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PubMed1998

s-IgA and cytokine levels in whole saliva of Sjögren's syndrome patients before and after oral pilocarpine hydrochloride administration: a pilot study.

Previous investigations have found elevated levels of s-IgA in the parotid saliva and normal levels in submandibular saliva of patients with Sjögren's syndrome (SS). Fox et al. also found elevated levels of cytokines (i.e., IL-2 and IL-6) in serum, salivary epithelial cells and parotid saliva of patients with SS. The oral administration of pilocarpine hydrochloride stimulates whole and parotid salivary flow. The purpose of this study was to determine the levels of s-IgA and IL-2 and IL-6 in whole saliva before and after administration of pilocarpine hydrochloride in SS subjects. Ten definitively diagnosed SS subjects were enrolled in the study, as were ten controls (C). The mean age was 57.2 years and all subjects were female. Whole unstimulated saliva (WUS) was collected by standard techniques for 5 min, after which the volume and flow rate were determined (mean WUS: SS = 0.047 vs C = 0.480 ml/min). Samples were centrifuged and the immunoglobulin analysis performed on the supernatants by immunoreactivity in a double-sandwich technique as previously described by Rudney et al. Cytokine analysis was performed similarly utilizing commercially available kits from R&D Systems. The results as analyzed by pairwise t-tests revealed comparable levels of s-IgA in the saliva of the SS patients, as compared to controls at baseline (means +/- SEM: SS-IgA = 348.1 +/- 82.0 vs C-IgA = 284.0 +/- 65.1 micrograms/ml; NS). Whole salivary flow was significantly increased (328%) in the SS subject group 60 min after the administration of 5 mg pilocarpine hydrochloride (means +/- SEM: 0.0472 +/- 0.017 vs 0.1546 +/- 0.054 ml/min; P < 0.01). There was no significant change in the concentration of s-IgA in the SS subject group following the pilocarpine dose (means +/- SEM: SS-IgA = 439.9 +/- 121.2 microliters/ml; P = NS). There were elevated levels of IL-2 in the saliva of four out of the ten and IL-6 in two out of the ten SS patients, as compared to controls (means +/- SEM: SS-IL-2 = 127.8 +/- 11.4 vs C-IL-2 = 30.8 +/- 1.6 pg/ml and SS-IL-6 = 41.4 +/- 7.1 vs C-11.6 +/- 2.8 pg/ml). There was also a significant decrease in the concentration of IL-2 in the same four out of ten SS subjects following the pilocarpine dose (means +/- SEM: SS-IL-2 = 32.4 +/- 10.3; P < 0.01). These preliminary results indicate that s-IgA levels do not change with increased salivary flow following the administration of pilocarpine hydrochloride in patients with Sjögren's syndrome. While cytokines are elevated in the whole saliva of some SS patients, a decrease in IL-2 concentration may occur with increased salivary flow.

Administration, Oral↗
PubMed1979

Efficacy and patient acceptance of pilocarpine gel.

Fifteen patients with symmetrically increased intraocular pressure (IOP) participated in a single-masked random 30-day clinical trial comparing 4% pilocarpine hydrochloride gel applied at bedtime to one eye with 4% pilocarpine hydrochloride drops instilled four times daily in the fellow eye. Both forms of pilocarpine reduced IOP significantly at 8 A.M., 12 noon, and 4 P.M. (P less than .01). At these times there was no significant difference in effect between the two forms of pilocarpine (P greater than .05). The mean IOP of eyes treated with gel showed no significant difference from the pretreatment value at 10 P.M. (P = .37), whereas at this time eyes treated with drops did maintain a significant IOP reduction (P = .02). At 10 P.M. pilocarpine drops reduced IOP significantly more than did pilocarpine gel (P = .002). Pupil diameter was affected by the gel and drops in a similar pattern to that of IOP. Patients tolerated the gel with few side effects and were pleased by the convenience of administration once daily.

Administration, Topical↗
PubMed1986

Can ophthalmologists correctly identify patients defaulting from pilocarpine therapy?

