prolonged bout of eating, while lesioned Ss consumed the meal in numerous small bouts of eating. Lesioned Ss were active for longer periods, exhibiting continuous alternation of brief bouts of eating, drinking, exploring, and resting throughout the meal. In tests in which water was not available during the diet access period, both groups increased their intrameal bout size, but lesioned Ss still showed much smaller bouts of ingestion than did controls. Data suggest that the small-bout pattern of ingestion may reflect a general disruption in the control of behavioral sequences, rather than processes uniquely related to the regulation of eating or drinking. (16 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Trigeminal orosensation and ingestive behavior in the rat.

Used a deafferentation procedure with male Wistar rats to examine the contributions of trigeminal orosensation to control of ingestive behavior. The procedure removed somatosensory input from the mouth while sparing olfaction, lingual taste, vibrissae inputs, and proprioceptive afferents from and efferents to the jaw muscles. Ss with sections of tongue or jaw muscle efferents served as controls. Bilateral trigeminal orosensory deafferentation was followed by effects on ingestive behavior, the magnitudes of which were proportional to the extent of the deafferentation. The trigeminal syndrome includes aphagia and adipsia, impairments in the sensorimotor control of eating and drinking, decreased responsiveness to food and water, and a reduction in the level of body weight regulation. Trigeminal deafferentation spared elementary ingestive movement patterns (biting, licking, and chewing) but disrupted their control by the perioral stimuli. Deficits in food intake varied with the sensory properties of the diet. Recovery of intake took place along a palatability gradient, and recovery of water intake paralleled that of dry food. The chronically reduced body weight was caused by persistent hypophagia and reflected reduced responsiveness to food. Findings suggest a considerable degree of overlap in the neural mechanisms mediating the sensorimotor and motivational control of intake in the rat. (76 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Orogastric determinants of drinking in rats: Interaction between absorptive and peripheral controls.

In 3 experiments with 24 female Sprague-Dawley rats, water intake of water-deprived Ss, drinking with absorption prevented by pyloric occlusion, was compared with that of Ss drinking normally. Drinking without absorption, under the control of only orogastric factors, was not graded in response to varied deprivation (Exp I). Orogastric controls effectively inhibited intake after absorbed water, but not isotonic saline, preloads (Exp II). The extent of orogastric inhibition was directly related to absorbed preload volume (Exp III). With large absorbed water preloads (9 ml), intakes with and without absorption were equal. Normal function of orogastric controls may thus be based on their interaction with absorption, which progressively enhances peripheral inhibition of drinking. (32 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Interaction between penile reflexes and copulation in male rats.

Placed intact, unanesthetized Long-Evans male rats in a supine position, with the penile sheath continuously retracted. Three forms of penile reflex were displayed: erections, cups, and flips. The reciprocal relation between copulation and the penile reflexes occurring in supine tests was explored in 4 experiments. In Exp I, sexual exhaustion depressed all penile reflexes, but the reflexes returned to baseline levels within 8 hrs, long before copulatory potential. In Exp II, reflexes were depressed to exhaustion levels after fewer ejaculations than were required for sexual exhaustion, an indication that reflexes are more readily evoked during copulation than in supine tests. Exp III determined that a rat's penile-reflex potential may be enhanced by placing the rat in a copulation-test cage, by allowing the male a few antecedent intromissions, or by allowing an antecedent ejaculation. The display of penile reflexes within 1 min after ejaculation suggested that the period of reduced sexual arousability following ejaculation is not due to reduced excitability in the spinal mechanisms controlling penile reflexes. In Exp IV, 1 hr of penile-reflex elicitation had no effect on subsequent copulatory behavior. Thus, sexual stimulation may increase or decrease penile-reflex potential, but a reciprocal influence was not detectable. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

ACTH and ACTH4–20 modification of neophobia and taste aversion responses in the rat.

