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PubMed1996

Behavioural feedback to risk variation ensues from unsatisfied appetency.

For a long time, but particularly since the last two decades, the phenomenon of behavioural feedback to risk variation, especially to highway safety measures, has been the subject of numerous papers and debates. It has been advanced that human behaviour ensues from the interaction between two motivational systems: (1) appetency, governed by a homeostasic mechanism, wherein the individual seeks to satisfy needs, and (2) aversion, guided by the principle of zero aversion, whereby the individual seeks to avoid aversive stimuli. When an individual considers the possibility of undertaking an action, he weighs the advantages (appetency) and the disavantages (aversion). If the appetency proves to be stronger than the aversion, the action is completed and ipso facto, the individual accepts the risk associated with it. In this article, it is suggested that the behavioural feedback following a variation in the risk (aversion) ensues from unsatisfied appetency. If the unsatisfied appetency is nil (the individual is already satisfied), a drop in the aversive constraint (e.g. lowered risk of an accident) will not cause any behavioural feedback. On the other hand, if there is an unsatisfied appetency (the individual is not fully satisfied), a drop in the aversive constraint will bring about behavioural feedback in proportion to the level of unsatisfied appetency. Cases in which behavioural feedback is likely to arise and the implications for public policy-making are briefly discussed.

Accidents, Traffic↗
PubMed1982

The behavioural effects of a novel substance P analogue following infusion into the ventral tegmental area or substantia nigra of rat brain.

The behavioural response following infusion of a novel, stable substance P (SP) analogue, DiMe-C7, into the ventral tegmental area (VTA) of rats was characterized and contrasted with the response to an equal dose of the parent compound SP. DiMe-C7 produced a longer-lasting behavioural stimulation than SP as evidenced in several behaviours, including locomotor activity, wet dog shakes, rearing and grooming. DiMe-C7-induced locomotor activity and rearing were potentiated by concurrent peripheral administration of D-amphetamine and blocked by pretreatment with haloperidol. Such responses to DiMe-C7 may thus be dependent upon dopaminergic activity. When given immediately following VTA infusion of DiMe-C7, morphine decreased, while naloxone had no effect upon most behavioural measures. The effect of methysergide on DiMe-C7 or SP into the substantia nigra reticulata produced a pattern of responses similar to nature to those produced by VTA infusion but different with respect to time course. These findings suggest that DiMe-C7 is a metabolically stable analogue of substance P which manifests prolonged actions on behaviour when centrally administered. Further, a role for central dopaminergic mechanisms is implicated in DiMe-C7-induced behavioural action.

Animals↗
PubMed1991

Behavioural effects of NMDA injected into the hypothalamic paraventricular nucleus of the rat.

Electrical stimulation of the hypothalamic paraventricular nucleus (PVH) and of the adjacent dorsal hypothalamic area (DHA) evokes grooming behaviour. Microinjections of low doses of kainic acid, an agonist of the kainate type of glutamate receptors, into the same area evokes the same behaviour. To test whether other glutamate receptors are involved, microinjections with N-methyl-D-aspartic acid (NMDA) were made into the PVH/DHA area and the behaviour was observed. From the total observation time (30 min) up to 73% was spent on grooming, accompanied by yawning. Pronounced feeding behaviour was also noticed at 3 injection sites but not until 23 min after injection. Conclusions are that neurones within the PVH/DHA area are involved in grooming behaviour, possibly via glutamatergic innervation. The interaction between grooming and feeding behaviour at the level of the PVH is discussed.

Animals↗
PubMed1996

Spinally-mediated behavioural responses evoked by intrathecal high-dose morphine: possible involvement of substance P in the mouse spinal cord.

