Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Piloerection”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

Vasoconstrictor and pilomotor fibres in skin nerves to the cat's tail.

Postganglionic neurones to the tail's skin of the cat were investigated with regard to their spontaneous activity, response characteristics to somatic stimuli and asphyxia, the conduction velocity of their axons, and the conduction velocity of the preganglionic axons converging on them. The cats were anaesthetized with chloralose, immobilized, and arteficially ventilated. With this regimen the postganglionic neurones were divided into two types: 1. Type 1 neurones are spontaneously active and exhibit reflexes upon somatic stimulation. During asphyxia they are mostly first depressed and then excited for about 2-3 min. Their axons conduct with 0.57 +/- 0.13 m/s (mean +/- SD). The pregaglionic axons converging on them conduct with 5.4 +/- 1.6 m/s. 2. Type 2 neurones are not spontaneously active and exhibit with few exceptions no reflexes on somatic stimuli. During asphyxia they are activated after 3-4 min, concomitantly with piloerection, when the activity in type 1 neurones is already decreasing. Their axons conduct with 0.84 +/- 0.14 m/s, the preganglionic axons converging on them conduct with 9.9 +/- 2.9 m/s. 3. From these characteristics it is concluded that type 1 neurones have vasomotor function and most type 2 neurones pilomotor function.

Action Potentials↗

Effects of intracerebroventricularly administered mu-, delta- and kappa-opioid agonists on locomotor activity of the guinea pig and the pharmacology of the locomotor response to U50,488H.

The effects of intracerebroventricular administration of morphine, the selective mu-agonist DAMGO, the delta-agonist DPDPE, the kappa-preferring peptide dynorphin A(1-13) and the kappa-agonist U50,488H on locomotor behaviour in the guinea pig were investigated. Morphine (total dose = 0.01, 0.1, 1, 10, 200 nmol), DAMGO and DPDPE (total dose = 0.1, 1, 10, 100 nmol of each) produced piloerection and sedation, indicating that the responses of guinea pigs to mu- and delta-opioid agonists differed from those of rats and mice. In contrast, U50,488H (total dose = 10, 100 nmol) and dynorphin A(1-13) (total dose = 100 nmol) produced increased locomotor activity which was attenuated by pretreatment with naloxone and norbinaltorphimine, thus confirming the involvement of kappa-opioid receptors. Furthermore, pretreatment with spantide, baclofen, muscimol, bicuculline, MK-801, raclopride and atropine also inhibited the U50,488H-induced locomotor activity, suggesting the involvement of GABA, dopamine, excitatory amino acids, substance P and acetylcholine in this response.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Further characterization of the behavioral effects of peripherally administered corticotropin-releasing factor in guinea pigs.

Guinea pig pups were either not injected (NI) or given SC injection of either saline vehicle (SAL) or 14 micrograms of corticotropin-releasing factor (CRF). In an isolation test, mean number of vocalizations and several measures of locomotor activity were markedly lower for CRF pups than for NI or SAL controls. CRF pups defecated less than did SAL pups. No differences were found among conditions for self-grooming. Behavioral freezing was shown by only two pups in the entire study. Significantly more CRF pups displayed piloerection, eye-closing, and a characteristic crouched stance than did controls. In a defensive withdrawal test, no differences among conditions were found for the proportion of pups entering a darkened chamber or for the latency to enter the chamber; however, CRF pups entered the chamber significantly fewer times during the 60-min test than did controls. There were no differences among conditions in the distance swum or number of turns made in a forced-swim test. These results replicate our earlier findings that peripheral injection of CRF suppresses vocalizing and a measure of locomotor activity in isolated guinea pig pups and identifies a number of additional behavioral effects. Of central interest here, the results indicate that the suppression of vocalizing and locomotion during isolation is not due to an increase in competing stress-related behavior or to diminished motor capacity.

Aggression↗

Effects of antibodies against acetylcholinesterase on the expression of peptides and catecholamine synthesizing enzymes in the rat adrenal gland.