We determined whether clinical measurements and assessments available to ophthalmologists could be used to identify patients who default from pilocarpine treatment. The measurements and assessments included intraocular pressure, pupillary diameter, pupillary reactivity to light, the patient's report of compliance, the physician's prediction of compliance, the patient's log of pilocarpine administration, and the weight of pilocarpine eyedrops utilized. Compliance with the pilocarpine regimen was measured with an unobtrusive eyedrop medication monitor. Intraocular pressure and pupillary diameter did not correlate with compliance to the regimen as measured by the eyedrop monitor. Pupillary reaction to light, the physician's prediction of compliance, a daily log of pilocarpine administration, the weight of pilocarpine utilized, and the patient's report of compliance correlated modestly with compliance as measured by the monitor (range of correlations, 0.19 to 0.24). However, none of these measures taken by itself or combined in any manner adequately distinguished patients with lower rates of compliance from those with higher rates of compliance. At present, the eyedrop monitor is the only reliable method for detecting patients who default from treatment.

Glaucoma↗
PubMed1988

Differential effects of non-steroidal anti-inflammatory drugs on seizures produced by pilocarpine in rats.

The muscarinic cholinergic agonist pilocarpine induces in rats seizures and status epilepticus followed by widespread damage to the forebrain. The present study was designed to investigate the effect of 5 non-steroidal anti-inflammatory drugs, sodium salicylate, phenylbutazone, indomethacin, ibuprofen and mefenamic acid, on seizures produced by pilocarpine. Pretreatment of rats with sodium salicylate, ED50 103 mg/kg (60-174), and phenylbutazone, 59 mg/kg (50-70) converted the non-convulsant dose of pilocarpine, 200 mg/kg, to a convulsant one. Indomethacin, 1-10 mg/kg, and ibuprofen, 10-100 mg/kg, failed to modulate seizures produced by pilocarpine. Mefenamic acid, 26 (22-30) mg/kg, prevented seizures and protected rats from seizure-related brain damage induced by pilocarpine, 380 mg/kg. These results indicate that non-steroidal anti-inflammatory drugs differentially modulate the threshold for pilocarpine-induced seizures.

Animals↗
PubMed1990

Biochemical and behavioral responses of pilocarpine at muscarinic receptor subtypes in the CNS. Comparison with receptor binding and low-energy conformations.

Pilocarpine was tested biochemically in vitro for its ability to stimulate phosphoinositide (PI) turnover in the hippocampus (M1/M3 responses) where it displayed 35% of the maximal carbachol response with an EC50 value of 18 microM, and low-Km GTPase in the cortex (M2 response), where it had 50% of the maximal carbachol response with an EC50 value of 4.5 microM. Behaviorally, pilocarpine was able to restore deficits in a representational memory task (sensitive to M1 antagonists) produced by intrahippocampal injections of AF64A. Twenty-three low-energy conformations of protonated pilocarpine were generated using the program MacroModel. The data indicate that pilocarpine is a partial agonist at both M1 and M2 muscarinic receptors in the CNS. Behaviorally, with respect to the memory task, M1 effects of pilocarpine apparently predominate. It also is conceivable that different conformations of pilocarpine are active as agonists at different muscarinic receptor subtypes.

Animals↗
PubMed1992

Excitatory neurotransmitters in the lateral habenula and pedunculopontine nucleus of rat modulate limbic seizures induced by pilocarpine.

The involvement of the excitatory neurotransmitter system in the lateral habenula and pedunculopontine nucleus in the initiation and propagation of limbic seizures induced by pilocarpine has been investigated in the rat. Limbic seizures occur in animals following bilateral microinjection into the lateral habenula of N-methyl-D-aspartate (NMDA) (5 and 12.5 nmol) or kainate (100 and 200 pmol), 15 min prior to a subconvulsant dose of pilocarpine (150 mg/kg, i.p.). In the absence of pilocarpine NMDA (5 and 12.5 nmol) or kainate (100 and 200 pmol), injected focally into the lateral habenula or pedunculopontine nucleus, produced sniffing, grooming and tremor but no electrographic or behavioural seizures. Limbic seizures also occur after a subconvulsant dose of pilocarpine when it is preceded by injection of NMDA (5 and 12.5 nmol) or kainate (50, 100 and 200 pmol) into the pedunculopontine nucleus. Behavioural and electrographic signs of limbic seizures following pilocarpine (380 mg/kg, i.p.) were attenuated or completely antagonized by focal injection into the lateral habenula of the NMDA antagonist, 2-amino-7-phosphonoheptanoate (AP7) (10 and 50 pmol) or kainate antagonist, gamma-D-glutamylaminomethylsulphonate (GAMS) (20 nmol). In addition, AP7 (0.05, 0.1 and 1.0 nmol) or GAMS (40 nmol) injected into the pedunculopontine nucleus suppressed limbic seizures induced by i.p. administration of pilocarpine (380 mg/kg). The relative efficacy of NMDA and non-NMDA receptor antagonists revealed that the selective NMDA antagonist, AP7, was more potent in its anticonvulsant activity in comparison to GAMS, a non-NMDA receptor antagonist.

