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At least 271 records · Page 15Linked to original sources
PubMed1984

Symposium on the management of ventricular dysrhythmias. Concept of reentry versus automaticity.

Arrhythmias can result from abnormal impulse initiation or conduction. Abnormal initiation results from either automaticity or triggered activity. Enhanced automaticity may be due to a normal automatic mechanism (a normal property of the sinus node and specialized conducting fibers) or to an abnormal mechanism such as automaticity in depolarized fibers. Triggered activity is caused by afterdepolarizations that occur either during repolarization (early afterdepolarization) or after repolarization is complete (delayed afterdepolarization). Triggered activity due to delayed afterdepolarizations is dependent on critical heart rates. Overdrive pacing may distinguish between normal and abnormal automaticity. Antiarrhythmic drugs can alter arrhythmias that result from abnormal impulse initiation. To suppress an arrhythmia resulting from abnormal impulse generation, a drug may (1) suppress the abnormal automatic mechanism, i.e., specific effect on ionic current; (2) suppress afterdepolarizations; (3) depress conduction in tissue surrounding automatic focus; or (4) modify refractory period of tissue in and around automatic focus. Abnormal impulse conduction results in reentrant excitation. Conditions necessary for reentry include a combination of unidirectional block and slowed conduction. A reentrant mechanism can be determined by an anatomically defined circuit or solely by the functional properties of the tissue (leading circle mechanism). Circus movement reentry around an anatomic obstacle may respond to antiarrhythmic drugs differently from reentry caused by a leading circle mechanism. Initiation and perpetuation of a reentry mechanism depends on a delicate interplay between conduction velocity and duration of the functional refractory period in the reentry circuit.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1985

Usefulness of programmed stimulation in predicting efficacy of propafenone in long-term antiarrhythmic therapy for paroxysmal supraventricular tachycardia.

The electrophysiologic effects of intravenous (i.v.) and oral propafenone were evaluated in 14 patients with Wolff-Parkinson-White syndrome and in 10 patients with atrioventricular (AV) nodal reentrant tachycardia. The effective refractory periods of the right atrium and the AV node increased after both preparations. In patients with Wolff-Parkinson-White syndrome, i.v. propafenone blocked anterograde accessory pathway conduction in 2 patients and retrograde conduction in 1; during oral therapy, accessory pathway conduction block occurred in 2 additional patients. The mean cycle length of the supraventricular tachycardia (SVT) increased from 338 +/- 60 ms to 387 +/- 56 ms (p less than 0.05) after i.v. application, and from 336 +/- 65 ms to 367 +/- 65 ms (p less than 0.05) during oral propafenone. The shortest pacing interval maintaining a 1:1 AV conduction increased from 325 +/- 65 ms to 368 +/- 81 ms (p less than 0.05) after i.v. infusion, and from 333 +/- 57 ms to 369 +/- 75 ms (p less than 0.05) during oral therapy. There was no difference in the electrophysiologic effects between i.v. and oral propafenone. The induction of SVT was prevented by i.v. propafenone in 10 of 20 patients and in 4 additional patients with oral propafenone. During follow-up, 6 of 7 patients, whose SVT could not be initiated by electrophysiologic drug testing, remained free from recurrences, whereas 5 of 7 patients with inducible tachycardia had recurrences of SVT. Thus, in patients with SVT, propafenone prolonged accessory pathway and AV nodal conduction and had a beneficial effect on circus movement tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Electrophysiology in assessing supraventricular arrhythmias: value of programmed stimulation in predicting and understanding efficacy of encainide.

