Ear Twitching Research Articles

Catcalls: exotic cats discriminate the voices of familiar caregivers.

The ability to differentiate familiar from unfamiliar humans has been considered a product of domestication or early experience. Few studies have focused on voice recognition in Felidae despite the fact that this family presents the rare opportunity to compare domesticated species to their wild counterparts and to examine the role of human rearing. We tested whether non-domesticated Felidae species recognized familiar human voices by exposing them to audio playbacks of familiar and unfamiliar humans. In a pilot study, we presented seven cats of five species with playbacks of voices that varied in familiarity and use of the cats' names. In the main study, we presented 24 cats of 10 species with unfamiliar and then familiar voice playbacks using a habituation-dishabituation paradigm. We anticipated that human rearing and use of the cats' names would result in greater attention to the voices, as measured by the latency, intensity, and duration of responses regardless of subject sex and subfamily. Cats responded more quickly and with greater intensity (e.g., full versus partial head turn, both ears moved versus one ear twitching) to the most familiar voice in both studies. They also responded for longer durations to the familiar voice compared to the unfamiliar voices in the main study. Use of the cats' name and rearing history did not significantly impact responding. These findings suggest that close human contact rather than domestication is associated with the ability to discriminate between human voices and that less social species may have socio-cognitive abilities akin to those of more gregarious species. With cats of all species being commonly housed in human care, it is important to know that they differentiate familiar from unfamiliar human voices.

Neuromotor Development in the Shank3 Mouse Model of Autism Spectrum Disorder.

Although autism spectrum disorder (ASD) is mainly characterized by developmental delay in social and communication skills, it has been shown that neuromotor deficits are an early component of ASD. The neuromotor development of B6.129-Shank3tm2Gfng/J (Shank3B−/−) mice as an animal model of autism has not been analyzed yet. The aim of this study was to compare the early neuromotor development of Shank3B−/− to wild-type mice. The mice underwent a multitude of neurodevelopmental tests and observations from postnatal day 1 (PND = 1) to weaning. Shank3B−/− mice opened their eyes later than their wild-type litter mates (p < 0.01). Shank3B−/− mice were also slower in the negative geotaxis test from PND = 13 to PND = 16 (p < 0.001) in both sexes. The results of this study indicate neurodevelopmental deficits in Shank3B−/− mice. The test is partially dependent on truncal motor control, and these lines of evidence suggest a phenotype of developmental hypotonia, which corresponds with the phenotypes seen in patients with Phelan-McDermid Syndrome. There was no observable effect of sex in any of the tests. There were no observed differences in upper and lower incisor eruption, ear unfolding, air righting, surface righting and ear twitch reflexes. Further studies should prove whether the delay in neuromotor development is linked to social or communication deficits, and thus, whether it may serve as an early indicator of autistic-like phenotype in mice.

Neurological diseases in cattle caused by plants and mycotoxins in Santa Catarina state, Brazil

ABSTRACT: This study described the epidemiological and clinical-pathological aspects of 25 outbreaks of neurological diseases in cattle caused by plants and mycotoxins in Santa Catarina state. Six of them were due to Sida carpinifolia poisoning, five to Solanum fastigiatum, five to Phalaris angusta, three to Claviceps paspali, three to Claviceps purpurea, and three outbreaks were of unknown etiology. The clinical signs observed in the affected cattle were mild to severe and characterized by generalized muscle tremors, incoordination, hypermetria, wide-based stance, intentional head tremors, dull staring eyes, and frequent ear twitching, with convulsions in some cases. At necropsy, lesions were observed only for P. angusta poisoning, characterized by gray-greenish discoloration in thalamus and midbrain. Microscopically, rarefaction and/or disappearance of Purkinje neurons with substitution by Bergmann cells were observed for S. carpinifolia and S. fastigiatum poisoning. For P. angusta poisoning, thin granular brown-yellowish pigment was observed in the cytoplasm of some neurons. Gross and microscopic findings were not observed in three outbreaks of tremorgenic disease of unknown etiology. Experiments conducted with leaves, flowers and seeds of Ipomoea indivisa and Ipomoea triloba, as well as with maize and soybean residues contaminated with Ipomoea spp. did not reproduced clinical signs.

