Discriminative learning occasioned by the administration of a dopamine agonist

RATIONALE: The repeated administration of psychostimulants usually brings about a progressive increment of the behavioral responses that they induce. We examined to what extent this sensitization is due to an associative learning process. OBJECTIVES: The dopamine agonist apomorphine elicits stereotyped pecking in pigeons, a response that increases with successive intramuscular injections. We tested whether this sensitized pecking would be discriminatively directed at environmental stimuli that had been present during the sensitization phase. METHODS: In a preliminary experiment we identified a pair of stimulus compounds that attracted an equal number of apomorphine peck responses. During discrimination training naive pigeons were exposed on 5 days to both a cage furnished with one of these stimuli after having been injected with apomorphine and to a cage furnished with the other stimuli after having been injected with saline. Then the birds were administered apomorphine (or saline) and tested in a cage that offered both compound stimuli simultaneously. A discrimination reversal training and renewed tests followed. RESULTS: The tests under apomorphine and saline showed that the pecking by the pigeons was virtually exclusively aimed at the specific environmental stimuli under which the sensitization to apomorphine had taken place. This discriminative stimulus control was reversed after the pigeons had been retrained with converse stimulus compound allocations. CONCLUSIONS: The sensitized apomorphine pecking of pigeons was subject to close control by environmental stimuli. The results thus support the hypothesis that the sensitization to psychostimulants may be due to a conditioning process. The conditioning occasioned by apomorphine injections in birds could be a useful model for the study of sensory-motor learning processes.     

Sensitization to apomorphine in pigeons: unaffected by latent inhibition but still due to classical conditioning

When administered apomorphine, pigeons exhibit protracted bouts of pecking behavior. This response is subject to sensitization, as it initially increases with repeated drug injections. The hypothesis is examined that the sensitization is due to a Pavlovian conditioning of the drug-induced pecking to the environment in which it first takes effect. In a first experiment, we attempted to suppress this conditioning by extensively pre-exposing the birds to the test environment and saline injections (latent inhibition procedure). As the experiment yielded undiminished sensitization, it cast doubt on the conditioning hypothesis. However, while inhibitory pretraining also proved ineffective in a second experiment, a shortening of response latencies specific to the environment in which the animals had first experienced the apomorphine effect supported the conditioning hypothesis. It is suggested that the absence of latent inhibition may be due to the interference of a context-dependent conditioning effect. A third experiment that examined the hypothesis that the reinforcing properties of apomorphine might be attributable to its well known anorectic properties. The results provided some support for this notion. At the same time, they also confirmed that apomorphine-induced pecking conditions reliably to environmental cues. These cues are then by themselves capable of provoking conditioned pecking.     

Haloperidol blocks the acquisition but not the retrieval of a conditioned sensitization to apomorphine

The dopamine agonist apomorphine (apo) elicits stereotyped pecking bouts in pigeons, a response which increases with successive apo injections. The present study sought, first, to confirm the hypothesis that this sensitization arises through a Pavlovian conditioning driven by both external and internal cues; and, secondly, to advance the hypothesis that during this learning the dopaminergic activation only initiates a process that probably ends in glutamatergic synapse modifications. The conditioned nature of the sensitization to apo was examined in two separate experiments that compared context contingent and context uncontingent apo treatments. The role of dopaminergic mechanisms in the acquisition, maintenance and retrieval of sensitization-conditioned pecking was examined by administering the dopamine antagonist haloperidol (hal) either before, during or after apo sensitization treatments. A contingency between context and apo was found to be essential for the acquisition and retrieval of apo-sensitized pecking. A pretreatment with hal did not curtail a subsequent sensitization to apo. When hal was co-administrated with apo it suppressed the initial pecking response to apo and blocked the acquisition of sensitized responding. A pecking response normally observed when apo-sensitized pigeons are challenged with saline (sal) in the same cage in which they were sensitized, was also absent. When hal was co-administered with apo after the sensitization was complete this led at first to an only partial apo response suppression. When treated with hal in the same cage, already sensitized pigeons responded much as if they had been challenged with sal. The sensitization induced by apo was thus blocked by hal co-administered during acquisition, but during the maintenance or retrieval phase hal did not impair a previously sensitized responding. It is concluded that when pigeons are sensitized to apo, dopaminergic mechanisms are implicated in initiating the neural modifications that underlie the conditioned sensitization, but that they themselves are not importantly altered.     