A series of 6 experiments assessed the effects of ACTH and the ACTH analog ACTH4–20 on drinking in conditioned taste aversion and neophobic situations using a total of 168 male Sprague-Dawley rats as Ss. Both substances delayed the extinction of a conditioned taste aversion established by a single pairing of lithium chloride with milk (Exp I). However, in this situation, the ACTH parent peptide was more potent behaviorally. ACTH supressed milk consumption in Ss with no toxicosis experience (Exp II). This effect was apparently not due to the conditioning of a taste aversion (Exp III) with ACTH serving as a weak aversive UCS. Exogenous ACTH (Exp IV) or ACTH4–20 (Exp V) did not enhance neophobia; however, repeated injections of ACTH suppressed drinking. This ACTH suppression was related to the familiarity/novelty of the substance being consumed. The neophobic response to milk was not accompanied by pituitary-adrenal activation (Exp VI). Both neophobic and conditioned taste aversion situations appear to be useful for assessing peptide effects on consummatory behavior. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Reflex jaw motions and jaw stiffness pertaining to whiplash injury of the neck

Because a so-called mandibular whiplash injury requires the absence of short-latency jaw-closing reflexes in order to explain the postulated mechanism of injury (excessive jaw opening); the authors studied the presence and absence and more importantly, the kinematics (duration, displacement, velocity, acceleration) of monosynaptic and possibly, polysynaptic myotatic (stretch) reflexes in the jaw elevator muscles. In six healthy adults jaw jerk maneuvers were elicited through a brisk tap on the chin, and surface electromyography identified elevator reflexes while translational electrognathography identified the kinematics of the reflexes. The maneuvers were done while maintaining the rest position (3% MVC) and moderate clenching of the teeth (30% MVC). Electromyography was also used to identify phasic elevator excitations during a passive brisk neck extension maneuver. A sudden and unexpected elongation of the jaw elevators released autogenic reflex responses that, in conjunction with augmented tissue elasticity (stiffness), elevated the mandible into centric occlusion within approximately 150 milliseconds. In 86% of trials, the responses occurred regardless of the prevailing resting and clenching contractile activities. There was no evidence of a depressor force that consistently would and could anchor the mandible in a position of extreme or moderate depression, the theoretical linchpin of the mandibular whiplash injury. It was concluded that the mandibular locomotor system is very efficient in maintaining the rest and intercuspal positions of the mandible. This study found no evidence corroborating the mechanism claimed to release a so-called mandibular whiplash injury.     

Localization of receptors for the dipsogenic action of angiotensin II in the subfornical organ of rats.

Investigated the proposal that the subfornical organ (SFO) is a site of receptors for drinking induced by angiotensin II (AII). A total of 159 male albino Holtzman rats was used. Intracranial injections of physiological doses of AII elicited drinking if and only if applied directly to the SFO (Exp I). Ablation of the SFO selectively (Exp II) and permanently (Exp IV) eliminated drinking elicited by physiological doses of iv infused AII. Animals in which SFO had been ablated responded normally to cellular dehydration but reduced responding to the extracellular thirsts of beta-adrenergic activation and hyperoncotic colloid dialysis (Exp III). Infusion of saralasin, an AII antagonist, directly into the SFO selectively and reversibly antagonized iv AII drinking (Exp V). The hypothesis that the SFO contains dipsogenic receptors for circulating AII was supported. (2 p ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Changes in self-stimulation at stimulation-bound eating and drinking sites in the lateral hypothalamus during food or water deprivation, glucoprivation, and intracellular or extracellular dehydration.

Examined the effects of hunger induced by food deprivation, 2-deoxy-{d}-glucose (200 mg/kg), or insulin (2 U/kg) and thirst induced by water deprivation, sodium chloride (4 M), or polyethylene glycol (5 ml of 30% w/w) on lateral hypothalamic self-stimulation in 40 male Long-Evans rats. Changes in self-stimulation were evaluated at electrodes that produced stimulation-bound eating and/or drinking or neither behavior. Daily 30-min test sessions consisted of 3 5-min periods of self-stimulation alternated with 3 5-min periods when barpresses resulted in 5-sec time-out from experimenter-delivered stimulation (stimulation escape). Food deprivation significantly increased self-stimulation; insulin, 2-deoxy-{d}-glucose, and sodium chloride significantly suppressed self-stimulation; water deprivation mildly inhibited self-stimulation; and polyethylene glycol had no effect. This pattern of findings was noted at electrodes that did and those that did not elicit eating and/or drinking. Findings do not support the hypothesis that the magnitude of lateral hypothalamic self-stimulation is differentially and predictably controlled by specific drive mechanisms indexed by the consummatory behaviors also elicited by the stimulation. (41 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Water drinking induced in sheep by angiotensin: A physiological or pharmacological effect?