2-Amino-5-phosphonovalerate↗
PubMed1983

Role of ganglionic M-1 and M-2 receptors in the neuronal control of the cardiovascular system of the normotensive rat as determined with pilocarpine.

The adrenoceptors involved in the increase in diastolic pressure and heart rate elicited by i.v. administration of pilocarpine to the pithed rat were assessed using as pharmacological tools the alpha 1-adrenoceptor antagonist prazosin, the alpha 2-adrenoceptor antagonist rauwolscine, the beta 1-adrenoceptor blocker atenolol and the beta 2-adrenoceptor blocker ICI 118,551. Pilocarpine indirectly activated vascular alpha 1- and cardiac beta 1-adrenoceptors. By using the M-1 antagonist pirenzepine and the mixed M-1/M-2 antagonist dexetimide, pilocarpine was shown to be a mixed M-1/M-2 agonist. Pilocarpine initiated antagonistic effects on intrasynaptic alpha 2-adrenoceptor-mediated pressor responses and not on those triggered by extrasynaptic alpha 2-adrenoceptors. During vasopressin infusion to counteract a possible vasodilator action of pilocarpine, it was demonstrated that pilocarpine indirectly activated alpha 1- and alpha 2-adrenoceptors. The results support the hypothesis that intra- and extrasynaptic alpha 2-adrenoceptors comprise different populations and that the neuronal control of alpha 2-adrenoceptors is mediated by ganglionic M-2 receptors.

Animals↗
PubMed1989

Reduction of paired pulse inhibition in the CA1 region of the hippocampus by pilocarpine in naive and in amygdala-kindled rats.

Subconvulsant doses (20 mg/kg) of pilocarpine administered to a kindled rat convert a kindled seizure to status epilepticus. The hippocampus is involved in such status epilepticus. Furthermore, evidence is accumulating that GABA-mediated inhibition in the hippocampus is chronically diminished by kindling. The studies presented here compared the electrophysiologic effects of pilocarpine in vivo in the CA1 region of the hippocampus in naive and amygdala-kindled rats. A paired pulse paradigm previously shown to quantify the potency of GABAergic inhibition was employed. Stimuli were delivered in the CA3 region of urethane-anesthetized rats and population spikes were recorded in the contralateral CA1 region. In naive rats, pilocarpine (6-60 mg/kg) caused a left shift in the input-output curve measuring stimulus intensity vs population spike amplitudes, indicating an increase in neuronal excitability. In addition, paired pulse inhibition was reduced for interpulse intervals less than 70 ms. In amygdala-kindled rats, neuronal excitability was also enhanced following pilocarpine administration. The potency of baseline paired pulse inhibition was decreased in kindled rats compared to naive controls. Following pilocarpine, inhibition for interpulse intervals less than 70 ms was further reduced, but to a lesser extent than in naive rats. These findings suggest that the ability of subconvulsive doses of pilocarpine to change a discrete kindled seizure triggered by one stimulus to status epilepticus depends on the suppression of GABAergic inhibition below a critical level.

Amygdala↗
PubMed1987

Pilocarpine-induced reciprocal hindlimb scratching in mice.