Conditioned effects of apomorphine are manifest in regional EEG of rats both in hippocampus and in striatum

Summary Previously, in own studies, it was shown that stereotyped behaviour produced by apomorphine can be conditioned if the drug is repeatedly paired with defined environmental stimuli (conditioned stimuli, CS). Eventually, the presentation of CS alone produces stereotyped behaviour as conditioned response (CR). Furthermore, in electrocorticographic recordings it could be demonstrated that the characteristic pattern following acute apomorphine treatment, namely a selective increase in the power of the alpha-1 band, could be conditioned as well.In the present study, regional EEG was recorded in the striatum and in the hippocampus of freely moving rats. For conditioning, apomorphine (0.5 mg/kg s.c.) was paired with auditory and olfactory stimuli as CS for seven times, and on the eighth day the drug was substituted by the solvent in the presence of the CS. The effects were compared with those obtained in pseudoconditioned controls.Acute apomorphine administration led to an increase in power in the alpha-1 band (7.00–9.50 Hz), which effect was obvious in the hippocampus, above the cortex and in the striatum. After performing the conditioning procedure, these effects in regional EEG were found to be conditioned as well: as CR, activation in power in the alpha-1 band in hippocampus and striatum were manifest in the presence of the CS, but in absence of the drug. These effects occurred sporadically, but with a significantly higher frequency than in the pseudoconditioned controls.The results suggest that both the hippocampus and the striatum play important roles in classical conditioning of apomorphine effects which are primarily mediated by the striatum. Correspondence to K. Kuschinsky at the above address     

Effects of white and infrared lighting on apomorphine-induced pecking in pigeons

This experiment was concerned with the role of the environment in the production and form of apomorphine-induced pecking of pigeons. Earlier literature has suggested that the pecking occurs even when pigeons are placed in complete darkness, but there are no systematic or quantitative reports of such pecking. Six pigeons were tested with doses of 0.1, 0.3, and 1.0 mg/kg apomorphine. Tests were made in conditions of white and infrared light. The apparatus used novel force transduction measures that provided for both the detection of a peck as well as its peak forcefulness. At the lowest dose tested, apomorphine elicited pecking when the pigeon was placed in white light, but not when the dose was examined under infrared lighting. As the dose increased, however, pecking was observed regardless of lighting condition. No consistent differences were found in forcefulness of pecking as a function of lighting condition or dose. Though response output was seemingly unaffected by the lighting condition at higher doses, videotaped analysis revealed important changes in the formal characteristics of pecking. In white light, apomorphine elicited pecking at stimuli in the chamber (e.g. screw heads or the pigeon's own toes), whereas in infrared light pecking was directed at the floor directly in front of the pigeon. Such differences may be attributable to shifts in control to other stimulus modalities when vision is limited. Additionally, apomorphine may have direct effects on retinal dopamine function modulating the expression of pecking in the dark.     

Sensitization to apomorphine in pigeons is due to conditioning, subject to generalization but resistant to extinction

Apomorphine (Apo) administration induces a persistent bout of pecking in pigeons and other birds. Repeated injections of Apo in pigeons lead to sensitization, i.e. the pecking response to a particular dose increases up to a dose-dependent asymptotic level. It is also known that Apo-induced pecking can be classically conditioned to the cage environment where the animals experience the effect of the drug. Here we address the question of whether, and to what extent, the sensitization effect arises as a consequence of a conditioning or of a pharmacological process. An extinction experiment demonstrated that an extinction procedure supposed to be effective in inhibiting the conditioned pecking response was not effective in suppressing the sensitization to Apo, thus casting provisional doubt on the conditioning hypothesis. However, a conditioning experiment demonstrated that the sensitization effect undoubtedly involved an important component of conditioning to an experimental cage environment, but also suggested that there was an additional component possibly not due to learning. A generalization experiment, however, showed that this second component was very probably due to a stimulus generalization effect deriving from conditioning to the home cage, suggesting that learning can account for most, if not all, of the increase in Apo-induced pecking and that an exclusively pharmacological sensitization process plays, at best, a minor role. The apparent contrast between the results of the first experiment, indicating that the sensitization is not affected by inhibitory conditioning, and the results of the last two experiments, suggesting that the sensitization is due to excitatory conditioning, can be resolved by assuming that Apo induces a drug-state-dependent conditioning. These results are related to findings and arguments concerning the sensitization to psychostimulant drugs in mammals.     

