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At least 37 records · Page 2Linked to original sources

Acute repetitive pilomotor seizures (goose bumps) in a patient with right mesial temporal sclerosis.

A 26 year old female with right mesial temporal sclerosis presented with events characterized by repetitive piloerection (goose bumps). These events were monitored using prolonged video-EEG. The events occurred at a rate of one per every 15 min, and were demonstrated to be simple partial seizures of right mesial temporal origin. The manifestations included piloerection, cold shivers and ictal tachycardia. These were effectively treated with lorazepam. Acute repetitive pilomotor seizures are rare. This is the first reported case with right mesial temporal sclerosis.

Acute Disease↗

Disruption of prepulse inhibition after stimulation of central but not peripheral alpha-1 adrenergic receptors.

Prepulse inhibition (PPI) refers to the attenuation of startle when a weak prestimulus precedes the startling stimulus. PPI is deficient in several psychiatric illnesses involving poor sensorimotor gating. Previous studies indicate that alpha1 adrenergic receptors regulate PPI, yet the extent to which these effects are mediated by central vs peripheral receptors is unclear. The present studies compared the effects of intracerebroventricular (ICV) vs intraperitoneal (IP) delivery of several alpha1 receptor agonists on PPI. Male Sprague-Dawley rats received either cirazoline (0, 10, 25, 50 microg/5 microl), methoxamine (0, 30, 100 microg/5 microl), or phenylephrine (0, 3, 10, 30 microg/5 microl) ICV immediately before testing. Separate groups received either cirazoline (0, 0.25, 0.50, 0.75 mg/kg), methoxamine (0, 2, 5, 10 mg/kg), or phenylephrine (0, 0.1, 2.0 mg/kg) IP 5 min before testing. PPI, baseline startle responses, and piloerection, an index of autonomic arousal, were measured. Cirazoline disrupted PPI; effective ICV doses were approximately six times lower than effective IP doses. Methoxamine disrupted PPI after ICV infusion but failed to affect PPI with IP doses that were up to 30-fold higher than the effective ICV dose. Phenylephrine disrupted PPI with ICV administration, but did not alter PPI after IP injection of even a 20-fold higher dose. None of the ICV treatments altered baseline startle magnitude, but phenylephrine and methoxamine lowered startle after administration of high systemic doses. Piloerection was induced by cirazoline via either route of administration, and by IP methoxamine and phenylephrine, but not by ICV infusion of methoxamine or phenylephrine. These findings indicate that alpha1 receptor-mediated PPI disruption occurs exclusively through stimulation of central receptors and is dissociable from alterations in baseline startle or autonomic effects.

Acoustic Stimulation↗

Brain stem tonic inhibition of thermoregulation in the rat.

It was shown, by selective levels of decerebration, that a drop in body temperature occurred in a midpontine rat due to impairment in thermoregulatory responses. Lowering the level of decerebration to the lower pons restored a coordinated thermoregulatory response. The response was inadequate to raise the core temperature to normal level, but it was nevertheless an integrated response of vasoconstriction, piloerection, and shivering and was appropriately turned off by warming the skin or core. In intact unanesthetized rats, microinjection of a local anesthetic in the pontine tegmentum resulted in thermoregulatory responses, such as curling of the body, piloerection, tremor in facial muscles, and shivering. Similar injections in the pontine tegmentum of the midpontine decerebrate rat also restored some heat gain responses, including shivering. These experiments suggest that in rats the heat gain responses are powerfully regulated by a tonic inhibitory mechanism located in the midbrain and upper pons that exerts a complete inhibitory effect on the thermoregulatory areas caudal to the midbrain in decerebrate rats and a partial inhibitory effect in intact animals. These experiments also confirm the previous observation in the cat of the presence of a facilitatory area(s) in lower levels of the central nervous system which is responsible for coordinated heat gain responses observed in low-level decerebrate animals. In addition, these experiments suggest that the brain stem thermoregulatory mechanisms are in fact functioning in intact unanesthetized animals.

Animals↗

Pilomotor seizures.