Intrathecal (IT) administration of pilocarpine (0.25-2.0 micrograms) to mice produced a vigorous and dose-related reciprocal hindlimb scratching response that lasted for 10-15 minutes. Neither the intracerebroventricular administration of pilocarpine at up to 10 times the intrathecal ED90 dose nor the subcutaneous administration of 10 mg/kg pilocarpine caused as robust an effect as IT administration. The reciprocal hindlimb scratching produced by the ED90 dose of pilocarpine (2 micrograms, IT) was antagonized in a dose-related manner by simultaneous IT administration of atropine (ID50 = 0.002 micrograms), methysergide (ID50 = 1.89 micrograms), the substance P antagonist [D-Pro2,D-Trp7,9]-SP (ID50 = 4.94 micrograms), and the putative neurokinin B antagonist [D-Pro2,D-Trp6,8,Nle10]-NK (ID50 = 3.33 micrograms), but not by yohimbine (5 micrograms), phentolamine (2 micrograms), or naloxone (2.5 micrograms). These results suggest that pilocarpine-induced reciprocal hindlimb scratching is mediated spinally, that the effect is produced by an action of pilocarpine on muscarinic receptors in the spinal cord, and that neurokinin, and perhaps 5-HT, mechanisms might also be involved.

Animals↗
PubMed1995

Extracellular potassium elevations in the hippocampus of rats with long-term pilocarpine seizures.

Pilocarpine injection into rodents leads to the development of chronic limbic seizures that follow an initial status epilepticus and a seizure-free interval. It has been proposed that a decreased efficacy of the mechanisms that buffer the extracellular concentration of K+ ([K+]o) leads to an increase in seizure susceptibility. Therefore, we analyzed the changes in [K+]o associated with the synchronous activity induced by 4-aminopyridine (4AP) in hippocampal slices obtained from control and pilocarpine-treated rats. At all recording sites (i.e. stratum radiatum of the CA1 and CA3 subfields, and hilus of the dentate gyrus), the amplitude of GABA-mediated synchronous field potentials induced by 4AP, as well as the associated [K+]o increases, were significantly reduced in slices obtained from the pilocarpine-treated rats. In the control group, the field-potential amplitudes reached 1 mV (i.e. 1.7 +/- 0.3 mV in CA1, 0.93 +/- 0.2 mV in CA3, and 1.03 +/- 0.12 mV in the hilus; mean +/- SEM), while the accompanying rises in [K+]o exceeded 4 mM (i.e. 4.17 +/- 0.15 mM in CA1, 4.04 +/- 0.12 mM in CA3, 4.04 +/- 0.11 mM in the hilus) from a baseline of 3.25 mM. The corresponding values in slices from the pilocarpine-treated group were rarely greater than 0.4 mV (i.e. 0.3 +/- 0.09 mV in CA1, 0.27 +/- 0.03 mV in CA3 and 0.38 +/- 0.06 mV in the hilus), and larger than 3.6 mM (i.e. 3.63 +/- 0.04 mM in CA1, 3.64 +/- 0.03 mM in CA3 and 3.60 +/- 0.04 mM in the hilus) from a similar baseline value. With pilocarpine, the rate of occurrence of the GABA-mediated potential significantly decreased from 0.035 to 0.016 s-1. Since the rises in [K+]o decreased rather than increased and their overall duration was unchanged (possibly reflecting cell loss), we conclude that a modification of [K+]o buffering capacity is unlikely to account for the appearance of in vivo seizures in the pilocarpine model of epilepsy.

4-Aminopyridine↗
PubMed1993

Determination of pilocarpine in aqueous humour by liquid chromatography-atmospheric pressure chemical ionization mass spectrometry.

A new method has been developed for rapid analysis and determination of pilocarpine in aqueous humour using liquid chromatography-atmospheric pressure chemical ionization mass spectrometry. The chromatography was carried out on a reversed-phase phenyl column with 0.1% acetic acid-acetonitrile (95:5, v/v). Pilocarpine and its analogues, isopilocarpine, pilocarpic acid and isopilocarpic acid, were separated. An aqueous humour sample was deproteinized with methanol. After evaporation, the residue was dissolved in the mobile phase. The method was applied to the analysis of the metabolite in aqueous humour after the topical application of 2% pilocarpine (w/v) eye-drops. The main metabolite, pilocarpic acid, was easily identified. The protonated molecular ion of pilocarpine was used for the determination. The calibration curve had a good linearity within the concentration range investigated (2 ng to 10 micrograms/ml). The limit of determination was estimated to be an aqueous humour concentration of ca. 2 ng/ml. The method was applied to the determination of unchanged pilocarpine after the topical application of 2% pilocarpine (w/v) eye-drops.