A comparison of different sensory stimuli in producing conditioned apomorphine effects

In previous studies, it was shown that apomorphine-induced stereotyped behaviour could be conditioned when apomorphine was repeatedly paired with sensory stimuli (CS). Since in these experiments, the sum of various sensory stimuli were applied, it seemed of interest to use each sensory stimulus separately in order to evaluate the relevance of each of the stimuli for the development of the conditioned responses (CRs). Therefore, apomorphine (0.5mg/kg s.c.) was repeatedly (six times) paired either with an auditory, an olfactory, a tactile or a compound (auditory + olfactory + tactile) stimulus. On the seventh (drug-free test) day, the rats were injected with solvent in the presence of the CS previously applied. It was shown that the olfactory stimulus alone when used as CS produced similar CRs (in particular, stereotyped sniffing and licking) as the compound stimulus, whereas the other stimuli applied did not noticeably contribute to the development of the CRs. Furthermore, similarly to the compound stimulus, the olfactory stimulus, but not the auditory or tactile one, enhanced the apomorphine-induced stereotypies in the presence of the CS. This result suggests that the application of olfactory stimuli might be of particular relevance for the development of conditioned dopaminergic responses.     

Conditioning of behavioural effects produced by an intermediate dose of apomorphine: hypokinesia,ptosis and stereotypies

Summary Apomorphine, in an intermediate dose (0.18 mg/ kg s.c.) decreased dopamine turnover and produced signs generally attributed to a decrease in dopaminergic neurotransmission, e.g. ptosis and yawning, as well as signs of an increased stimulation of dopamine receptors in dopaminoceptive target neurones, e.g. stereotyped sniffing. In contrast, the former signs were exclusively observed after smaller doses and the latter after larger doses of apomorphine. Since it had been shown in previous studies that these signs, except yawning, could be conditioned in association with discriminative stimuli in the environment, the present study using conditioning experiments with this intermediate dose aimed at determining, 1. the time course of each conditioned response, 2. the interaction of conditioned and unconditioned responses, and 3. the conditions under which hypokinesia occurred. In each series, conditioned animals were compared with pseudoconditioned controls. Rats were conditioned for 8 days with apomorphine, and on day 9, treated with saline in presence of the conditional stimuli (a test cage in combination with acoustic and olfactory stimuli). In contrast to pseudoconditioned controls, ptosis and stereotyped behaviour were observed in conditioned rats, sometimes occurring alternatingly. These signs closely resembled the direct, unconditioned pharmacological effects. In addition, akinesia occurred after conditioning, although it was never manifest as a pure drug response, nor during the conditioning period. In contrast, yawning was observed in pseudoconditioned as well as in conditioned rats, although slightly more frequently in the former animals. Subsequently, the rats were again conditioned (or pseudoconditioned) on days 10–14 with apomorphine and both groups tested with the same dose (0.18 mg/kg) of apomorphine in the presence of the conditional stimuli. Both ptosis and stereotypies were significantly enhanced in conditioned animals, indicating synergistic interactions between conditioned and direct, pharmacological behavioural effects. In all cases the conditioned effects lasted for about 30 min.The results show that, after conditioning with an intermediate dose of apomorphine, both signs typical of a low dose of apomorphine and those characteristic of a large dose can be conditioned and sometimes occur alternately. Send offprint requests to K. Kuschinsky     

Conditioned behavioural responses to apomorphine: extinction and haloperidol-induced inhibition