The effect of val5-angiotensin II amide on water drinking in sheep was studied against a background of comprehensive data on arterial blood and cerebrospinal fluid angiotensin II levels in sheep under a variety of physiological conditions. 10 sheep of Corriedale or Merino breeds were used in Exp I and 4 in Exp II; 5 ewes were used in Exp III. Physiological range of blood angiotensin II concentration is 1-100 ng/100 ml. Intravenous infusion of angiotensin II within the physiological range did not increase water drinking. Intracarotid infusion of angiotensin II, or injection into 3rd ventricle or hypothalamus, consistently caused immediate drinking of large amounts of water. Dosages necessary for effect were in the supraphysiological range. Quantitative examination of data in sheep and other species suggests that a physiological role for angiotensin II in thirst is not proved. (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Taste avoidance, but not aversion, learning in rats lacking gustatory cortex.

Control rats rapidly learned to avoid drinking either a sucrose solution (Exp 1) or an NaCl solution (Exp 2) when the taste was paired with illness. These rats also produced aversive reactivity to each of these solutions in a taste reactivity test. Rats that lacked gustatory cortex (GC) learned to avoid drinking sucrose and NaCl, albeit at a slower rate than control rats. GC rats failed to display aversive reactivity to these tastes. The GC rats did show normal aversive reactivity to a strong quinine HCl solution during additional tests. It is suggested that the avoidance developed by GC rats did not entail a palatability shift of the conditional stimulus as it did in control rats. This altered learning strategy may account for the consistent learning deficits found in GC rats trained to avoid tastes. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Schedule constraint on the average drink burst and the regulation of wheel running and drinking in rats.

Two experiments compared predictions of a molar-pattern model and a general molar behavior regulation model by requiring 16 Sprague-Dawley rats to wheel run for access to water. In both experiments, schedule parameters constrained the baseline average burst length of drinking without constraining total drinking. Five levels of schedule constraint were imposed on time spent per drinking burst (Exp I) or the number of drinks per burst (Exp II). Results support the general molar behavior regulation view but not the molar-pattern model by showing no increase in total wheel running and no decrease in total drinking under schedule constraint. However, both experiments also showed local effects of drink burst constraint, including a direct relation between the degree of constraint and the local rate of drinking, and an approximation of the temporal distribution of baseline drinking under all degrees of schedule constraint. Most local changes support the view that rats defend the baseline temporal distribution of responding under schedule constraint, though some changes appear related to disruption of local response pattern characteristics. (35 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Drinking in the pigeon (Columba livia): Topography and spatiotemporal organization.

Analyzed drinking response of 5 male White Carneaux pigeons by means of high-speed cinematography. Like eating, drinking may be subdivided into 3 movement patterns involving the effector systems of the neck, eyelids, and beak. The major topographic difference between the 2 responses involves beak opening (gape). In eating, beak opening begins prior to contact with the food, and the amount of gape is directly proportional to seed size. In drinking, the beak remains almost closed during descent and opens intermittently and with a relatively small gape during water intake. The topography of drinking in the pigeon differs from that of many birds, and these differences reflect a difference in the mechanism of water ingestion. Data in this study confirm previous observations of a general resemblance between certain features of the pigeon's drinking behavior and the topography of water-reinforced key pecks. (9 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Transition from suckling to drinking at weaning: a kinematic and electromyographic study in miniature pigs