Intrathecal (i.t.) administration of morphine in the spinal subarachnoid space of mice produced a severe hindlimb scratching followed by biting and licking. The onset of the scratching behaviour was observed 60-70 s after i.t. injection of morphine (60 and 90 nmol), and had a duration of 3-4 min. The morphine-induced behaviour was increased additively by i.t. co-administration of substance P (SP). This characteristic behavioural response was inhibited dose-dependently by i.t. co-administration of the tachykinin NK-1 receptor antagonists, sendide and CP-96,345. Significant antagonistic effects of SP (1-7), a putative antagonist for NK-1 receptors and [D-Phe7, D-His9]SP (6-11), a selective antagonist for SP receptors, were observed against the morphine-induced behaviour. Pretreatment with i.t. SP antiserum and i.t. capsaicin resulted in reduction of the response to morphine. I.t. administration of somatostatin (SOM) antiserum, cysteamine, a relatively selective depletor of SOM and cyclo-SOM, a SOM receptor antagonist, produced no inhibitory effect on the morphine-induced behaviour. These results demonstrate that a spinal system of neurones containing SP may be involved in elicitation of the behavioural episode following i.t. injection of morphine in mice.

Animals↗
PubMed1982

The role of catecholamines, 5-hydroxytryptamine and m-tyramine in the behavioural effects of m-tyrosine in the rat.

The behavioural and neurochemical effects of m-tyrosine and a monoamine oxidase inhibitor in the rat are described. Systemic injections of m-tyrosine (50-150 mg/kg) 30 min after the administration of pargyline (75 mg/kg) produced intense behavioural stimulation which was not evident after injection of either compound alone. The behavioural syndrome induced consisted of forepaw padding, headweaving, backward walking, splayed hindlimbs, wet dog shakes, hyperactivity and hyperreactivity. m-Tyrosine alone or in combination with pargyline caused a significant increase in brain m-tyramine levels and a significant depletion of catecholamines. 5-Hydroxytryptamine (5-HT) levels, however, were unaffected by the administration of m-tyrosine at most of the times studied. The increase in levels of m-tyramine produced by m-tyrosine plus pargyline was 10 times greater than that produced by m-tyrosine alone, whereas the depletion in levels of the more abundant amines was not potentiated by pargyline pretreatment. The biochemical results suggest that an increased formation of m-tyramine may have been responsible for the observed behavioural stimulation and that a threshold level of m-tyramine in the brain appears to be necessary to produce an overt behavioural effect. The behavioural components observed indicate that m-tyramine could act by releasing newly synthesized catecholamines or 5-HT. Alternatively, m-tyrosine may function as a direct agonist at 5-HT or dopamine receptors, although an action on a specific tyraminergic receptor cannot be ruled out at present.

Animals↗
PubMed1987

Dopamine D-1 receptor agonists combined with the selective D-2 agonist quinpirole facilitate the expression of oral stereotyped behaviour in rats.

The behaviour of rats was studied after combined treatment with the selective DA D-2 agonist quinpirole and three selective D-1 agonists (SK & F 38393, SK & F 75670 and Lu 24-040). The effects on behaviour were compared with those on receptor binding and adenylate cyclase (AC). While the D-1 agonists alone did not induce stereotyped behaviour, quinpirole induced dose-dependent hyperactivity (locomotion, sniffing, head movements and rearing), whereas licking/biting was absent or seen only occasionally. Combined treatment with quinpirole and a D-1 agonist was followed by dose-dependent licking and occasional biting behaviour. The D-1 agonists had similar efficacies, but SK & F 75670 and Lu 24-040 were more potent than SK & F 38393. The maximal effects of SK & F 38393 plus quinpirole were effectively blocked by either a D-1 antagonist (SCH 23390) or a D-2 antagonist (YM 09151-2) confirming the close relation between D-1 and D-2 receptor sites in the brain. Good correspondence was found between affinities to D-1 receptors [( 3H]SCH 23390 binding) in vitro and the EC50 values for stimulation of AC activity. However, the maximal effects on DA-sensitive AC activity were less for SK & F 75670 and Lu 24-040 than for SK & F 38393. Thus, the results indicate that efficacies in the adenylate cyclase assay are dissociated from those on behaviour. Furthermore, the data indicate that in normal rats D-1 receptors are functionally relevant since D-1 agonists facilitate the expression of oral stereotyped behaviour after combination with a D-2 agonist.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Substance P analogues containing D-histidine antagonize the behavioural effects of intrathecally co-administered substance P in mice.