Summary In previous studies it was established that stereo-typies (sniffing, licking, gnawing) produced by apomorphine can be conditioned and after repeated pairings with defined conditioned stimuli (auditory, tactile + olfactory) these stereotypies can be observed in the presence of the conditioned stimuli alone. In the present experiments, the extinction of these conditioned stereotypies was studied in one series; in another series, the possible inhibition of conditioned stereotypies by the blocker of dopamine receptors, haloperidol, was measured. The rats were conditioned (or the controls pseudoconditioned, respectively) for either 3 or 10 days with 2.0 mg/kg s. c. apomorphine or 6 days with 0.5 mg/kg s. c. of the drug and by placing them into particular cages in the presence of an auditory and an olfactory stimulus. Under all these conditions, episodes of conditioned stereotypies were observed, when solvent + conditioned stimuli instead of apomorphine was applied 1 day after the last conditioning session (first session of extinction). The conditioned responses seemed to be on the highest level after conditioning with 2.0 mg/kg apomorphine 3 days, lower after conditioning with the same dose on 10 days, and even lower after conditioning for 6 days with 0.5 mg/kg. Under all these conditions, the stereotypies summed up and averaged for the total observation period of 60 min rapidly decreased during the extinction period, so that on day 4 of the extinction period, no further significant differences between conditioned and pseudoconditioned animals were observed, although a short initial period was still observed on the fourth day. On day 3 of extinction, not only an early, but also a late episode of conditioned stereotypies was manifest, interrupted by an almost silent period. The acute (unconditioned) stereotypies produced by 0.5 mg/kg s. c. apomorphine were almost completely suppressed by pre-treatment with 0.1 mg/kg i. p. haloperidol. In contrast, the same dose of haloperidol produced a much less pronounced inhibition of conditioned stereotypies after conditioning with the same dose of apomorphine for 6 times. These results, together with previous findings, suggest that the conditioned behavioural effects are not due to an activation of dopaminergic mechanisms during conditioning with apomorphine. Send offprint requests to K. Kuschinsky at the above address     

Nature of receptors involved in apomorphine responses in pigeons

Apomorphine provokes pecking and emesis in pigeons. These effects are mediated through activation of dopamine receptors. In the present paper the effect of apomorphine on the body temperature was studied and an attempt made to determine whether the receptors mediating pecking, emesis, thermoregulatory effects, etc. were similar or different in their transmitter reactivity.Apomorphine was injected by either an intravenous or intracerebroventricular route. It produced dosedependent pecking and hypothermia. Pecking occurred in the form of a syndrome comprised of preening and visual exploratory movements of the head preceding and following a period of pecking. Large intraventricular doses produced emesis, vocalization, and opisthotonus. When apomorphine was injected intravenously, the dose required was smaller than that required by intraventricular route, suggesting that the receptors involved are located away from the ventricular surface. The reverse was true for hypothermia.The effects of apomorphine were prevented by the dopamine receptor-blocking substance pimozide, but were unaffected by the adrenoceptor-blocking substances phenoxybenzamine and propranolol. Pecking alone was suppressed by 5-HT and facilitated by cyproheptadine.The results indicate that the activation of dopamine receptors mediates the different apomorphine responses, of which only pecking is modulated by activation of tryptamine receptors.     

The role of D1 and D2 dopamine receptors in the acquisition and expression of cocaine-induced conditioned increases in locomotor behavior

Certain motoric effects of cocaine increase in intensity with repetitive administration. Conditioned drug effects are among primary determinants of such sensitization. The purpose of these experiments was to evaluate the role of D1 and D2 dopamine (DA) receptor mechanisms in the acquisition and expression of cocaine conditioning. On Day 1, rats were injected with cocaine (40mg/kg) either before (PAIRED) or after (UNPAIRED) exposure to a locomotor activity chamber. On Day 2, all animals were injected with a low dose of cocaine (10mg/kg) prior to placement in the locomotor chambers. Conditioning on Day 2 was evidenced by significantly higher activity levels in the PAIRED group relative to the UNPAIRED or saline-treated groups. Pretreatment with D1 (SCH 23390) or D2 (raclopride, sulpiride, haloperidol) DA antagonists on Day 1 prevented the development of conditioning as assessed on Day 2, indicating that both receptor subtypes are involved in acquisition. However, pretreatment with raclopride or SCH 23390 on Day 2, prior to cocaine injections, did not eliminate the differences in behavior between the conditioned and non-conditioned groups. Neither D1 (SKF 82958, SKF 38393) nor D2 (quinpirole) agonists administered alone were effective in establishing conditioning, while a combination of SKF 82958 and quinpirole was effective, suggesting that conditioning in this experimental paradigm requires the concurrent activation of both receptor subtypes. In the final study it was found that conditioned cocaine effects could be revealed only in the presence of quinpirole or apomorphine on Day 2. The D1 agonists (SKF 38393 and SKF 82958) were ineffective. This would suggest either that only quinpirole and apomorphine are effective in amplifying the conditioned effects of cocaine on Day 2 or that the cues produced by these drugs are more similar to those produced by cocaine than those produced by D1 agonists.     