In the rat, systemic administration of murine monoclonal antibodies against acetylcholinesterase caused rapid piloerection and ptosis (within 30-60 min after the injection). Using indirect immunohistochemistry the effect of these antibodies on peptides and enzyme expression was studied in the rat adrenal gland. Four days after antibody administration a total disappearance of acetylcholinesterase-immunoreactive fibers was observed. However, groups of acetylcholinesterase-immunoreactive chromaffin cells and intramedullary ganglion cells, both cell types showing acetylcholinesterase immunoreactivity also in the control adrenal medulla, expressed increased immunoreactivity. Analysis revealed that the acetylcholinesterase-immunoreactive chromaffin cell groups lacked phenylethanolamine-N-methyltransferase staining both in controls and treated rats. Antibody administration also affected levels of several peptides present in nerve fibers and chromaffin cells. Thus, the number of cells expressing enkephalin, calcitonin gene-related peptide and galanin was dramatically increased compared to the very few cells observed containing these three peptides in the normal gland. The majority of cells expressing enkephalin after antibody treatment also showed phenylethanolamine-N-methyltransferase immunoreactivity. In contrast, the few chromaffin cells expressing strong enkephalin-like immunoreactivity in controls were phenylethanolamine-N-methyltransferase negative. The sparse networks of calcitonin gene-related peptide- and galanin-positive fibers found in control adrenals were unchanged after the antibody treatment. However, the dense network of enkephalin varicose fibers totally disappeared after the antibody injection. A few substance P- and somatostatin-immunoreactive cells, not present in the normal gland, appeared after administration of the antibodies, whereas no changes were encountered with regard to immunoreactive nerve fibers. No clear differences between normal and treated animals could be observed in chromaffin cells with regard to immunoreactivity for neuropeptide Y or any of the four catecholamine-synthesizing enzymes, tyrosine hydroxylase, aromatic 1-amino acid decarboxylase, dopamine beta-hydroxylase or phenylethanolamine-N-methyltransferase. The present findings demonstrating a disappearance of acetylcholinesterase- and enkephalin-immunoreactive nerve fibers in the adrenal gland after intravenous injection of acetylcholinesterase antibodies support earlier reports showing that these antibodies cause degeneration of preganglionic fibers, and that neuronal decentralization of the adrenal gland induces marked increases in the levels of several peptides in chromaffin cells.

Acetylcholinesterase↗

Alpha-melanocyte stimulating hormone reduces putative stress-induced sickness behaviors in isolated guinea pig pups.

We have proposed that passive responses observed following maternal separation in guinea pig pups represent "stress-induced sickness behaviors" mediated by proinflammatory processes. In this study, the anti-inflammatory peptide, alpha-melanocyte stimulating hormone (alpha-MSH) administered intracerebroventricularly, but not intraperitoneally, reduced the passive responses of crouching, eye-closing, and extensive piloerection relative to levels following administration of vehicle. These findings support our hypothesis and are as would be expected if pro-inflammatory processes act centrally to promote the passive behaviors of separated guinea pig pups.

Age Factors↗

Nandrolone decanoate has long-term effects on dominance in a competitive situation in male rats.

The aim of the present study was to examine possible long-term effects of the anabolic androgenic steroid (AAS), nandrolone decanoate (ND), on dominance in a provoking and competitive situation in sexually matured male rats. The experimental group (n=10) received daily injections of ND [15 mg/kg in a volume of 1 ml/kg subcutaneous (s.c.) injection for 14 days]. During the corresponding period, the controls (n=10) were given daily injections of an oil vehicle (1 ml/kg s.c.). All animals were tested in a competitive situation at four occasions after the end of the treatment period (week 5, 8, 11 and 14). Water-deprived pairs of rats, consisting of one ND-treated rat and one control, had to compete for access to water. The results showed that the ND-treated rats approached the water spout significantly more often compared to the controls. During the competition tests, the ND-treated rats spent more time drinking, an effect that was prominent for 11 weeks after the end of the treatment period. The ND-treated rats also displayed more frequently piloerection than the controls. The results indicate that ND has long-term effect on dominance in a provoking and competitive situation.

Anabolic Agents↗

Toxicity of botulinum neurotoxins in central nervous system of mice.