The effects of a maternal advanced glycation end product-rich diet on somatic features, reflex ontogeny and metabolic parameters of offspring mice.

Maternal exposure to a Western type diet during pregnancy might predispose the offspring to manifestation of metabolic and behavioral disturbances in later life. The Western type diet contains large amounts of advanced glycation end products (AGEs). In humans and experimental rodents, the intake of an AGE-rich diet (AGE-RD) negatively affected glucose homeostasis, and initiated the production of reactive oxygen species. Rats consuming the AGE-RD presented changes in behavior. It remains unclear whether maternal intake of the AGE-RD might affect developmental plasticity in offspring. We examined early somatic (weight, incisor eruption, ear unfolding, and eye opening) and neuromotor development, oxidative status, insulin sensitivity (HOMA index) and locomotor activity assessed in PhenoTyper cages in the offspring of mice fed during pregnancy with either the AGE-RD (25% bread crusts/75% control chow) or control chow. Until weaning, the somatic development of offspring did not differ between the two dietary groups. The AGE-RD offspring manifested physiological reflexes (auditory startle, eye lid, ear twitch and righting reflexes) earlier. As young adults, the male offspring of the AGE-RD dams were heavier and less insulin sensitive compared with their control counterparts. The AGE-RD offspring showed higher locomotor activity during the active phase. Our data indicate that the maternal AGE-RD during pregnancy might accelerate the maturation of reflexes in offspring, predispose the male progeny to weight gain and affect their glucose homeostasis. These effects manifest without the direct consumption of the AGE-RD by offspring. Further work is needed to determine the mechanisms by which the maternal AGE-RD affects neurobehavioral pathways in offspring, as well as sex differences in adverse metabolic responses.

EXERCISE, MANUAL THERAPY AND POSTURAL RE-EDUCATION FOR UNCONTROLLED EAR TWITCHING AND RELATED IMPAIRMENTS AFTER WHIPLASH INJURY: A CASE REPORT

Whiplash Associated Disorders and the interventions used to remediate them are well documented in physical therapy literature. However, specific interventions for spasms of the neck musculature that also involve constant ear twitching have yet to be addressed. The purpose of this case report is twofold. First, to describe comprehensive physical therapy management and outcomes for a subject with uncontrolled ear twitching and related musculoskeletal impairments, and second, to discuss the physical therapist's approach to evidence-based care when faced with a paucity of literature addressing physical therapy interventions for subjects with uncontrolled ear twitching. The subject was a 14-year-old female who sustained a right anterolateral whiplash injury when struck in the head by a volleyball seven months prior to physical therapy. Beginning five months after that injury, she experienced uncontrolled and constant superior/inferior movement of her right ear (hereafter described in this report as a twitch) in addition to facial and cervical pain from her initial injury. She was unable to participate in high school athletics due to her pain. A multimodal treatment approach including exercise, manual therapy, and postural reeducation was utilized during the subject's episode of care. After eight treatment sessions, the subjects's cervical range of motion and upper extremity strength improved. The reported frequency of ear twitching decreased, as did reports of neck and shoulder pain. In addition, her Neck Disability Index improved from a score of 22, indicating moderate disability, to 9, indicating mild disability and she was able to return to sport activity. With limited research to direct intervention, clinical reasoning was utilized to formulate an effective therapeutic intervention. A combination of manual therapy, exercise, and postural reeducation intervention was effective for this subject and could assist in guiding interventions for similarly unique clinical presentations in the future. Further research is needed to examine the etiology of ear twitching caused by muscle spasm and to develop additional evidence-based interventions for Whiplash Associated Disorders. Level 4.

Twitching in veterinary procedures: How does this technique subdue horses?