A 44-year-old man had frequent episodes of piloerection, or " gooseflesh ." Clinical and EEG evidence suggested that the attacks were pilomotor seizures, originating in the right temporal lobe. The cause was a glioblastoma. Paroxysmal piloerection is a rare manifestation of epilepsy.

Adult↗

Effect of methoxamine on maximum urethral pressure in women with genuine stress incontinence: a placebo-controlled, double-blind crossover study.

The aim of the study was to evaluate the potential role for a selective alpha1-adrenoceptor agonist in the treatment of urinary stress incontinence. A randomised, double-blind, placebo-controlled, crossover study design was employed. Half log incremental doses of intravenous methoxamine or placebo (saline) were administered to a group of women with genuine stress incontinence while measuring maximum urethral pressure (MUP), blood pressure, heart rate, and symptomatic side effects. Methoxamine evoked non-significant increases in MUP and diastolic blood pressure but caused a significant rise in systolic blood pressure and significant fall in heart rate at maximum dosage. Systemic side effects including piloerection, headache, and cold extremities were experienced in all subjects. The results indicate that the clinical usefulness of direct, peripherally acting sub-type-selective alpha1-adrenoceptor agonists in the medical treatment of stress incontinence may be limited by associated piloerection and cardiovascular side effects.

Adrenergic alpha-Agonists↗

Cyclophosphamide cystitis as a model of visceral pain in rats: model elaboration and spinal structures involved as revealed by the expression of c-Fos and Krox-24 proteins.

The evoked expression of the immediate early gene (IEG)-encoded proteins c-Fos and Krox-24 was used to monitor spinal visceronociceptive processing that results from cyclophosphamide cystitis in behaving rats. Animals received a single dose of 100 mg/kg i.p. of cyclophosphamide and survived for 30 min to 5 h. Longer survival times were not considered because of ethical considerations. Cyclophosphamide-injected animals developed characteristic behavioral signs in parallel with development of bladder lesions and spinal evoked expression of IEG-encoded proteins. Histological examination of the urinary bladder was used to evaluate the degree of cystitis and as a criterion for selection of groups of animals to be quantitatively analyzed. Controls consisted of freely behaving animals including control (un-injected), sham (saline-injected) or diuretic (furosemide-injected) animals. Behavioral modifications consisted of lacrimation, piloerection, assumption of a peculiar "rounded-back" posture, which was accompanied by head immobility and various brief "crises" (tail hyperextension, abdominal retractions, licking of the lower abdomen, backward withdrawal movements). Abnormal behaviors, which first appeared (lacrimation, piloerection) at the end of postinjection hour 1, progressively increased in severity (rounded-back posture) over the following 90 min to reach a plateau at about postinjection hour 2; the rounded-back posture was maintained up to time of death. Histological modifications of bladder tissue were assessed using a 4-grade scale in a blind setting. The 1st grade consisted of control or sham animals with no bladder lesion; 2nd grade, animals with simple chorionic edema; 3rd grade, animals with chorionic edema associated with mucosal abrasion, fibrin deposit, and onset of polymorphonuclear leukocyte infiltration; 4th grade, animals with complete cystitis corresponding to an increase in severity and spread of all the signs of cystitis described above plus petechial hemorrhage. Simple chorionic edema was observed from 30 min to 3 h postinjection, but with a progressive increase in severity over time. Edema accompanied by epithelial abrasion was observed for animals that survived 3-4 h postinjection; complete inflammation was observed in animals that survived 4-5 h postinjection. The study of c-Fos- and Krox-24-encoded protein expression demonstrated that few lumbosacral spinal areas were specifically involved in the processing of visceral inputs in response to bladder stimulation. These areas were the parasympathetic column (SPN), the dorsal gray commissure (DGC as the caudal extent of lamina X), and superficial layers of the dorsal horn.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Acute and subacute inhalation toxicity of dichlorosilane in male ICR mice.