Antagonism of apomorphine-induced pecking in pigeons

Central nervous system stimulants, tranquillizers and other central nervous system depressants, antiemetics, antihistamine drugs and autonomic blocking agents were examined for their ability to prevent the pecking response in pigeons induced by apomorphine (250 μg/kg intramuscularly). Reduction in the proportion of positive responses or significant increase in the latent period of pecking were taken as the criterion of effectiveness. Protection was afforded by caffeine, lysergic acid diethylamide, morphine, rauwolscine, triflupromazine and yohimbine. In addition, a significant increase in latent period was produced by artane, pentobarbitone, benactyzine, 2-bromolysergic acid diethylamide, cyclizine, diphenhydramine, ergotoxine, hyoscine, promethazine, 5-(2-chloroethyl)-4-methylthiazole and trimethobenzamide. Most of these drugs influenced the pecking and emetic responses to apomorphine in an identical manner. It is possible that identical receptors may be concerned with apomorphine pecking (in pigeons) and emesis (in other species).     

Influence of response topography on the effect of apomorphine and amphetamine on operant behavior of pigeons

Key-pecking and treadle-pressing behavior were maintained in five pigeons by a mult. FI 5 key FI 5 treadle schedule of food presentation. Dose-effect curves for apomorphine and amphetamine on overall rates of responding in both FI components of the multiple schedule were determined. Effective doses of apomorphine caused dose-dependent decreases on treadle-pressing rates in all animals. Similarly, key pecking rates were decreased by increasing doses of apomorphine in two of the five pigeons. However, dose-dependent increases in key-pecking rates were caused by apomorphine in the other three birds. In this group of pigeons, the mean key-pecking rate was increased to over 500 % of the control rate by the dose of 1 mg/kg of apomorphine. Observation of the animals under the effect of apomorphine showed continuous pecking at the operative key in these three animals while the other two pecked at different places of the floor and walls of the experimental chamber. Appropriate doses of amphetamine caused rate-increasing effects on key-pecking as well as treadle-pressing rates of all pigeons. These results suggest that the increases in keypecking rate caused by apomorphine in some pigeons in a conventional operant situation are due to the orientation of the drug-induced stereotyped pecking toward the response-key, as a consequence of the topographic compatibility between this behavioral effect of apomorphine and the operant selected for study.This investigation was supported in part by Grant 72/1419 of the FundaÇÃo de Amparo à Pesquisa do Estado de SÃo Paulo (FAPESP).     

Some observations on pecking in pigeons

An attempt was made to analyse the pecking behaviour in pigeons induced by apomorphine. The pecking was completely suppressed by tranquillizers, barbiturates and cortisone. It was intensified by histamine, nicotine, lobeline, testosterone, progesterone and sodium taurocholate. None of the drugs tested could induce in pigeons pecking typical of apomorphine. Apomorphine induced pecking in other birds too. It was concluded that the pecking phenomenon after apomorphine is similar to the natural feeding movements performed by pigeons while eating grains and possibly it is the function of a specialized area in the limbic system of the brain which is stimulated by apomorphine.     

Dopaminergic nature of apomorphine-induced pecking in pigeons

Apomorphine induces a pecking response in pigeons and the effects of various drugs on this pecking response were studied. The pecking induced by apomorphine (1.64 μmole/kg) has a rapid onset, and lasts for approximately 1 hr. Pecking induced by apomorphine can be blocked by dopaminergic receptor-blocking agents such as chlorpromazine, haloperidol, bulbocapnine and morphine, but not by α- or β-adrenergic receptor-blocking agents. Cholinergic agents have an inhibitory effect on pecking. The inhibitory effect of oxotremorine can be reversed by the prior administration of atropine. Apomorphine can induce both pecking and emesis while apomorphine methiodide causes only emesis. This ivestigation indicates that the pecking induced by apomorphine is caused by the stimulation of central dopaminergic receptors and that central cholinergic systems have a modulating effect on pecking. Serotonergic systems might also inhibit the pecking induced by apomorphine.     

Apomorphine-induced pecking in pigeons

Apomorphine produced persistent pecking in pigeons, the latent period, intensity and duration of which were related to the dose. The ED50 was estimated as 78.1±11.1 μg./kg. On chronic administration of apomorphine there was a significant decrease in latent period and weight which quickly returned to normal on stopping the drug. No conditioning and no tolerance were observed. The uncertain emetic effect of apomorphine in pigeons has been confirmed. Ten other centrally acting agents tested (caffeine, cocaine, 5-hydroxytryptamine, lysergic acid diethylamide, methamphetamine, morphine, nalorphine, pentylenetetrazol, strychnine, and yohimbine) failed to produce similar effects in pigeons.     