Abstract This study investigates the mechanisms by which 2 forms of restraint (lip twitch and ear twitch) subdue horses. Prior research suggests that the lip twitch subdues horses through an analgesic effect; the mechanism of the ear twitch is unknown. Heart rate (HR) and heart rate variability (HRV) were measured to determine autonomic nervous system activity before and during application of the twitches, and salivary cortisol levels were analyzed to assess stress levels before and after application of the twitches. Twelve male horses (all geldings) were divided into 2 groups. One group received the lip twitch, and the other received the ear twitch. Results show that the lip twitch significantly decreased HR and increased HRV when applied for 5 minutes. However, when the lip twitch was applied for a longer period, it significantly increased HR and decreased HRV. The ear twitch significantly increased HR, decreased HRV, and increased salivary cortisol levels regardless of the length of application. It is concluded that the lip twitch might initially subdue horses through a calming, probably analgesic effect at least in the initial 5 minutes, whereas the ear twitch evokes a stressful response, immobilizing horses through fear and/or pain.

Proconvulsive effects of oxytocin in the generalized pentylenetetrazol mouse model are mediated by vasopressin 1a receptors

The possible involvement of oxytocin (OT) in the generation of seizures has not received a lot of attention in the past, although generalized epileptic convulsions were observed in humans following intravenous OT infusion. We here aimed to investigate the effect of exogenous OT administration on seizure susceptibility in C57Bl/6 mice subjected to the pentylenetetrazol (PTZ) model. In addition, we studied via which receptor possible effects on seizure thresholds could be mediated since OT binds to both the OT receptor (OTR) and the vasopressin 1a receptor (V1aR). We showed that C57Bl/6 mice treated with 0.5mg/kg OT had decreased PTZ thresholds for ear twitch, myoclonic twitch, tail twitch, forelimb clonus and falling. This pronconvulsive effect was reversed by the OTR antagonist L-368.899, however, it was not mimicked by the OTR agonist carbetocin (CBT). Nevertheless, CBT had antidepressant-like effects in the forced swim test that could be reversed by L-368.899. These experiments shed some doubt on the involvement of OTR in the observed effect of OT on seizure thresholds. Therefore, we investigated the role of the V1aR as a possible mediator of the proconvulsive effects of OT. We found that the proconvulsive effects of both arginine vasopressin and OT were reversed by the V1aR antagonist SR49059. In summary, OT has proconvulsive effects in our mouse model of generalized seizures that could not be mimicked by CBT. Our results suggest that the binding of OT to V1aRs is the most plausible explanation for the proconvulsive effects of OT.

Evaluation of medetomidine-ketamine and dexmedetomidine-ketamine in Chinese water deer (Hydropotes inermis)

ObjectiveTo investigate physiological and sedative/immobilization effects of medetomidine or dexmedetomidine combined with ketamine in free-ranging Chinese water deer (CWD). Study designProspective clinical trial. Animals10 free-ranging adult Chinese water deer (11.0 ± 2.6 kg). MethodsAnimals were darted intramuscularly with 0.08 ± 0.004 mg kg−1 medetomidine and 3.2 ± 0.2 mg kg−1 ketamine (MK) or 0.04 ± 0.01 mg kg−1 dexmedetomidine and 2.9 ± 0.1 mg kg−1 ketamine (DMK) If the animal was still laterally recumbent after 60 minutes of immobilization, atipamezole was administered intravenously (MK: 0.4 ± 0.02 mg kg−1, DMK: 0.2 ± 0.03 mg kg−1). Heart rate (HR) respiratory rate (fR) and temperature were recorded at 5-minute intervals. Arterial blood was taken 15 and 45 minutes after initial injection. Statistical analysis was performed using Student’s t-test or anova. p < 0.05 was considered significant. ResultsAnimals became recumbent rapidly in both groups. Most had involuntary ear twitches, but there was no response to external stimuli. There were no statistical differences in mean HR (MK: 75 ± 14 beats minute−1; DMK: 85 ± 21 beats minute−1), fR (MK: 51 ± 35 breaths minute−1; DMK; 36 ± 9 breaths minute−1), temperature (MK: 38.1 ± 0.7 °C; DMK: 38.4 ± 0.5 °C), blood gas values (MK: PaO2 63 ± 6 mmHg, PaCO2 49.6 ± 2.6 mmHg, HCO3− 30.8 ± 4.5 mmol L−1; DMK: PaO2 77 ± 35 mmHg, PaCO2 45.9 ± 11.5 mmHg, HCO3− 31.0 ± 4.5 mmol L−1) and biochemical values between groups but temperature decreased in both groups. All animals needed antagonism of immobilization after 60 minutes. Recovery was quick and uneventful. There were no adverse effects after recovery. Conclusion and clinical relevanceBoth anaesthetic protocols provided satisfactory immobilisation. There was no clear preference for either protocol and both appear suitable for CWD.