Using male ICR mice, the LC50 and acute and subacute inhalation toxicity of dichlorosilane (SiH2Cl2, DCS) and the fate of DCS released into the air were investigated. DCS resolved and minute particles including silicon and chloride were observed, when DCS was released into the air. Most particles were under 1 micron in diameter. The LC50 of DCS at 4-h exposure was 144 ppm (nominal concentration). In the acute inhalation study, ten mice in each group were exposed to 64 ppm (nominal concentration) DCS for 1, 2, 4 or 8 h. Body weight loss, wheezing and piloerection were observed in mice exposed for 2 h or more. Histopathologically, injury to the nasal mucosa and trachea were observed in all exposed mice. Mice exposed to 32 ppm (nominal concentration) DCS for 2 or 4 weeks also exhibited depression of body weight gain, wheezing and piloerection. Squamous metaplasia of the nasal mucosa and tracheal epithelium was observed in both 2- and 4-week exposure groups. Exposure to DCS was irritant or corrosive to the respiratory tract with both acute and subacute inhalation. Apart from silane (SiH4), toxic effects of DCS seem to be characterized by chloride compounds derived from DCS.

Administration, Inhalation↗

Involvement of both opiate and catecholaminergic receptors in the behavioural excitation provoked by thyrotropin-releasing hormone: comparisons with amphetamine.

Following direct administration of thyrotropin-releasing hormone (TRH), but not thyroid-stimulating hormone (TSH) or vehicle solution, into the lateral cerebral ventricle in rats, three main categories of behaviour were provoked: activity of the normal type--stimulation of forward locomotion, head and body rearing (as shown by an enhancement in gross movements); stereotyped activity--increased grooming and head swaying (as shown by an enhancement in fine movements); abnormal behaviour--tail elevation and piloerection (as observed grossly). The behavioural excitation caused by TRH was antagonized by pretreatment of the rats with either a narcotic receptor antagonist, naloxone, an alpha-adrenergic receptor antagonists, yohimbine, or a dopaminergic receptor antagonist, haloperidol, but not with a beta-adrenergic receptor antagonist, propranolol. Intraventricular administration of amphetamine to rats caused stimulation of forward locomotion, head and body rearing, increased grooming and sniffing. Unlike TRH, amphetamine did not produce wet-dog shakes, tail elevation and piloerection. Furthermore, the amphetamine-induced excitation was antagonized by pretreatment with a dopaminergic receptor antagonist, haloperidol, but not with either naloxone, yohimbine or propranolol. The data indicate that both opiate and catecholaminergic receptors are involved in the TRH-induced behavioural excitation, whereas dopaminergic receptors are involved in amphetamine-induced excitement in the rat.

Amphetamine↗

Medial hypothalamic lesions in the rat enhance reactivity and mouse killing but not social aggression.

In rats subjected to lesions of the medial hypothalamus, 8 of 11 animals became mouse killers and all manifested some degree of hyperreactivity to the experimenter. When introduced as intruders into a mixed sex colony group, the lesioned rats did not manifest piloerection nor did they emit flank attacks characteristic of social aggressive behavior. However, the lesioned animals did respond to the attacks of the resident male rats with significantly more counterattacks and biting than did sham-lesioned control rats. Spontaneous mouse killing rats also failed to show a level of social aggressive behavior significantly greater than that of sham-operated control rats, but the spontaneous mouse killers did kill rat pups in the colony groups. Alpha-male rats when introduced as an intruder into a colony group did exhibit piloerection and emit flank attacks characteristic of social aggressive behavior. These results demonstrate that the mouse killing and heightened reactivity associated with medial hypothalamic lesions do not represent an indiscriminant release of all forms of agonistic behavior.

Aggression↗

Peripheral administration of a corticotropin-releasing factor antagonist increases the vocalizing and locomotor activity of isolated guinea pig pups.