Animals↗
PubMed2006

Damage of the medial preoptic area impairs peripheral pilocarpine-induced salivary secretion.

The existence of neural connections between the medial preoptic area (MPOA) and the salivary glands and the increase in salivation by thermal or electrical stimulation of the MPOA have suggested an important role of MPOA in the control of salivary gland function. Although direct cholinergic activation of the salivary glands induces salivation, recent studies have suggested that salivation produced by i.p. pilocarpine may also depend on the activation of central mechanisms. Therefore, in the present study, we investigated the effects of bilateral electrolytic lesions of the MPOA on the salivation induced by i.p. pilocarpine. Adult male Holtzman rats (n = 11-12/group) with bilateral sham or electrolytic lesions of the MPOA were used. One, five, and fifteen days after the brain surgery, under ketamine anesthesia, the salivation was induced by i.p. pilocarpine (1 mg/kg of body weight), and saliva was collected using pre-weighed small cotton balls inserted into the animal's mouth. Pilocarpine-induced salivation was reduced 1 and 5 days after MPOA lesion (341 +/- 41 and 310 +/- 35 mg/7 min, respectively, vs. sham lesions: 428 +/- 32 and 495 +/- 36 mg/7 min, respectively), but it was fully recovered at the 15th day post-lesion (561 +/- 49 vs. sham lesion: 618 +/- 27 mg/7 min). Lesions of the MPOA did not affect baseline non-stimulated salivary secretion. The results confirm the importance of MPOA in the control of salivation and suggest that its integrity is necessary for the full sialogogue effect of pilocarpine. However, alternative mechanisms probably involving other central nuclei can replace MPOA function in chronically lesioned rats allowing the complete recovery of the effects of pilocarpine.

Animals↗
PubMed2004

Monoamine levels after pilocarpine-induced status epilepticus in hippocampus and frontal cortex of Wistar rats.

Pilocarpine-induced status epilepticus (SE) is an useful model to study the involvement of neurotransmitter systems as epileptogenesis modulators. Some researches have shown that pharmacological manipulations in dopaminergic, serotonergic, and noradrenergic systems alter the occurrence of pilocarpine-induced SE. The control group was treated with 0.9% saline (control group, s.c.). Another group of rats received pilocarpine (400mg/kg, s.c.) and both groups were sacrificed 24 h after the treatment. This work was performed to determine the alterations in monoamine levels (dopamine (DA), serotonin (5-HT) and norepinephrine (NE)) and their metabolites (3,4-hydroxyphenylacetic acid (DOPAC), homovanilic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA)) after pilocarpine-induced SE in hippocampus and frontal cortex of adult rats. The monoamines and their metabolites were determined by reverse-phase high-performance liquid chromatography with electrochemical detection. DA and 5-HIAA concentrations were not altered in the hippocampus of the pilocarpine group, but in the same group the 5-HT (160%), DOPAC (316%) and HVA (21%) levels increased, whereas, the NE (47%) content declined. For the frontal cortex determinations, there was an increase of 20 and 72% in DA and DOPAC levels, respectively, and a decrease in NE (32%), 5-HT (33%) and 5-HIAA (19%) concentrations, but HVA content remained unaltered. These results indicate that pilocarpine-induced SE can alter monoamine levels in different ways depending on the brain area studied, suggesting that different mechanisms are involved.

Analysis of Variance↗
PubMed2002

Pupillary response to four concentrations of pilocarpine in normal subjects: application to testing for Adie tonic pupil.