Effect of depth of anaesthesia and postganglionic sympathetic blockade on reflex heart rate control in rodents during lower body negative pressure

We tested the hypothesis that depth of anaesthesia affects heart rate (HR) control during orthostatic stress in rodents. Urethane (UR) and a‐chlorolose (a‐CL) were injected IP to reach either a Light (n=4; 25mg UR/100g rat mass, 3.5mg a‐CL/100g rat mass) or Deep (n=3; 40mg UR/100g rat mass, 4.0mg a‐CL/100g rat mass; IV top‐ups as needed) plane of anaesthesia, verified by the respective presence or absence of ear twitch, palpebral and pedal reflexes. Orthostatic stress was achieved with lower body negative pressure (LBNP), adapted for a rat model. Cardiac output (Q; transonic flow‐meter at descending aorta) and HR (ECG) were measured during graded bouts of LBNP between ‐1 and ‐10 mmHg, ordered randomly. At each anaesthetic depth LBNP was repeated with saline or hexamethonium (HEX; 25mg/kg IV) to block postganglionic sympathetic nerve activity. The reduction in Q during LBNP (main effect, P&lt;0.05) was not affected by anaesthetic depth or HEX. HR increased with LBNP when suction exceeded ‐4 mmHg (main effect, P&lt;0.05). Focusing on ‐10 mmHg, the HR increase was not different between Light (24±10 bpm) and Deep (24±7 bpm) planes, but was attenuated with HEX (4±1 and 5±5 bpm, P&lt;0.001 vs. Light and Deep, respectively). These preliminary results suggest that the majority of the HR response to LBNP in rodents is mediated by postganglionic sympathetic outflow and is not affected by depth of anaesthesia.Support provided by CIHR and NSERC.

Postnatal inflammatory rat model for cerebral palsy: Too different from human

Postnatal inflammatory rat model for cerebral palsy: Too different from human

Neurological reflexes and early motor behavior in rats subjected to neonatal hypoxic–ischemic injury

Severe perinatal hypoxia–ischemia is an important cause of brain injury in both full-term and premature newborns, with a high risk of future behavioral and neurological deficits. The most commonly used animal model of neonatal hypoxia–ischemia is the unilateral ligation of the common carotid artery followed by exposure to hypoxia in 7-day-old rats. In spite of the wide use of this model, lot of contradictions and discrepancies exist between the results obtained by different laboratories regarding behavioral deficits and there are no data regarding the possible delay of the appearance of neurological reflexes and the time-course of reflex performances following neonatal hypoxic–ischemic injury in rats. In the present study we showed that neonatal hypoxia–ischemia retarded the development of somatic growth and several neurological reflexes (ear twitch, grasping, gait and negative geotaxis). Hypoxic animals also displayed retarded performance in righting, geotaxis and gait reflexes. Although hypoxic pups performed worse in most tests for motor coordination, they reached normal levels by 5 weeks of age except in the footfault test. In the open-field, hypoxic animals were generally more active, except at 3 weeks, when activity of normal pups increased enormously as well. Brain areas were significantly reduced in hypoxic animals, but no close correlation was found with behavioral deficits.