Guinea pig pups vocalized more and were more active during a 60-min period of isolation in a novel environment when injected SC with 50 micrograms of the corticotropin-releasing factor (CRF) antagonist, [D-Phe]CRF12-41, than when injected with saline vehicle only. More pups exhibited eye closing and extensive piloerection when injected with saline than when injected with the antagonist. Plasma levels of cortisol following testing were not affected by the injections. These results support the hypothesis that endogenous CRF contributes to the normal decline in vocalizing and locomotor activity that guinea pig pups show with continued isolation. The results also suggest that endogenous CRF plays a role in the eye closing and piloerection of isolated pups. The finding that the dose of the antagonist used altered behavior, yet was not sufficient to lower plasma cortisol levels, supports earlier evidence that the observed effects of CRF are not due to the actions of ACTH or glucocorticoids.

Animals↗

Genetic differences in the development of physical dependence upon diazepam in Lewis and Fischer 344 inbred rat strains.

The purpose of the present study was to investigate physical dependence upon diazepam systematically in two inbred strains of rats, Lewis (LEW) and Fischer 344 (F344). Rats were chronically fed food containing diazepam on an escalating drug dosage schedule, from 1 and 2 to 12 mg/g of food, over a period of 30 days. During treatment, the growth curve in LEW and F344 rats was suppressed compared with the respective controls. Motor incoordination was evaluated by a rotarod performance test. The ranking of the motor incoordination during the final concentration of diazepam was as follows: F344 greater than LEW. After substitution of normal food for the diazepam-admixed food, various signs of diazepam withdrawal occurred 16-120 h later. These signs included vocalization, irritability, muscle rigidity, ear-twitching, Straub's tail, piloerection, fascicular twitch, tremor, convulsion, and death. The incidences of vocalization, ear-twitching, piloerection, and tremor in F344 were significantly higher than those in LEW rats. Furthermore, two of six F344 rats showed spontaneous convulsions and one rat died of convulsions. Overall withdrawal scores were significantly greater in F344 (16.0) than in LEW (6.3) rats. These results suggest that diazepam withdrawal severity is strongly influenced by genetic factors, and F344 rats are highly susceptible to dependence upon benzodiazepines.

Animals↗

Behavioral and physiological effects of a single injection of rat interferon-alpha on male Sprague-Dawley rats: a long-term evaluation.

Interferon-alpha (IFN-alpha) is a cytokine used as a first line of defense against diseases such as cancer and hepatitis C. However, reports indicate that its effectiveness as a treatment is countered by central nervous system (CNS) disruptions in patients. Our work explored the possibility that it may also cause long-term behavioral disruptions by chronicling the behavioral and physiological disturbances associated with a single injection of vehicle, 10, 100, or 1,000 units of IFN-alpha in male Sprague-Dawley rats (n = 5/dose). Following 1 day of locomotor baseline collection, we monitored sickness behaviors (ptosis, piloerection, lethargy, and sleep), food and water intake, body weight, temperature, and motor activity. Observations were recorded 4 days prior to and 4 days following the IFN-alpha injection. Temperature and sickness behaviors were recorded three times daily at 9:00, 15:00, and 21:00 h, and all other indices, once daily. On the injection day, temperature values were highest in the animals receiving the 10-unit IFN-alpha dose 15 min and 13 h post-injection. In the case of sickness behaviors, a significant increase was observed in piloerection in all IFN-alpha groups at each time point measured, while the scores of the rats in the vehicle condition remained unchanged between pre- and post-injection days. Analyses of overall sickness behaviors during morning and night observation periods indicated increased scores in all IFN-alpha groups following injection. Cumulatively, these data suggest that a single IFN-alpha exposure may elicit long-term behavioral disruptions and that its consequences should be thoroughly investigated for its use in clinical populations.

Analysis of Variance↗

Responses of guinea pig pups during isolation in a novel environment may represent stress-induced sickness behaviors.