PURPOSE: To determine the amount of pupillary constriction to four different concentrations of pilocarpine in normal human subjects and to determine if pupillary constriction correlates with bioavailability of the instilled concentrations. The amount of pupillary constriction to dilute pilocarpine is utilized as a diagnostic test for Adie tonic pupil as distinguished from a normal pupil response. DESIGN: Twenty healthy volunteers had automated binocular infrared pupillography in the dark after instillation of four different concentrations of dilute pilocarpine. Ocular penetration of eye drops was also assessed using 2% fluorescein sodium as a tracer. METHODS: Prospective institutional double-masked study of both eyes of twenty healthy volunteers, ten with brown irides, ten with blue irides, between the ages of 20-40 years. RESULTS: A pilocarpine dose-dependent curve showed decreased pupil size within 15 minutes, peaking at 30-60 minutes. No difference was noted between right and left eyes, iris color, or corneal permeability. CONCLUSIONS: Normal pupils constrict to dilute concentrations of pilocarpine (0.25% or 0.125%), but constrict insignificantly to concentrations of 0.0313% or 0.0625%. Pupil constriction with 0.0625% pilocarpine should distinguish an Adie pupil from normal. This confirms the utility of this simple office diagnostic procedure.

Adult↗
PubMed1999

Plateau iris syndrome: changes in angle opening associated with dark, light, and pilocarpine administration.

PURPOSE: To report changes in angle configuration associated with dark, light, and pilocarpine administration in plateau iris syndrome. METHOD: In 10 eyes of 10 patients with plateau iris syndrome and persistent narrow angles after patent peripheral Nd:YAG laser iridotomy, ultrasound biomicroscopy was used to image variations in angle opening, iris thickness, and trabecular-ciliary process distance. Measurements were taken in the dark, in full room light, and after administration of pilocarpine 2%. RESULTS: Average angle opening distance increased in the light compared with the dark (113+/-34 microm vs. 22+/-34 microm, P = .0001) and increased further after pilocarpine administration (171+/-52 microm vs. 113+/-34 microm, P = .0034). Average iris thickness decreased in the light compared with the dark (338+/-34 microm vs. 436+/-58 microm, P = .0009) and decreased further after pilocarpine administration (253+/-48 microm vs. 338+/-34 microm, P = .0002). Average trabecular meshwork-ciliary process distance measurements were smaller than normal and did not change significantly in the light compared with the dark (481+/-42 microm vs. 464+/-44 microm, P = .4001) or after pilocarpine administration compared with light (451+/-67 microm vs. 481+/-42 microm, P = .1304). CONCLUSIONS: In plateau iris syndrome, anteriorly located ciliary processes support the peripheral iris. Changes in angle opening in dark and light are solely related to changes in iris thickness. Pilocarpine produces iris thinning and is an effective method of opening the angle. Ultrasound biomicroscopy can be used to perform a darkroom provocative test, which provides information on whether the angle anatomically closes in the dark.

Anterior Eye Segment↗
PubMedDate not supplied

Comparison of the intraocular pressure lowering effect of latanoprost and carteolol-pilocarpine combination in newly diagnosed glaucoma.

PURPOSE: To evaluate the comparative efficacy of latanoprost monotherapy versus combined carteolol and pilocarpine therapy in patients with newly diagnosed glaucoma. METHODS: Masked randomized prospective trial. This study included 51 patients (64 eyes) with newly diagnosed glaucoma or ocular hypertension. The cases were randomly divided into two treatment groups for administration of latanoprost 0.005% once daily, or of carteolol 2% twice daily and pilocarpine 2% twice daily. Mean diurnal intraocular pressure (IOP) was measured at baseline, week 2, week 4, and month 3 after the beginning of treatment. Changes in mean IOP from baseline to the 3-month visit were determined by an analysis of variance. RESULTS: Mean diurnal IOP values were 25.1 +/- 3.1 mm Hg and 25.5 +/- 2.5 mm Hg at baseline in the latanoprost monotherapy group and in the carteolol-plus-pilocarpine group, respectively. Diurnal IOP was significantly decreased from baseline to 3 months in both groups (P <.001). At this time point, latanoprost monotherapy had reduced mean diurnal IOP by 7.2 +/- 2.5 mm Hg (28.7%) and carteolol plus pilocarpine had reduced mean diurnal IOP by 7.4 +/- 2.7 mm Hg (29%). There was no difference between the groups in terms of their IOP reduction effect (P =.51). Decreased visual acuity and twilight vision, blurred vision, and headache were more frequent in the carteolol-plus-pilocarpine group than in the latanoprost group (P <.05). CONCLUSIONS: We concluded that latanoprost monotherapy was at least as effective as the carteolol-pilocarpine combination therapy in reducing mean diurnal IOP in newly diagnosed glaucoma or ocular hypertension.