The effects of intravenous (1.5 mg/kg body weight given over 15 minutes) and oral (mean dose 164.8 +/- 56.2 mg/day) encainide were studied in 11 patients with recurrent, difficult to treat, supraventricular tachycardia. In 2 patients the arrhythmia was atrial in origin. In 9 patients a concealed (slow type in 3, fast type in 6) accessory atrioventricular pathway was used for retrograde conduction during a circus movement tachycardia. Intravenous encainide terminated tachycardia in 8 of the 11 patients. Oral encainide prevented clinical recurrence of tachycardia in 7 patients during a 5- to 20-month follow-up (mean 11). Programmed stimulation of the heart after intravenous encainide administration revealed significant (p less than 0.05) prolongation of HV interval, QRS width and refractory period of the right ventricle. Apart from a slower tachycardia rate no changes in electrophysiologic parameters were observed in 5 patients restudied while receiving oral encainide medication. Although encainide was an effective antiarrhythmic agent, programmed stimulation of the heart was not very helpful in providing insight into its mode of action, nor did programmed stimulation predict clinical efficacy. Prevention of the tachycardia-initiating premature beat seems to be the most likely mechanism for the clinical efficacy of oral encainide.

Administration, Oral↗
PubMed1987

A transcardiac lead system for identification and termination of supraventricular and ventricular tachycardia.

The value of a transcardiac lead system (coronary sinus to right ventricular apex) to record atrial and ventricular electrical activity and its pacing capabilities was assessed in 20 patients with a variety of tachycardias (atrial tachycardia in 3 patients, atrial flutter in 4, intranodal tachycardia in 6, circus movement tachycardia using an accessory pathway in 1 patient, and ventricular tachycardia in 9). The transcardiac lead invariably showed both atrial and ventricular electrical activity during sinus rhythm and tachycardias, allowing application of the same criteria as used when analyzing cardiac rhythm on the surface electrocardiogram. Atrial complexes had a mean amplitude of 4.2 mV during sinus rhythm and varied from 3.0 to 4.1 mV during the different types of tachycardia. Ventricular complexes had a mean amplitude of 9.8 mV during sinus rhythm, 13.8 mV during supraventricular tachycardia and 16.1 mV during ventricular tachycardia. The duration of the QRS complex on the transcardiac lead was equal to the duration of the QRS complex on the surface electrocardiogram during tachycardias with a small or wide QRS complex. By varying the intensity of current delivered through the transcardiac lead, only right ventricular pacing (mean current intensity 1.2 +/- 0.4 mA) or simultaneous atrioventricular pacing (mean current intensity 4.7 +/- 3.3 mA) could be achieved. Termination of all episodes of tachycardia was achieved with either ventricular pacing or simultaneous atrioventricular pacing. This transcardiac lead system allows clear identification of atrial and ventricular events, is suitable for tachycardia analysis using simple surface electrocardiographic algorithms and allows pacing termination of a variety of tachycardias.

Atrioventricular Node↗
PubMed1988

Termination of tachycardias by interrupting blood flow to the arrhythmogenic area.

The hypothesis that production of ischemia or cooling of an arrhythmogenic area or pathway could interrupt tachycardias was tested by subselective catheterization of the coronary artery supplying the site of origin of ventricular tachycardia (9 patients), the accessory pathway (2 patients) and the site of origin of atrial tachycardia (1 patient). Ventricular tachycardia was reproducibly terminated and reinduction temporarily prevented in 8 of the 9 patients by occlusion of the artery or administration of iced isotonic saline. Block in the accessory pathway was obtained in 1 of the 2 patients with Wolff-Parkinson-White syndrome. Selective cooling through the atrioventricular nodal artery in 1 patient terminated his circus movement tachycardia. Reproducible termination of a continuous atrial tachycardia was obtained by cooling of the atrial branch supplying the site of origin of the arrhythmia. These data demonstrate the feasibility of identification and selective catheterization of the coronary artery branch supplying blood to an arrhythmogenic area or pathway and suggest a new possibility for treatment of tachycardias by permanently blocking the blood supply to the site of origin or pathway of a tachycardia.

Coronary Circulation↗
PubMed1989

Multicenter long-term results of antitachycardia pacing for supraventricular tachycardias.