Effect of LSD on acquisition, maintenance, extinction and differentiation of conditioned responses

Three experiments were conducted to compare the effects of LSD (30 nmol/kg) on the acquisition, maintenance, extinction and differentiation of the rabbit's classically conditioned nictitating membrane response. LSD significantly enhanced the acquisition of conditioned responses to tone and light conditioned stimuli as compared with vehicle injected controls (Experiments 1 and 2), but had no detectable effect on differential conditioning in Experiment 3. The conditioned responses acquired under LSD in Experiments 1 and 2 exhibited some unusual features in that: they were more rapidly extinguished under continued injections of LSD; they demonstrated a significant decrement when animals were switched from LSD to vehicle during maintenance; and they were virtually eliminated when animals were switched from LSD to vehicle during extinction. In contrast, conditioned responses acquired under saline injections in Experiments 1 and 2 were not affected when animals were switched to LSD injections during either maintenance or extinction. These results of Experiments 1 and 2 were interpreted as indicating that LSD produces an asymmetrical state-dependent learning.     

Characterization of dopamine receptors involved in apomorphine-induced pecking in pigeons.

1. The possible involvement of subtypes of dopamine-receptors in apomorphine induced pecking was studied in pigeons. Different doses of apomorphine induced pecking in pigeons which was dose-dependent. 2. The response was decreased by SCH 23390 (D-1 antagonist) or high doses of sulpiride (D-2 antagonist) pretreatment, but increased by lower doses of sulpiride. 3. Combination of SCH 23390 with sulpiride completely antagonized the apomorphine effect. 4. Single dose administration of SKF 38393 (D-1 agonist) or bromocriptine (D-2 agonist) and combination of these drugs did not induce pecking, although either SK 23390 or bromocriptine increased the apomorphine-induced pecking which was decreased by SCH 23390 or sulpiride pretreatment. 5. It may be concluded that pecking, induced by apomorphine in pigeons, is elicited through activation of both D-1 and D-2 dopamine-receptors.     

Contextual control over the expression of fear in rats conditioned under a benzodiazepine

RATIONALE: Benzodiazepines disrupt fear conditioning, but this disruption is context-specific; if rats have been conditioned under a benzodiazepine, their fear is recovered if they are tested in a different context. The present experiments investigated how the conditioning context controls fear in rats conditioned under a benzodiazepine. OBJECTIVES: The experiments had three aims: (1) to replicate the finding that fear is recovered when rats are tested in a different context, (2) to test whether the conditioning context reduces fear generally or only for the specific stimulus conditioned in that context and (3) to test whether latent inhibition of the conditioning context reduces its control over fear. METHODS: Rats were injected with the benzodiazepine midazolam (1.25 mg/kg) or saline and exposed to a conditioned stimulus (CS) and shock in a distinctive chamber. Latent inhibition of the chamber was induced by extensively preexposing the rats to the chamber. The day after conditioning, fear was assessed by presenting the CS while rats were in either the conditioning chamber or a different chamber. RESULTS: The midazolam-induced reduction of fear was reversed (i.e. fear was partially recovered) if rats were tested in the different context, and was completely prevented if the conditioning context had been latently inhibited. These two effects were not additive since, when the conditioning context had been latently inhibited, rats showed less fear in the different context than in the conditioning context. CONCLUSIONS: We argue that midazolam does not disrupt conditioning, but imbues the conditioning context with control over retrieval of the CS-shock association. In this regard, the effects of midazolam closely parallel those of extinction.     

Stereotyped behavior affected by peripheral and intracerebroventricular apomorphine administration in pigeons

In pigeons, peripheral injection of apomorphine HCl (1.5 mg) produced a rapid pecking response while intracerebroventricular administration of the drug (60 μg) was ineffective in this respect. Both peripheral and to a larger extent central treatment with apomorphine stimulated another activity, that is headshaking. The frequency of other behavioral patterns was either decreased (preening) or unaffected (yawning, stretching) following both treatments. Together with previous studies, these data suggest that (a) apomorphine stimulates pecking in pigeons by activating dopaminergic mechanisms lying in brain areas situated away from the ventricles; (b) dopaminergic mechanisms situated in periventricular regions may take part in the control of some patterns, e.g. headshaking, and (c) other activities do not appear to depend directly on these mechanisms.