The antagonistic effect of newly synthesized substance P (SP) analogues containing D-histidine was examined on behavioural responses induced in mice by SP, neurokinin (NK) A, physalaemin, eledoisin, somatostatin and bombesin. [D-Pro2,D-Trp7,9]SP (DPDT-SP) and [D-Arg1,D-Trp7,9,Leu11]SP (spantide) were used as references for comparison. When co-administered with SP intrathecally, all the SP analogues used decreased the SP-induced response which consists of scratching, biting and licking. DPDT-SP and spantide attenuated non-specifically the SP-like behavioural responses induced by physalaemin, eledoisin, NK A and somatostatin. In general, the introduction of D-histidine in position 9 of the SP molecule resulted in potent antagonistic activity of the SP derivative on the behavioural responses to SP. Of these SP analogues, [D-Arg1,D-Pro2,4,D-Phe7,D-His9]SP attenuated selectively the behavioural responses produced by NK-1 receptor agonists such as SP and physalaemin. Simultaneous injection of [D-Phe7,D-His9]SP-(6-11) selectively inhibited the SP-induced behavioural response without affecting the other peptide-induced behavioral response. The results suggest that the behavioural antagonism induced by [D-Arg1,D-Pro2,4,D-Phe7,D-His9]SP and [D-Phe7,D-His9]SP-(6-11) is probably due to the specific blockade of spinal NK-1 receptors.

Amino Acid Sequence↗
PubMed1989

Induction of purposeless chewing behaviour in rats by 5-HT agonist drugs.

The 5-HT agonist m-chlorophenylpiperazine (m-CPP; 1-16 mg/kg i.p. or s.c.), trifluoromethylphenylpiperazine (TFMPP; 2-16 mg/kg i.p.) and quipazine (2.5-20 mg/kg i.p.) increased purposeless chewing behaviour in rats. However, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.025-4 mg/kg s.c.) and 5-methoxy-N,N-dimethyltryptamine (5-MeODMT; 0.25-8 mg/kg s.c.) were without effect on chewing behaviour. Chewing behaviour induced by m-CPP (6 mg/kg s.c.) was antagonised by pretreatment with the 5-HT antagonists methiothepin and mianserin, but not by ketanserin or spiperone, or ICS 205-930. m-CPP (6 mg/kg s.c.)-induced chewing behaviour was also antagonised by pretreatment with (-)-propranolol (20 mg/kg). Pretreatment with the anticholinergic drugs benzhexol (2.5 mg/kg), and scopolamine (1 mg/kg) antagonised m-CPP (6 mg/kg s.c.)-induced chewing behaviour, but methylscopolamine (1 mg/kg) had no effect. These data support the role of 5-HT receptors in the mediation of purposeless chewing behaviour and suggest an interaction between brain 5-HT and acetylcholine systems.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

The behavioural effects of MK-801 in rats: involvement of dopaminergic, serotonergic and noradrenergic systems.

The non-competitive NMDA receptor antagonist, MK-801 (dizocilpine), induces in rats a characteristic behavioural syndrome with ataxia, stereotypies and hyperlocomotion. At least part of this behavioural syndrome is thought to be related to interactions between glutamatergic and dopaminergic neurotransmission. Based on recent biochemical evidence that serotonin (5-HT) might also be involved in the effects of MK-801 several 5-HT receptor ligands were tested for effects on MK-801-induced behaviours. The 5-HT1A receptor ligands, ipsapirone and NAN-190, which are known to display antagonist-like properties in functional models of postsynaptic 5-HT1A receptor activity attenuated or blocked the hyperlocomotion and head weaving observed after administration of MK-801, whereas the 5-HT2 receptor antagonist, ritanserin, was ineffective in this respect. The dopamine receptor antagonist, haloperidol, and the alpha 1-adrenoceptor antagonist, prazosin, also attenuated behaviours induced by MK-801. In contrast to its effects on stereotypies induced by MK-801, ipsapirone potentiated rather than attenuated the stereotyped behaviour induced by the dopamine receptor agonist, apomorphine, indicating that antagonism of MK-801-induced stereotypies by ipsapirone may not be related to the dopaminergic system. The data indicate that, in addition to catecholaminergic systems, serotonergic neurotransmission is significantly involved in the mechanisms by which MK-801 alters behaviour in rats.

Adrenergic beta-Agonists↗
PubMed1992

Partial and full dopamine D1 receptor agonists in mice and rats: relation between behavioural effects and stimulation of adenylate cyclase activity in vitro.