This report describes the multicenter experience of the Tachylog antitachycardia pacemaker (Siemens-Elema) in the treatment of drug-refractory, recurrent supraventricular arrhythmias. The device has been implanted in 63 patients (mean age 47 years). The arrhythmias were atrial tachycardia in 4 patients (6%), atrioventricular nodal reentry tachycardia in 23 patients (37%), circus movement tachycardia via an overt bypass tract in 17 patients (27%) and via a concealed bypass tract in 19 patients (30%). The mean follow-up period was 30 months. In 28 patients (44%) arrhythmia control was achieved with the pacemaker therapy alone. In 31 patients (49%) drug therapy had to be reintroduced to obtain control of recurrent arrhythmias. Four patients (6%) were definite nonresponders. In 4 patients (6%) the pulse generator was explanted either because it was not tolerated or because of tachycardia-sensing failure. No syncope or death was observed during follow-up. Thus, antitachycardia pacing gives satisfactory results in selected patients with drug-refractory supraventricular tachycardias.

Cardiac Pacing, Artificial↗
PubMed1989

Electrophysiologic basis of catheter ablation in atrial flutter.

A reentrant mechanism is believed to be responsible for atrial flutter. The recent development of the entrainment criteria further supports this theory, and there is a general consensus that circus movement is the underlying abnormality that supports this arrhythmia. In most clinical studies, abnormal fragmented (or double spike) electrograms, suggesting the presence of areas of localized slowing of conduction or block, have been reported. They are almost always recorded in the lower and posterior portion of the right interatrial septum, but also frequently in the high lateral portion of the right atrium. The determination of their involvement in the reentry pathway is important for designing curative procedures such as surgery or ablation. The low atrial septal area surrounding the mouth of the coronary sinus was suspected as being the critical area of slow conduction in atrial flutter. Rapid pacing at that site can yield a surface electrocardiographic pattern similar to the clinically occurring arrhythmias. Additionally, the flutter circuit can be accelerated during atrial pacing at fixed and slightly faster rates than the intrinsic tachycardia rate--the so-called entrainment phenomenon. When entrainment criteria are fulfilled, tachycardia termination being by definition ruled out, any concomitant recorded local type II block identifies an area that must be outside the circuit. Such local block may be recorded either spontaneously or during entrainment and therefore helps in identifying atrial slow conduction areas that do not belong to the reentrant path. This approach was applied to identify the optimal ablation site in 8 patients with long-standing drug resistant atrial flutter. In 7 of 8 patients, we were able to identify a fragmented potential in the low posteroseptal area during sustained atrial flutter.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗
PubMed1991

Efficacy and safety of intravenous sotalol for termination of paroxysmal supraventricular tachycardia. The Sotalol Versus Placebo Multicenter Study Group.

A double-blind, placebo-controlled, crossover, multicenter study was conducted to study the efficacy and safety of a single intravenous dose of sotalol (1.5 mg/kg over 10 minutes) in achieving normal sinus rhythm in paroxysmal supraventricular tachycardia (SVT) lasting greater than or equal to 15 minutes. Patients were randomized to either sotalol or placebo as initial treatment, and if the SVT was not terminated a crossover was performed after 20 minutes. A total of 43 patients were enrolled, 38 of whom with spontaneous (n = 14) or induced (n = 24) SVT were analyzed for sotalol efficacy. Most patients (n = 27) had atrioventricular (AV) nodal reentrant tachycardia, and an important subgroup (n = 11) had circus movement tachycardia, using an accessory pathway for retrograde conduction. The number of patients converting to sinus rhythm as a result of the initial treatment was significantly higher in the sotalol group than in the placebo group, for spontaneous (p less than 0.005) as well as for induced tachycardia (p less than 0.001). Sinus rhythm was achieved within 30 minutes in 83% of all patients who received sotalol as the first drug, compared with 16% of the patients first receiving placebo (p less than 0.0001). For sotalol safety analysis, 42 patients were included. A total of 37 patients received sotalol, 19 as the first treatment, and 18 as the second treatment, while 25 patients received placebo. A total of 15 possible adverse effects were reported, occurring in 10 patients with sotalol versus 4 with placebo. The only severe side effect (hypotension) necessitating termination of drug administration occurred with placebo. No proarrhythmic effects were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Electrophysiologic study of dysrhythmias after atrial operations in dogs.