The movements of the tongue, hyoid, and jaw were recorded cineradiographically in preweaning pigs as they suckled bariumized milk from a veterinary teat or drank it from a bowl. The movements were quantified by measuring the X, Y coordinates of radioopaque markers embedded in the tongue and attached to both jaws and to the hyoid. EMG activity in masseter, anterior digastric, geniohyoid, genioglossus, hyoglossus, sternohyoid, stylohyoid, and omohyoid muscles was recorded synchronously with cineradiography at 100 frames/sec. In both suckling and drinking, the movements were characterized by minimal movements of the jaw and hyoid but extensive movements of the tongue. In suckling, the movements were largely confined to the midposterior part of the tongue. A seal was formed between the posterior tongue and soft palate while a depression formed in the mid-tongue; this was associated with fluid moving into the depression probably because of a reduced intraoral pressure. The depression was associated with increased EMG activity in the genioglossus muscle and overlapping activity in digastric, geniohyoid, hyoglossus, and sternohyoid muscles. In drinking cycles, significant movement occurred in all parts of the tongue; milk ingestion was associated with tongue movements that combined elements characteristic both of suckling (mid-tongue depression with a posterior seal) and of lapping (extensive anteroposterior movements within the tongue itself). In drinking, compared to suckling, there was a major reduction in EMG activity in masseter, digastric, geniohyoid, and sternohyoid muscles. After milk had accumulated in the valleculae, swallows usually occurred in every other cycle during suckling and in every third or fourth cycle during drinking. The emptying of the valleculae was an event that was embedded in the early jaw-opening phase of an otherwise normal suckling or drinking cycle. Emptying of the valleculae was associated with posteriorly directed movement of the back of the tongue and increased EMG activity in hyoglossus, styloglossus, and omohyoid muscles. No differences were noted in the kinematics associated with swallowing in the two activities, but, in the normalized and averaged EMG data, there were significant differences in the timing of genioglossus activity and in the relative balance of hyoglossal and stylohyoid activity.     

Hypoxia inhibits gastric emptying and gastric acid secretion in conscious rats

This study examines the effects of hypoxia in the gastric function in conscious rats which adapted to a meal-feeding schedule, that allowed free access to a high protein (HP) diet (550 g casein/kg diet, Exp.1,2 and 4), a normal protein (NP) diet (200 g casein/kg diet, Exp.3) or a nonpurified rat (NPR) diet (Exp. 5 and 6) for 4 h every day for 2 wk. In Exp. 1, after 4 h of consuming the HP diet, rats were exposed to 7.6 or 10.5% O2 normobaric hypoxia. Hypoxia delayed the excretion of urinary urea for 12 h. In Exp.2 and 3, when rats were exposed to 7.6%O2 after 4 h of consuming the HP diet and exposed to 10.5% O2 after 4 h of consuming the NP diet, respectively, a significant delay in gastric emptying was found in the hypoxic rats. In Exp. 4, when rats were exposed to 7.6 O2 hypoxia after 4 hr of eating the HP diet, the plasma gastrin concentration in the 7.6% O2 hypoxic rats was 2.3-fold that of the normoxic rats after 6 h of hypoxia. Furthermore, when rats that did not consume any HP diet on the day of the experiment were exposed to 7.6 or 10.5% O2 hypoxia, the plasma gastrin concentration was higher in both hypoxic groups than in the normoxic group after 3 and 6 of hypoxia. In Exp. 5, rats that were not fed the NPR diet on the day of study were exposed to 7.6 or 10.5% O2 hypoxia for 3 h after pylorus ligation. Hypoxia inhibited the secretion of gastric acid and elevated the plasma gastrin concentration. In Exp. 6, unfed rats that had been consuming the NPR diet were exposed to 7.6% O2 hypoxia for 3 h after pylorus ligation and were orally administered HCl. The rise of the gastrin concentration due to hypoxia was completely inhibited by oral HCl. These results demonstrate that hypoxia inhibits gastric emptying and gastric acid secretion and that the inhibitory effect of hypoxia on gastric acid secretion stimulates gastrin release through positive feedback regulation.     