Indicators of Acute Pain and Fly Avoidance Behaviors in Holstein Calves Following Tail-docking

Previous work showed that the banding process of docking minimally affected mature cows’ behavior and physiology, but cutting off the necrotic tail increased haptoglobin. Additionally the docked cows had more flies on the rear legs and exhibited more fly avoidance behaviors. Because many producers dock young calves while they are in hutches where fly problems are more pronounced, we investigated changes in behavior and physiology of young calves following docking by banding. Twenty calves (3 to 5wk of age) were assigned to a docked or control group, at each of two locations (Indiana and Wisconsin). After applying a band to dock the tail, calves were tested every 15min for sensitivity to heat below the band at the Indiana location. Calf behavior was recorded for 2h postbanding and analyzed continuously for that period. After 3wk, tails were removed and then 1wk later, fly counts and fly avoidance behaviors were observed at both locations. Tails were sensitive to heat below the banding site, for 60 to 120min postbanding (mean 87min). Banded calves were more active than control calves during the 2h following banding. Percentage of time spent lying was greater for control calves, and the percentage of time spent walking was greater for docked than control calves. More importantly, movements of the head to touch the tail were increased for banded calves (eight-fold more movements). Fly avoidance behaviors directed toward the rear of the calf were evident at noon or in the afternoon. Ear twitches were more frequent for the docked calves and less frequent in the morning for all calves. Licking was more frequent for the docked calves at 1200 and 1600h. Tail swings were most frequent at 1200 and more frequent for control calves. Two acute phase proteins, haptoglobin and α1 acid-glycoprotein, were not different at any time. In this study, calves that were banded at 3-wk-of-age showed behaviors indicative of discomfort for 2h, were attacked by more flies, and showed increased fly avoidance behaviors when docked.

Mutant beta-spectrin 4 causes auditory and motor neuropathies in quivering mice.

The autosomal recessive mouse mutation quivering (qv), which arose spontaneously in 1953, produces progressive ataxia with hind limb paralysis, deafness and tremor. Six additional spontaneous alleles, qvJ, qv2J, qv3J, qv4J, qvlnd and qvlnd2J, have been identified. Ear twitch responses (Preyer's reflex) to sound are absent in homozygous qv/qv mice, although cochlear morphology seems normal and cochlear potentials recorded at the round window are no different from those of control mice. However, responses from brainstem auditory nuclei show abnormal transmission of auditory information, indicating that, in contrast to the many known mutations causing deafness originating in the cochlea, deafness in qv is central in origin. Here we report that quivering mice carry loss-of-function mutations in the mouse beta-spectrin 4 gene (Spnb4) that cause alterations in ion channel localization in myelinated nerves; this provides a rationale for the auditory and motor neuropathies of these mice.

Neurobehavioral Development of Neonatal Mice Following Blockade of VIP During the Early Embryonic Period

Wu, J. Y., K. A. Henins, P. Gressens, I. Gozes, M. Fridkin, D. E. Brenneman and J. M. Hill. Neurobehavioral development of neonatal mice following blockade of VIP during the early embryonic period. Peptides 18(8) 1131–1137, 1997.—Previous work has shown that blockade of VIP function in the early postimplantation embryo results in growth retardation and microcephaly. In the present work, the neurobehavioral development of neonatal mice was examined following treatment of dams with a VIP antagonist during this period. Inhibition of VIP functions during early embryogenesis impaired the performance of 5 of 10 developmental behaviors. These behaviors included developmental milestones (first appearance of ear twitch and eye opening) and complex motor behaviors (negative geotaxis, surface righting, and air righting). The retardation of neurobehavioral development produced by inhibition of VIP action indicates that this peptide is important to the progression of embryonic development. Published by Elsevier Science Inc.

Effects of 8-OHDPAT and 5-HT1A antagonists WAY100135 and WAY100635, on guinea-pig behaviour and dorsal raphe 5-HT neurone firing.