Experiments were conducted with 159 dogs to investigate the mechanism of persistent dysrhythmias clinically encountered after atrial-level operations. Those found after incisions to the internodal pathways (INPs) of the right atrium were analyzed using cardiac mapping in an anesthetized or extracorporeally perfused state. Longitudinal incisions of the posterior INP often allowed inducible sustained atrial flutter, with circus movement of excitation around the right atrium near the tricuspid orfice. Sustained atrial flutter thus produced was modified in cycle length by coexisting division of the middle INP but inhibited by that of the anterior INP. Its incidence increased at chronic stage, with marked cicatricial changes. The disrupted anterior INP markedly prolonged conduction time to the atrioventricular node and A-H interval compared with the other disruptions. Persistent atrioventricular junctional rhythm developed in about 50% of the animals after disruption of all three INPs or anterior and posterior INPs; division of the anterior INP was the common potent factor, although no single blocked INP produced persistent junctional rhythm. Our results support the "summation theory." The incidence of junctional rhythm and hypoxia of the sinoatrial node (flow rate of less than 10 mL.100 g-1.min-1) were markedly enhanced by coexisting blockade of atrial feeding arteries in addition to division of the anterior INP. In conclusion, massive posterior INP disruption is a potent anatomic substrate in producing sustained atrial flutter, middle INP division a modifier, and anterior INP division an inhibitor. Division of the anterior INP is a potent anatomic substrate in producing junctional rhythm, and hypoxia involving the sinoatrial node reacts as its synergic factor.

Animals↗
PubMed1982

Study of the neural basis of circling behavior induced by L-dopa in lesioned entopeduncular cats.

Experiments were carried out in cats bearing unilateral electrolytic lesion of the entopeduncular nucleus. The animals were tested for circling 1-2 weeks after surgery. Postoperatively the cats displayed transient spontaneous ipsiversive turning. The administration i.p. of L-DOPA (80 mg/kg) plus CarbiDOPA (30 mg/kg), suspended in 10% Tween 80, induced rotational behavior toward the lesioned side. This effect began about 26 min after drug administration and reached its maximum 40-110 min after the injection. Electrolytic lesions placed in the superior colliculus, strionigral pathway or pedunculopontine nucleus, contralateral to the lesioned entopeduncular nucleus did not modify the circling behavior induced by L-DOPA. Similar results were observed following unilateral lesion of the sensorimotor cortex or the VL thalamic nucleus. These results suggest that the circus movements induced by L-DOPA, in animals with unilateral lesion of the entopeduncular nucleus, is not mediated by the classic outflow of the striopallidal system.

Animals↗
PubMed1996

The antiarrhythmic effect of verapamil on atrioventricular re-entry in the Wolff-Parkinson-White syndrome: a computer model study.