Refractory periods of neurons directly excited in stimulus-bound eating and drinking in the rat.

Studied male hooded rats to determine whether the amygdaloid, or the brainstem, or neither population of neurons is involved in eating and drinking. Latency to the onset of eating or drinking became short when the intrapair interval of twice-threshold stimulating pulse pairs was increased beyond .50-.65 msec. This indicates that the absolute refractory periods of neurons directly excited in eating and in drinking elicited by lateral hypothalamic stimulation are between .50-.70 msec. The previous finding that the absolute refractory period characteristic of basolateral amygdaloid neurons directly excited by the same lateral hypothalamic stimulation is also in this range is considered evidence that the amygdaloid neurons are involved in the eating and drinking. Results also indicate either that the eating and drinking are elicited through different neurons with similar characteristics, or through the same neurons. (17 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Oropharyngeal control of ingestion in rats: Acquisition of sham-drinking patterns.

Conducted 3 experiments with female Sprague-Dawley rats with esophageal fistulas (3 Ss in Exp I, 3 in Exp II, and 4 in Exp III). Offered a concentrated glucose solution, Ss sham drank relatively small amounts on the 1st session, whether or not such a solution was familiar. Intake rose to high levels over ensuing sham-drinking sessions, showing that the initial small volumes were not attributable to fixed properties of the solution itself. The gradual acquisition of copious sham drinking was not affected by previous "practice" at sham drinking other commodities; it was not simply an alteration in motor habits. The gradual acquisition of the sham-drinking pattern did not occur with more dilute solutions; in response to these, sham drinking was copious and continuous from the onset. The following conclusions are made: (a) Rats must learn to respond, by continuous drinking, to the absence of the postingestive inhibition normally produced by concentrated solutions. (b) No such learning is required in the case of more dilute solutions. This is further evidence that controlling factors with differing properties operate at different levels even of the single commodity, glucose in solution. (17 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Punishment of saccharin drinking by amphetamine in rats and its reversal by chlordiazepoxide.

Demonstrates, in a conditioned taste-aversion paradigm, that doses of dextroamphetamine which are intravenously self-administered by rats may punish saccharin drinking. Ss were male Wistar rats. In Exp I (n = 42), single-trial, dose-related aversion was shown. Aversion was not antagonized by chlorpromazine. Exp II (n = 32) demonstrated dose-related acquisition of taste aversion with repeated administration of very low amphetamine doses. In Exp III (n = 18), drug-induced saccharin aversion was reversed by chlordiazepoxide; this action paralleled the action of chlordiazepoxide in numerous other aversive-conditioning situations. Exp IV (n = 30) ruled out the possibility that depression of saccharin drinking was due to a direct pharmacological action of the drug and not to learned saccharin avoidance. Results indicate that the reinforcing action of amphetamine depends on the response with which its effects are correlated. (20 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Angiotensin III-induced dipsogenic and pressor responses in rodents.

Three experiments examined responses to angiotensins in 64 male Sprague-Dawley rats, 64 male Mongolian gerbils, and 40 Octodon degus—a South American rodent. In Exp I, injections of [des-Asp–1]-angiotensin I ([des-Asp–1]-AI), angiotensin II (AII), and angiotensin III (AIII), at doses of .001–2 mg/kg (sc), induced drinking in the rat and degus, but not in the gerbil. In Exp II, pretreatment with captopril (50 mg/kg), an angiotensin converting enzyme inhibitor, prevented the endogenous conversion of sc injected [des-Asp–1]-AI to AIII and prevented drinking in rats and degus. The pharmacological artifact of hypovolemia caused by angiotensin-induced increases in vascular permeability was not observed in members of these species. In Exp III, blood pressure changes resulting from injections of AII and AIII in rats and gerbils were measured. Significant pressor elevations were seen following the administration of both analogs, although AII was more potent. Results demonstrate that AIII is dipsogenic in rats and degus and serves as a pressor agent in rats and gerbils. No explanation was found for the gerbil's relative lack of dipsogenicity to the presently tested angiotensins. (54 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)