When guinea pig pups are isolated in a novel environment, they show an initial active phase of behavioral responsiveness characterized by vocalizations and locomotor activity. One earlier study found that after about an hour, pups began to exhibit a second, passive stage of responsiveness marked by a crouched stance, eye-closing, and extensive piloerection. The present experiments tested the hypothesis that the responses during the second, passive stage result from the isolation experience activating pathways underlying the acute phase response, i.e., that behaviors of the second stage represent "stress-induced sickness behaviors". We found the following: (1) the passive stage did not emerge if pups remained with the mother during exposure to a novel cage; (2) injection of lipopolysaccharide, which induces an acute phase response, also led pups to exhibit crouching, eye-closing, and piloerection; and, (3) isolation in the novel cage produced a rise in rectal temperature, but did not affect peripheral or central levels of interleukin-1beta (IL-1beta)-immunoreactivity. Overall, these results are consistent with the notion that stress-induced sickness behaviors can account for some of the behaviors of isolated guinea pig pups, though if this is the case, cytokines other than IL-1beta appear to be involved.

Acute-Phase Reaction↗

Ethological analysis of morphine withdrawal with different dependence programs in male mice.

This work was performed to clarify the differences between a long or short development of morphine dependence as well as between a recently installed or a long-term dependence. Morphine withdrawal in rats is a well-characterized phenomenon but this is not so in mice. A study of the principal withdrawal signs have been performed in mice, evaluating their specificity and particular profile of appearance in each type of dependence. Mice were divided into two groups that received increasing doses of morphine every 24 h, three groups that received increasing doses of morphine twice a day for 3 days, and a control group that received saline. Naloxone-induced opiate withdrawal was evaluated following short-term exposition to morphine [Test 1 (T1)--saline and Test 2 (T2)--naloxone] and long-term exposition to morphine [Test 3 (T3)--naloxone and Test 4 (T4)--saline]. Morphine administration twice a day is more effective in inducing opiate dependence than once a day, and with the latter, the duration of morphine exposure increases the intensity of withdrawal signs. Weight loss, diarrhea, body shakes, jumping, paw tremor, ptosis, piloerection, and the modified Gellert-Holtzman scale for mice are specific patterns of naloxone-induced withdrawal. The first four signs allow the discrimination between different levels of opiate dependence. Body care, piloerection, and the modified Gellert-Holtzman scale could be useful to detect conditioned withdrawal.

Animals↗

Effects of peripherally administered corticotropin-releasing factor (CRF) and a CRF antagonist: does peripheral CRE activity mediate behavior of guinea pig pups during isolation?

Guinea pig pups vocalized and ambulated when first isolated in a test cage; at 1 and 24 hr, levels of these behaviors had waned, and pups frequently exhibited a crouched stance, eye-closing, and piloerection. Injection (s.c.) of corticotropin-releasing factor (CRF) prior to isolation diminished the initial vocalization and locomotor responses and induced pups to exhibit the crouched stance, eye-closing, and piloerection at the beginning of the isolation period. Pretreatment with a CRF-receptor antagonist reversed the behavioral effects of CRF. CRF had no effect on blood pressure. Thus, s.c. CRF produced the same behavioral profile as seen with the passage of time in untreated isolated pups. The behavioral effects appeared to be CRF-receptor-mediated events and were not secondary to hypotension. These results support the hypothesis that during prolonged isolation, high or sustained peripheral CRF activity modulates behavior.

Animals↗

Prevalence and etiology of autonomic dysreflexia in children with spinal cord injuries.

OBJECTIVE: To delineate the prevalence, etiologies, clinical manifestations, complications, and management of autonomic dysreflexia in individuals who sustained spinal cord injury (SCI) as children. METHOD: Retrospective chart review. PARTICIPANTS: All individuals with > or = T6 SCI who were injured at 13 years of age or younger and who were cared for at one pediatric SCI program. OUTCOME MEASURES: Outcome measures included prevalence, etiologic factors, and symptoms of autonomic dysreflexia as documented in both inpatient and outpatient records. Blood pressure and heart rate for observed episodes of autonomic dysreflexia also were recorded. RESULTS: Of 121 participants who met the study criteria, 62 (51%) had experienced autonomic dysreflexia. The most common causes of dysreflexia were urologic (75%) and bowel impaction (18%), and the distribution of causative factors were similar in the 3 age ranges (0-5 years, 6-13 years, and 14-21 years). For all age groups, the most common symptoms were facial flushing (43%), headaches (24%), sweating (15%), and piloerection (14%). However, headaches (5%) and piloerection (0%), were uncommonly seen in children 5 years of age and younger. For observed episodes of autonomic dysreflexia, the majority (93%) demonstrated blood pressure elevations consistent with published guidelines, 50% experienced tachycardia, and 12.5% experienced bradycardia. Autonomic dysreflexia was significantly more common in individuals with complete lesions and in those who were injured between 6 and 13 years old compared with those injured at a younger age. Individuals with cervical injuries were not at significantly higher risk of dysreflexia than were those with upper thoracic level injuries. However, among individuals with complete lesions, autonomic dysreflexia was significantly more common in those with tetraplegia. CONCLUSION: Autonomic dysreflexia has a similar prevalence in pediatric-onset SCI compared with the adult SCI population. Dysreflexia is diagnosed less commonly in infants and preschool-aged children, and these 2 populations may present with more subtle signs and symptoms.