Verapamil is supposed to suppress the initiation of circus movement supraventricular tachycardia by affecting the atrioventricular node. In electrophysiological tests, programmed stimulation is usually performed by using the same location for pacing and premature stimulus. Spontaneous ectopic activity starts from a different location than the sinus node and can therefore find altered re-entry conditions. In this study a 3D computer model based on Huygen's principle is used for simulation of the spread of excitation in the human heart in combination with a posterobasal, right or left lateral accessory pathway (AP). The effect of verapamil on properties of the atrioventricular node were modelled by prolonging the effective refractory period and basal conduction time. For each of the three APs, ectopic foci at the atrial base and between sinus node and AP were modelled at various coupling intervals for investigating re-entrant activation. In the control state (without verapamil) only orthodromic echoes were found. The maximum echo zone (EZ) range was found near the AP. If stimuli were selected further away from the AP on the atrial basis, the EZ range decreased until no EZ was found. The EZ range decreased from it's maximum value near the AP, towards the difference of the effective refractory periods between AP and AV-node near the sinus node Verapamil abolished the EZ in case of a posteroseptal AP. For a lateral AP the administration of verapamil resulted in an orthodromic and antidromic EZ depending on the atrial premature activation site. A maximum orthodromic EZ was found for premature stimuli near the AP. As stimulus site moved away from the AP, the EZ range first decreased continuously to zero leading eventually to an antidromic EZ. These findings suggest the important influence of the site of premature stimuli with respect to the accessory pathway and AV-node on the inducibility of atrial re-entry.

Anti-Arrhythmia Agents↗
PubMed1990

Clinical experience with a new catheter for His bundle ablation.

Eleven patients aged 33-66 years were referred for treatment of refractory supraventricular arrhythmias. Each patient had failed to respond to medical treatment. One patient had a paroxysmal atrial flutter with a rapid ventricular response. Six patients had a chronic atrial fibrillation. Two others had a supraventricular tachycardia due to reentry in the atrioventricular (AV) node, and two patients suffered from circus movement tachycardia using a concealed left free wall accessory pathway. A specially built United States Catheter and Instruments (USCI) women Dacron polyurethane electrode catheter (bipolar 8F with an internal lumen, 90 A, 5,000 V, 5.5 omega) was positioned in the His bundle area to record unipolar large atrial and His signals. When the maximal ratio low right atrium/His spike was recorded, the pole was connected to the output of a standard defibrillator. A shock of 200-250 J was delivered through this pole. Ten patients developed complete AV block (CAVB) immediately. After 72 hours, these patients were implanted with a rate-responsive pacemaker. The procedure was without side effects. Nine patients remain in CAVB after 3-17 months; in one case AV conduction resumed but the patient is free of arrhythmia. Another patient needed a second catheter ablation after 1 month.

Adult↗
PubMed1991

Vagally induced depression of impulse propagation as a cause of atrial tachycardia.

It is known that parasympathetic influence favors induction of re-entrant atrial tachycardias (ATs). This effect is usually interpreted as a result of inhomogeneous shortening of atrial refractoriness leading to increased probability of circus movement following a premature impulse. However, early microelectrode studies showed that in spontaneously beating isolated frog atria, intensive vagal stimulation (VS) induced paroxysms of rapid AT in the absence of myocardial extrastimulation. This AT was found to correlate with inexcitability of some of the impaled fibers of the atria. It was supposed that temporary, vagally induced, inexcitable areas of the atria could lead to re-entry, serving as a site of unidirectional conduction. This hypothesis was recently evaluated by direct multielectrode mapping of excitation sequence during vagally induced AT in frog atria. Recording from 32 sites with a spatial resolution of 1-2 mm clearly showed that the AT was due to re-entry. The ATs were always preceded by vagally induced depression of conduction, with some areas of the atria being completely blocked. As the vagal influence decreased, the blocked areas recovered in an inhomogeneous manner. The re-entrant AT was initiated when a sinus impulse arrived during a certain phase of the recovery. Unlike the well-known mechanism of re-entry, which is based on inhomogeneous refractoriness and extrabeat(s), the re-entrant AT in our model depended on vagally induced conduction block and could be launched by a single sinus impulse.

Animals↗
PubMed1984

Structural comparison of purified dynein proteins with in situ dynein arms.