Adult↗
PubMedDate not supplied

Tremulous characteristics of the vacuous jaw movements induced by pilocarpine and ventrolateral striatal dopamine depletions.

Vacuous jaw movements induced by the muscarinic agonist pilocarpine and striatal dopamine depletions were examined using a slow motion videotape system. With this procedure, rats were videotaped in a Plexiglas tube so that the profile of the head region could be seen. Vacuous jaw movements were analyzed by examining the tape at 1/6 normal speed. An observer recorded each jaw movement using a computer, and the computer program re-calculated the temporal characteristics of jaw movement responses back to normal speed. The interresponse time was recorded for each jaw movement, and each jaw movement interresponse time was assigned to a 50 ms wide time bin. Thus, the distribution of interresponse times could be used to analyze the temporal characteristics of jaw movement responses. In the first experiment, rats were administered saline vehicle, 1.0 mg/kg and 2.0 mg/kg pilocarpine. The rats were videotaped 10-15 min after injection, and the data were analyzed as described above. Pilocarpine induced very high levels of vacuous jaw movements, and the vast majority of all movements occurred in "bursts" with interresponse times of 1.0 s or less. Analysis of the interresponse time distributions showed that most of the jaw movements were within the 150-350 ms range. The modal jaw movement interresponse time was in the 150-200 ms range, which corresponds to a local frequency of 5-6.66 Hz. In the second experiment, the neurotoxic agent 6-hydroxydopamine was injected directly into the ventrolateral striatum in order to produce a local dopamine depletion. The dopamine-depleted rats were observed for jaw movements 7 days after surgery. The overall level of jaw movement activity resulting from dopamine-depletion was much lower than that produced by pilocarpine. There was a significant inverse correlation between ventrolateral striatal dopamine levels and total number of vacuous jaw movements. Videotape analysis indicated that the temporal characteristics of jaw movements induced by dopamine depletions were similar to those shown with pilocarpine. These experiments indicate that vacuous jaw movements induced by pilocarpine and striatal dopamine depletion occur in a frequency range similar to that shown in parkinsonian tremor.

Animals↗
PubMed1997

Inhibition of grooming by pilocarpine differs in high- and low-yawning sublines of Sprague-Dawley rats.

A comparative study of the effect of pilocarpine, a muscarinic receptor agonist, on grooming, scored during 45 min via a time-sampling procedure, was carried out on two sublines of male rats selectively bred for high-(HY) and low-yawning (LY) frequency. In one condition, we introduced rats in a novel cage and observed them immediately after receiving an I.P. injection of pilocarpine (0.5-3.75 mg/Kg) or an equivalent volume of saline. Besides grooming, the occurrence of yawns was continuously recorded. In the other condition, we immersed rats in water for 60 s, then they received an I.P. injection of pilocarpine (3.75 mg/Kg) or an equivalent volume of saline and we placed them in an open field, in which we recorded the number of crossed squares. Grooming scores were significantly higher in the condition after water immersion than in the novel situation; in both conditions HY had a grooming response higher than that of LY rats. Pilocarpine produced a dose-dependent inhibition of novelty-induced grooming in HY rats, whereas LY grooming was reduced only with the highest dose. In contrast, yawning increased in a dose-dependent manner with HY rats curve over that of LY animals, except for the highest dose. Pilocarpine inhibited water immersion-induced grooming in both sublines of rats, but it did not reduce grooming as much as it did in the novel condition. Pilocarpine affected distinctly each of the components of grooming, without inhibiting animals locomotor activity. The results indicate that HY rats also have a higher number of grooms than LY rats, and because grooming and yawning can appear after stressful circumstances, HY rats may be used to study the role that both behaviors could have in counteracting the effects of stress. Similarly, HY animals might be utilized to study the underlying neurochemical mechanisms of grooming. This study also indicates that the cholinergic systems exert an inhibitory influence on grooming which contrasts with the excitatory effect on yawning.

Animals↗