1. The effects of 5-HT1A antagonists on guinea-pig behaviour and dorsal raphe neuronal activity were investigated. 2. WAY100135 (10 mg kg-1, s.c.) and WAY100635 (1 mg kg-1, s.c.) significantly reduced the behaviours induced by 8-hydroxy-2-(di-n-propylamino) tetralin (8-OHDPAT) (1 mg kg-1, s.c.) indicative of post-synaptic 5-HT1A receptor antagonism. WAY100635 (10 mg kg-1, s.c.) alone induced ear twitches, which were antagonized by ketanserin (1 mg kg-1, s.c.), but no other overt behaviours. 3. WAY100635 (0.125 mg kg-1, i.v.) produced a right-ward shift in the dose-related inhibition of neuronal firing by 8-OHDPAT (5-100 micrograms kg-1, i.v.) but did not affect the maximum inhibition induced by 8-OHDPAT indicating competitive antagonism between 8-OHDPAT and WAY100635 at the 5-HT1A somato-dendritic autoreceptor in the dorsal raphe nucleus of the guinea-pig. WAY100635 also produced a dose-related increase in the basal firing of 5-HT neurones in the dorsal raphe nucleus and restored the firing of dorsal raphe neurones previously inhibited by 8-OHDPAT (10 micrograms kg-1, i.v.). 4. The results indicate that WAY100635 is a competitive 5-HT1A antagonist in the guinea-pig. Furthermore WAY100635 can increase 5-HT neuronal firing, suggesting that it blocks a 5-HT1A receptor-mediated inhibitory tone acting on guinea-pig 5-HT neurones resulting in increased 5-HT release and 5-HT2 receptor-mediated behaviours.

Otoacariasis in Bengal goats of Bangladesh

The clinical findings and therapy of otoacariasis, caused by Psoroptes cuniculi, were studied in 12 Bengal goats. The major presenting signs included marked discomfort, rubbing of the ears against fixed objects or scratching by the toes, ear twitching and head shaking. In some severe cases violent head dashing against fixed objects was also noticed. Crackling sounds were detectable by gentle digital pressure on the ear base. In all cases, external auditory meatuses were found to be filled with yellowish-brown laminated scabs or waxy materials. Ten animals recovered after three to five applications of Lorexane cream 1% (ICI Ltd.) applied at an interval of 7 days. Two animals died after 2–3 days of treatment. Terramycin Otic Drop (Pfizer) was also applied to inhibit secondary bacterial infections and to promote the healing process. It is suggested that otoacariasis should be included in the list of differential diagnoses of brain diseases in goats.

Precipitated abstinence in the diazepam-dependent rat.

Physical dependence was produced in the rat by exposure to continuous release of diazepam from silastic capsule implants (recrystallized diazepam) or by dosing through a gastric fistula. The precipitated abstinence syndrome induced by the IV infusion of flumazenil was characterized by clonic and tonic-clonic seizures, retropulsion, digging, rearing, head, limb and body tremors, twitches and jerks of the body, and ear twitches. This abstinence syndrome differed both qualitatively and quantitatively from the milder syndrome induced in previous experiments by the intragastric administration of flumazenil in the diazepam-dependent gastric fistula rat. Capsule-implanted rats had free plasma and extraneuronal brain levels of diazepam, oxazepam, and nordiazepam in the 10(-3) and 10(-4) mg/ml range, and their brain: plasma ratios were not significantly different from 1. The diazepam capsules had a sustained release of over 28 days. These studies show that the capsule implantation technique is an efficacious way of maintaining plasma levels of diazepam and its metabolites, and producing a high level of physical dependence in the rat.