Using the quick-freeze deep-etch technique, we describe the structure of outerarm dynein proteins from Chlamydomonas and Tetrahymena after adsorption to a mica surface, after high-salt dissociation, and after glutaraldehyde fixation, and compare these images to the configuration of outer arms bound to microtubules. After adsorption to mica, the extracted dyneins from both organisms look like three-headed "bouquets", as reported for Tetrahymena by Johnson & Wall (1983b). High magnification images demonstrate that each head carries a slender "stalk" and a long "stem", and that small subunits decorate the stems and create a "flowerpot" domain at the base of the bouquet. Exposure to high salt induces this trimer to dissociate into a two-headed species and a single-headed species; it also stimulates the decorative elements to dissociate from the stems. Dynein is thus constructed on the same general plan as myosin, with large globular heads, narrow stems and additional small subunits that associate with the stems. The splayed-out image of the bouquet appears to be a distortion arising during adsorption to mica since, after brief glutaraldehyde fixation, the three heads remain closely associated as vertices of a triangular unit. In situ, the three heads also adopt this trigonal configuration. Two of the three are visible from the exterior of the axoneme and constitute the bilobed rigor head we described previously (Goodenough & Heuser, 1982). The third head faces the interior of the axoneme where, we propose, it forms the "hook" of the outer arm as seen in thin section. We further propose that the decorative elements associated with the stem coalesce to form the two outer-arm "feet" seen in situ, and that at least one of the in vitro stalks is equivalent to the in situ stalk, which extends from the head to the B microtubule. Deep-etch images of stretched axonemes, partially extracted axonemes, and dynein-decorated brain microtubules indicate that each outer arm, as traditionally viewed, is a hybrid of two dynein molecules: its two feet derive from one molecule, whereas its trigonal head derives from the molecule located distally. The resultant overlapping configuration creates the diagonal "linkers" seen in situ, which correspond to the in vitro stems. Thus, a row of dynein arms is essentially a dynein polymer that extends from the tip to the base of a doublet microtubule, each head riding on its neighbor's feet like a row of circus elephants.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphatases↗
PubMed1990

A dual electrophysiologic test for atrial antireentry and ventricular antifibrillatory studies. Effects of bethanidine, procainamide, and WY-48986.

We have developed a dual electrophysiologic test that allows measurement of both antireentry and antifibrillatory activities of potential antiarrhythmics in the same anesthetized dog. The reentry portion of the model was created surgically by a Y-shaped crushing around the tissue between the superior and inferior vena cava and tissue parallel to the AV groove. The pacing-induced tachycardia that results from circus movements around the tricuspid ring is very persistent in duration and regular in cycle length. The antifibrillatory activities were assessed by determination of the ventricular fibrillation threshold (VFT) using train-stimuli method. Control VFT was measured every 15-20 min in duplicate and followed by induction of atrial reentry. A drug was infused to intervene the atrial tachycardia. After the conversion of the arrhythmia (either by drug regimens or pacing), postdrug VFT was measured, again in duplicate. Bethanidine (20 mg/kg), procainamide (30 mg/kg), and WY-48986 (10 mg/kg), a Class III antiarrhythmic, were evaluated in this dual test. Bethanidine and procainamide prolonged the cycle length of atrial reentry to a greater extent than WY-48986. The atrial arrhythmias were consistently terminated by procainamide and WY-48986 whereas bethanidine converted the tachycardias in one of the five dogs studied. All three agents elevated VFT with bethanidine producing higher values than procainamide and WY-48986. In conclusion, the dual electrophysiologic testing system offers both economic and scientific advantages for the study of modes of action of antiarrhythmic agents.

Animals↗
PubMed1990

Combined sotalol and flecainide given at low dosage in patients with the Wolff-Parkinson-White syndrome.

We determined the effects of combined sotalol (160 mg/day) and flecainide (200 mg/day) in 15 patients with the Wolff-Parkinson-White syndrome. After medication given for 3 days, the plasma levels were 0.8 +/- 0.3 micrograms/ml for sotalol and 232 +/- 104 ng/ml for flecainide. Electrophysiologic testing showed complete blockade of the accessory pathway in 4 patients and a decrease in the anterograde conduction capacity by 27% in the remainder. The effect on the accessory pathway was unrelated to the resting conduction properties. Initiation of circus movement tachycardia was prevented in 5 of 11 patients. During a median period of 28 months of follow-up, 87% of patients were either free of tachycardia or satisfactorily improved. No proarrhythmic or adverse drug effects were observed.