Adolescent↗

The local side effects of transdermally absorbed nicotine.

Percutaneous nicotine administration induces predominant sudorific and rubiform responses in the skin which may be accompanied by subtle piloerection, hyperalgesia and pruritus (although these signs are not overtly manifest). These dermal responses are complex and mechanisms have been proposed for the direct nicotine-stimulation of sweat glands, piloerection and vasoconstriction. These reactions are accompanied by secondary activation and release of vasodilator peptides which produce a predominating vasodilator tone following topical administration, this response masking the direct axon reflex-mediated vasoconstriction.

Administration, Cutaneous↗

[Single-dose toxicity studies of prulifloxacin (NM441) in mice, rats and dogs and the active metabolite (NM394) in rats].

Single-dose toxicity studies of prulifloxacin, a new antibacterial agent, were conducted in mice, rats and dogs. In addition, a single-dose toxicity study of (+/-)-6-fluoro-1-methyl-4-oxo-7- (1-piperazinyl)-4H-[1,3]thiazeto[3,2-a]quinoline- 3-carboxylic acid (NM394), an active metabolite of prulifloxacin, was performed in rats. Prulifloxacin was administered orally, intraperitoneally (i.p.) or subcutaneously (s.c.) to mice and rats, and orally to dogs. NM394 was administered intravenously (i.v.) to rats. When prulifloxacin was administered orally or s.c., LD50 values were more than 5000 mg/kg in both sexes of mice and rats; when it was administered i.p., LD50 values were 1757 mg/kg in male mice, 1652 mg/kg in female mice, 915 mg/kg in male rats, and 1076 mg/kg in female rats. The lethal doses of this drug were more than 5000 mg/kg in both sexes of dogs by the oral route. The LD50 values of NM394 were 226 mg/kg in male rats and 238 mg/kg in female rats by the i.v. route. In mice, the major clinical signs observed following the administration of prulifloxacin were sedation, oligopnea, abnormal gait, piloerection, closed eye and tremor by the i.p. route and a scab at the site of injection by the s.c. route; in rats, decreased spontaneous locomotor activity by any of the three routes, oligopnea, lacrimation, hypothermia, piloerection and abnormal gait by the i.p. route, and a scab at the site of injection by the s.c. route; and in dogs, vomiting, reddening of the skin, and loose stool by the oral route. When NM394 was administered i.v., rats showed clonic convulsion and dyspnea. The site of injection was hyperemic, swollen and necrotic. Mice showed a decrease in body weight or an inhibition in weight gain when prulifloxacin was administered i.p. and rats showed the same effects when prulifloxacin or NM394 was administered by any of the above-mentioned routes. Macroscopic findings detected following the i.p. administration of prulifloxacin in mice were pale color of the liver and spleen, thickening of the liver, and adhesion of intra-abdominal organs; and in rats, hydrothorax, congestion and edema of the lung, adhesion of intra-abdominal organs, swelling of the kidney accompanied by fine yellowish-white foci, and atrophy of the testis. When NM394 was administered i.v. to rats, congestion of the lung was macroscopically observed.

Administration, Oral↗