Botulinum neurotoxins (BoNTs) act specifically on cholinergic nerve terminals, where they cause a sustained block of acetylcholine release, and therefore they are powerful tools to study the role of cholinergic neurons in neuronal processes. Peripheral effects of BoNTs are widely documented while central effects have not been studied. Here, we report for the first time on the central toxicity of BoNT serotypes A and B following their direct intracerebroventricular (icv) injection in CD1 mice. The LD50 values were found to be in the range 0.5-1.0 x 10(-6)mg/kg. We recorded the following signs preceding animal death: piloerection and weight decrease appear first, followed by temperature decrease, eyelid closure, loss of sensorimotor reflexes, dehydration, dyspnea. Mice died of heart or respiratory failure. The surviving mice recovered completely within 4-6 days and regained the initial healthy conditions. At sub-lethal doses, the same clinical signs appear in a lighter form and with a longer time course.

Animals↗

Posttraumatic pilomotor seizures: a case report.

Pilomotor epilepsy is a rare phenomenon. A 35-year-old man suffered a traumatic contusion of the right temporal lobe and subsequently developed spells characterized by diffuse piloerection and sweating. We believe this to be the first reported association between pilomotor epilepsy and posttraumatic head injury. Although pilomotor seizures may result from diverse etiologies, they appear to have a common involvement of temporolimbic structures.

Adult↗

Fever produced by endotoxin injected into the hypothalamus of the monkey and its antagonism by salicylate.

1. A suspension of the killed cell bodies of either E. coli, S. dysenteriae or S. typhosa was micro-injected through cannulae implanted chronically at specific sites within the diencephalon and mid-brain of the unanaesthetized monkey. A biphasic, monophasic or an undifferentiated fever could be induced by each type of micro-organism, but the type of response depended solely upon the locus of injection.2. Although little difference in the potency of the three pyrogens was found, the rise in body temperature was in each instance dependent upon the concentration of the endotoxin. A more intense fever was accompanied by shivering, vasoconstriction of the ear vessels, piloerection and huddling behaviour. Tolerance to the pyrexic effect of repeated injections of endotoxin did not develop.3. The febrile response having the shortest latency, greatest maximum rise in temperature and largest 10-hr fever index was evoked by micro-injections into the anterior hypothalamic, preoptic area. The incidence of biphasic fevers was also greater after endotoxin was injected into this same region. Endotoxin given similarly in the posterior hypothalamus or in the mesencephalon had either no effect or produced a smaller elevation in temperature after a longer latency. The distance of an injection site from the coronal plane formed by the optic chiasm and anterior commissure correlated significantly with the latency and magnitude of the temperature change as well as the fever index.4. When given intravenously, endotoxin in a quantity at least 100 times greater was required to evoke a fever similar to that produced when the pyrogen was micro-injected into the anterior hypothalamic, preoptic region. However, a biphasic fever was evoked with a latency of from 3 to 15 min when a larger amount of endotoxin was injected intravenously. Tolerance developed rapidly to the febrile effect of endotoxin administered by this route although toxic reactions were not observed.5. After the fever evoked by the hypothalamic injection of endotoxin had reached a plateau, 300-1200 mg sodium salicylate administered intragastrically produced a dose-dependent fall in temperature, but had no effect on the body temperature of an afebrile monkey.6. It is concluded that in the rhesus monkey, a bacterial pyrogen can evoke a fever which is mediated entirely by an action on the central nervous system, the principal site being the anterior hypothalamic, preoptic area. The first phase of a biphasic fever caused by bacteria acting either by the central or peripheral route seems to be due either to a direct action of the pyrogen on the cells of the anterior hypothalamus, or to the secondary release within this region of an intermediary thermogenic substance such as 5-hydroxytryptamine or prostaglandin. The finding that sodium salicylate counteracts a centrally evoked fever is not compatible with the hypothesis that an antipyretic exerts its action by preventing a pyrogen that is circulating in the blood stream from entering the central nervous system.

Animals↗

Pilomotor seizures.

We report pilomotor seizures in two patients who had piloerection or gooseflesh spreading in a pattern like the 'Jacksonian march', confined ipsilaterally to the lesion side. The first patient presented this in conjunction with complex partial seizures. Left anterior temporal lobectomy abolished pilomotor and other seizures. Pathological study demonstrated hippocampal sclerosis. A meningioma near the left sphenoid region, incompletely removed, is the likely cause of pilomotor seizures in the second patient. Carbamazepine reduced these attacks. To our knowledge, hippocampal sclerosis and meningioma have never been linked to pilomotor seizures.