Electroencephalographic changes after short-term exposure to agonists of benzodiazepine receptors in the rat

Naive rats receiving IV diazepam (10 mg/kg), flunitrazepam (2.5 mg/kg) and clonazepam (2 mg/kg) show electroencephalographic (EEG) changes consisting of lengthening of the spindle bursts (7–12 Hz; 200–300 μV) and appearance of 15–30 Hz waves (β-like activity). These EEG manifestations are associated with signs of behavioral sedation (crouched, eyes open and myorelaxation) and stimulation (gnawing, running, ear twitches and sometimes wet-dog shakes), respectively. Bursts of 2–4 Hz waves can be occasionally observed associated with either marked sedation (lying down, eyes closed and presence of righting reflex) or sleep (stretched in the side with absence of rightning reflex). Measurements of the periods spent by the animals in the two EEG patterns within the first hour after intravenous injection show the large preponderance of the spindle bursts over the β-like activity. After the triazolopyridazine Cl 218,872 (10 mg/kg) the β-like activity is almost absent, and in no case loss of the righting reflex can be observed. These agonists of BDZ receptors have been injected at the above reported doses for 5 days, once-a-day. At the 5th day, animals receiving diazepam exhibit a preponderace of the EEG and behavioral activation within the first hour after injection. Rats receiving flunitrazepam show a significant increase of the periods of stimulation and a slight decrease of the periods of sedation. These phenomena of “habituation” are absent in animals treated with clonazepam and Cl 218,872.

Central nicotinic receptors: Vomiting, ear twitching and panting

Vomiting, ear twitching and panting produced by either nicotine or dimethylphenylpiperazinium (DMPP) administered intracerebroventricularly (ICV) to the unanesthetized cat were studied and compared. On a molar basis, nicotine evoked stronger effects overall in terms of the three responses studied, but the DMPP-induced vomiting and ear twitching responses, while weaker, were of longer duration. No significant differences were found in the duration of panting evoked by these nicotinic agonists. The nicotinic blocker hexamethonium injected ICV abolished the vomiting and ear twitching caused by either ICV nicotine or ICV DMPP, but vomiting and ear twitching persisted following the ICV administration of the muscarinic blocker, atropine. Both hexamethonium and atropine depressed or abolished the panting response evoked by either ICV nicotine or ICV DMPP. In cats with ablations of the area postrema, nicotine and DMPP injected ICV did not produce the vomiting response, but ear twitching and panting still occurred. It is concluded that the ICV injection of nicotine or DMPP evoked vomiting and ear twitching in the cat by way of an action on the central nicotinic receptors. However, panting produced by these nicotinic agonists is mediated by the mimicking action of acetylcholine on central receptors having mixed nicotinic and muscarinic properties.

Vasopressin release by nicotine in the cat

Our goal in this study was to examine where nicotine acted on the neurohypophysial release of arginine vasopressin (AVP). In the chamber-isolated, unanesthetized cat, an IV infusion of nicotine (25--50 micrograms/kg/min for 10 min) produced a 54-fold rise in plasma AVP (65 +/- 12.5 microU/ml) and a behavioral sequence of restlessness, ear twitching, salivation, chewing and retching. Chloralose anesthesia and acute surgical preparation increased plasma AVP (9.4 +/- 3.8 microU/ml) 4-times the control level in the unanesthetized state (2.4 +/- 0.1 microU/ml). In the anesthetized cat, an IV infusion of nicotine produced a 140-fold rise in plasma AVP (802.7 +/- 289.0 microU/ml) and a biphasic response in mean arterial blood pressure (MABP) which rose to 32% above control in the first 5 min and fell to 25% below control during the last 5 min. Bilateral surgical section of the carotid sinus and vagus nerves increased plasma AVP (47.6 +/- 25.8 microU/ml) to 5-times the control level in the anesthetized state (9.4 +/- 3.8 microU/ml). In the anesthetized, baroreceptor-denervated cat, an IV infusion of nicotine produced a 3-fold rise in plasma AVP (141.5 +/- 31.3 microU/ml) and a biphasic MABP response. Hypophysectomy abolished the nicotine-induced rise in AVP but did not modify the biphasic MABP response. These data suggest that in the cat nicotine releases AVP from the neurohypophysis by multiple sites of action within the receptive fields of te carotid sinus and vagus nerves and at unknown loci within the central nervous system.