Adult↗
PubMed1990

Morphology of the region of the coronary sinus in respect to coronary sinus rhythm.

The arterial supply to the region of the coronary sinus and the interatrial septum was examined in 18 normal canine hearts. In 13 of a further 18 dogs, coronary sinus rhythm was evoked by the ligation of atrial arteries, subsequent to which the arteries were visualized by injection of latex. A stable coronary sinus rhythm is evoked by producing ischaemia in an extensive area of the right atrium, including the sinus node, the interatrial septum and Bachmann's bundle, but preserving from ischaemia the posteroinferior part of the right atrium. Microscopical examination of the hearts with coronary sinus rhythm, and comparison with 9 control hearts, failed to demonstrate any morphological centre, in the form of nodal cells, which might have been responsible for the abnormal rhythm. In the posterior part of the right atrium, the ischaemic changes failed to affect the approaches of the atrioventricular node. The approaches were predominantly composed of cells poor in myofibrils mixed to a variable degree with cells of the working myocardium. We discuss the possibilities of the development of coronary sinus rhythm and "circus movement" with regard to the participation of the approaches to the atrioventricular node.

Animals↗
PubMed1983

Role of the ventromedial nucleus of the thalamus in motor behaviour--I. Effects of focal injections of drugs.

An assortment of drugs was injected into one or both ventromedial nuclei of the thalamus, to see how these influenced stereotypy, locomotion and posture in spontaneously behaving and actively rotating rats. Unilateral intrathalamic muscimol promoted weak ipsiversive circling, while bilateral treatment gave catalepsy. Similar injections of 4-amino-hex-5-enoic acid, which inhibits gamma-aminobutyrate metabolism, raised gamma-aminobutyrate levels in the ventromedial nuclei more than three-fold yet had none of these behavioural effects. The indirectly acting gamma-aminobutyrate agonists flurazepam and cis-1,3-aminocyclohexane carboxylic acid had little effect on posture and locomotion and, like muscimol and 4-amino-hex-5-enoic acid, elicited only very weak stereotypies. Procaine behaved like the gamma-aminobutyrate antagonist bicuculline, provoking vigorous locomotor hyperactivity and teeth chattering if given uni- or bilaterally. Pretreatment of one ventromedial nucleus with muscimol or 4-amino-hex-5-enoic acid, and to a lesser extent flurazepam or cis- 1,3-aminocyclohexane carboxylic acid, gave rise to pronounced ipsilateral asymmetries when combined with a large systemic dose of apomorphine. Contraversive rotations were initiated by unilateral stereotaxic injection of muscimol into the substantia nigra pars reticulata, or with apomorphine from the supersensitive striatum in unilaterally 6-hydroxydopamine lesioned rats. Drug treatments in the ipsilateral ventromedial nucleus showed a similar rank order of potency at inhibiting these circling behaviours, seemingly by reducing apomorphine-induced posture and muscimol-induced hypermotility. The suppression of circling by muscimol in these tests was highlighted by introducing the compound into the ventromedial nucleus at the height of circling activity. Both types of circling stimulus lost the capacity to increase locomotion, but still caused head turning and stereotypy in rats made cataleptic with bilateral ventromedial muscimol. Treating one ventromedial thalamus with muscimol greatly intensified any pre-existing posture directed towards that side, and vice versa. These data suggest that the ventromedial nucleus is not involved with the expression of stereotyped behaviours, but can profoundly influence posture and locomotion, especially in the presence of some other motor stimulus. The recovery of circus movements in rats with impaired ventromedial nucleus function implies this nucleus is not essential for the execution of circling in these models.

Amino Acids↗