Adult↗

Pilomotor seizures associated with sequential changes in magnetic resonance imaging.

Piloerection is rarely described in seizures. This symptom has been most frequently observed in patients with temporal lobe epilepsy and is rarely the principal clinical feature of seizures. No specific etiology of epilepsy associated with pilomotor seizures has been reported. We present the first case of a patient who experienced sudden and transitory epilepsy with pilomotor seizures occurring several times a day for months, and associated with sequential changes of the left hippocampus demonstrated by magnetic resonance imaging. [Published with video sequences].

Adult↗

Pilomotor epilepsy.

The case is reported of a patient presenting pilomotor seizures as the initial symptom of a tumour of the deep temporal lobe. Six other cases had previously been reported with the same type of seizures. The responsible lesion was often a tumour in deep temporal lobe and the distribution of the piloerection attacks was almost always ipsilateral. Pilomotor seizures deserve a definite role in the nosography of partial epilepsy.

Brain Neoplasms↗

Long-lasting hypersensitivity to methamphetamine following amygdaloid kindling in cats: the relationship between limbic epilepsy and the psychotic state.

This study attempts to analyze the biological mechanisms involved in the association of a psychotic state with temporal lobe epilepsy, and the inverse relation between the epilepsy and this psychotic state. Responses to a test dose of methamphetamine (MAP) were examined in amygdaloid-kindled cats. It was found that (i) MAP-induced stereotyped behavior was enhanced after amygdaloid kindling, and this hypersensitivity lasted for at least 10 days after the final convulsion, (ii) autonomic responses to MAP including piloerection, salivation, heart rate, and respiration rate were also enhanced by the kindling, (iii) kindled generalized convulsions were suppressed during MAP-induced stereotyped behavior in some cats, and (iv) this suppression was blocked by pretreatment with pimozide. Engel and Ackermann proposed that inhibitory events precipitated by each kindling stimulus could produce changes in the catecholaminergic system similar to the reverse tolerance seen with dopamine agonists, and that inhibitory hypersensitivity could parallel the development of kindled excitation. This was partially confirmed by the present study, and leads to the hypothesis that excitation of seizure-inhibiting activity, including activity of the dopamine system, may be related to the emergence of a psychotic state, and to the inverse relationship between epilepsy and the psychotic state in temporal lobe epilepsy.

Amygdala↗

Preclinical studies with triazinate (NSC-139105), an antifolate drug, in beagle dogs and rhesus monkeys.

The effects of the intravenous administration of triazinate by single and multiple injections were studied in beagle dogs and rhesus monkeys. In dogs, dose levels ranging from 0.3125 to 40 mg/kg were given either as single doses daily for 5 days, or once weekly for 6 weeks. The 5-day regimen was also studied in monkeys with dose levels from 2.5 to 40 mg/kg/day. Prominent drug-related and drug-dependent effects which appeared in both species were piloerection, muscular weakness, and respiratory difficulty which occurred during and immediately after the administration of dose levels of 10 mg/kg or greater. Gastrointestinal toxicity was severe in dogs but mild in monkeys. Lymphoid tissue toxicity was manifested by a circulating lymphopenia and localized cellular depletion in the germinal centers of lymphoid tissues. In dogs, signs of bone marrow toxicity consisted of a circulating neutropenia and, at necropsy, a reduction in the number of erythroid and myeloid elements plus megaloblastosis. Only the latter change was observed in monkeys. This difference in the hematopoietic toxicity between the beagle dog and the rhesus monkey was corroborated by the findings from in vitro studies with bone marrow. DNA synthesis in beagle bone marrow cells was depressed significantly by triazinate as compared with cells from rhesus marrow. A direct renal toxic effect was observed in monkeys given high doses of triazinate (20 and 40 mg/kg/day or 240-280 mg/m/day) for 5 days.

Animals↗

Toxicity of the novel anti-peptic ulcer agent catena-(S)-[mu-[Na- (3-aminopropionyl)histidinato(2-)-N1,N2,Q:N tau]-zinc in male cynomolgus monkeys.

A preliminary dose-range finding study and a 13-week toxicity study were performed in male cynomolgus monkeys with catena-(S)-[mu-[N a-(3-aminopropionyl) histidinato (2-)-N1,N2,O:N tau]-zinc] (Z-103, CAS 107667-60-7), a novel anti-peptic ulcer agent, as part of a safety evaluation program. In the preliminary ascending dose study emesis was observed in animals treated at 625 mg/kg and transient reductions in food intake with associated body weight loss in a male treated at 625 or 312.5 mg/kg. Plasma zinc levels were also increased in all animals treated at 625 or 312.5 mg/kg. As a result dosages of 0, 20, 63 and 200 mg/kg/day were selected for the 13-week toxicity study. In this study, treatment-related changes were confined to the 200 mg/kg/day dosage and consisted of emesis, piloerection and transient body weight loss in one animal, increased plasma zinc concentrations, and zinc and copper deposition in the liver and kidneys without any associated morphological change. The no observed effect level was estimated to be 63 mg/kg/day in this study.

Animals↗

Congenital smooth muscle hamartoma. A report of six cases and a review of the literature.

Congenital smooth muscle hamartoma (CSMH) represents a proliferation of randomly oriented dermal smooth-muscle bundles. Six patients with CSMH were observed, the largest series to date, and the literature was reviewed. Congenital smooth muscle hamartoma has presented as congenital patches or slightly indurated plaques with prominent overlying hair (88% of cases), or rarely as patches with perifollicular papules without prominent hair (12% of cases). Most lesions (61% of cases) have been somewhat hyperpigmented, but 39% of cases have been flesh colored. Congenital smooth muscle hamartoma has occurred on the torso and proximal extremities, except for one case on the eyebrow and eyelid (present study). A positive pseudo-Darier's sign (temporary induration or piloerection after rubbing) helped to differentiate CSMH from congenital hairy nevo-cellular nevus. Congenital smooth muscle hamartoma is a distinct entity that is at one end of a spectrum that includes Becker's nevus, and should be considered in the differential diagnosis of any congenital hairy lesion.

Biopsy↗

Model of Wernicke's encephalopathy.

After a week on a thiamine-free diet and daily injections of pyrithiamine hydrobromide, a group of rats began to lose weight; soon thereafter hypothermia, piloerection, and ataxia developed, followed by convulsions and death. Neuropathologic examination disclosed hemorrhagic necrotic lesions in the thalamus, hypothalamus, collicular plate, vestibular nuclei, and inferior olives. The control groups did not show neurologic signs or neuropathologic abnormalities. The lesions in thiamine-deficient rats were similar in character and distribution to those of human Wernicke's disease. Because this experimental regimen produces neuropathologic changes rapidly and consistently, this animal model should be useful in studies designed to examine the pathophysiologic aspects of experimental Wernicke's disease in particular and CNS thiamine deficiency in general.

Animals↗

Noradrenergic function in panic anxiety. Effects of yohimbine in healthy subjects and patients with agoraphobia and panic disorder.

Yohimbine, an alpha 2-adrenergic receptor antagonist that increases noradrenergic function, was administered to 20 healthy subjects and 39 drug-free patients with agoraphobia and panic attacks. Following drug administration, changes in plasma levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG), BP, pulse rate, and subjective ratings of feelings and somatic symptoms were examined during a four-hour period. Yohimbine produced significantly greater increases in patient-rated anxiety, nervousness, palpitations, hot and cold flashes, restlessness, tremors, piloerection, and sitting systolic BP in the total patient group compared with healthy subjects. There were significant correlations between the yohimbine-induced rise in plasma MHPG level and patient-rated anxiety and nervousness and the frequency of reported panic attacks. Patients experiencing frequent panic attacks (greater than 2.5 per week) had a significantly greater plasma MHPG response to yohimbine than the healthy subjects and patients having less frequent panic attacks. These observations support a hypothesis of increased sensitivity to augmented noradrenergic function in anxiety states associated with panic, and they suggest that impaired presynaptic noradrenergic neuronal regulation may exist in patients with frequent panic attacks.

Adult↗