The dopamine (DA) D1 agonists, SK&F 83959, SK&F 75670, SK&F 38993, SK&F 81297 and SK&F 80723, had variable abilities to stimulate adenylate cyclase activity in rat striatal homogenates. Their efficacies, in relation to the effect of 100 microM DA were 0, 33, 69, 68 and 81%, respectively. In rats, all compounds induced (1) contralateral circling behaviour after unilateral 6-hydroxy-DA lesions, (2) ipsilateral circling behaviour after midbrain hemitransection after cotreatment with the D2 agonist quinpirole and (3) oral stereotypies after their combination with quinpirole. Maximum effects and rank order of potencies were similar in the three test models. In mice SK&F 83959, SK&F 75670 and SK&F 38393 inhibited methylphenidate-induced gnawing behaviour and induced no or only weak hypermotility. SK&F 81297 induced marked hypermotility which was partially inhibited by SK&F 83959 and SK&F 75670 and was completely blocked by the D1 antagonist, SCH 23390. It is concluded that no relation could be demonstrated between the efficacy to stimulate adenylate cyclase and to induce circling behaviours and stereotypies in rats. In contrast, a relation between biochemical and behavioural efficacies was found in the mouse models. The results suggest that different subtypes of D1 receptors mediate the behavioural effects reported in this study.

Adenylyl Cyclases↗
PubMed1993

Effects of the novel 5-HT1A receptor antagonist, (+)-WAY 100135, on stereotyped behaviour induced by the NMDA receptor antagonist dizocilpine in rats.

We have recently shown that the stereotyped behaviour induced by the uncompetitive NMDA receptor antagonist dizocilpine (MK-801) can be attenuated or blocked by partial agonists at 5-HT receptors of the 5HT1A subtype, indicating that 5-HT (5-hydroxytryptamine, serotonin) is involved in the stereotyped behaviour produced by dizocilpine. In the present experiment, a selective, silent 5-HT1A receptor antagonist, (+)-WAY 100135 (N-tert-butyl 3-4(2-methoxyphenyl) piperazin 1-yl-2-phenylpropanamide dihydrochloride), was used to further study the role of 5-HT activation in dizocilpine-induced behaviours. At a dose of 10 mg/kg, (+)-WAY 100135 significantly reduced the intensity of head weaving induced by dizocilpine, but this effect was lost by increasing the dose to 20 mg/kg. At this higher dose, (+)-WAY 100135 induced marked but short-lasting increases in skeletal muscle tone and hindlimb abduction, resembling components of the '5-HT behavioural syndrome', which would explain its biphasic effects on dizocilpine induced behaviours. The data substantiate that, in addition to the well known activation of dopaminergic transmission, activation of the 5-HT system might be involved in the behavioural effects of NMDA receptor antagonists such as dizocilpine.

Animals↗
PubMed1995

Induction but not expression of behavioural sensitization to nicotine in the rat is dependent on glucocorticoids.

Behavioural sensitization has been implicated in the development of addictive behaviour, and several studies suggest that corticosteroids may be involved in this phenomenon. In the present study, the effects of adrenalectomy and steroid replacement treatments on the behavioural sensitization observed after daily injections of nicotine (0.4 mg/kg s.c.) were investigated in the rat. Adrenalectomy completely prevented sensitization to the locomotor stimulating effect of nicotine after repeated injections but did not influence the acute locomotor activating effect of the drug or an already established sensitization to nicotine. In adrenalectomized animals receiving replacement treatment with corticosterone or dexamethasone, but not aldosterone, repeated administration of nicotine produced behavioural sensitization. Repeated dexamethasone treatment per se failed, however, to sensitize rats to nicotine. Post mortem neurochemical studies showed that repeated administration of nicotine significantly increased homovanillic acid (HVA) levels, as well as the dihydroxyphenylacetic acid (DOPAC)/dopamine quotient, in the limbic forebrain. Adrenalectomy per se significantly increased HVA levels and tended to elevate the DOPAC/dopamine quotient. When repeatedly treated with nicotine, adrenalectomized rats displayed a higher DOPAC/dopamine quotient, but no significant difference in HVA levels, compared to nicotine-treated sham-operated controls. In the striatum and the cortex, no significant effects of nicotine treatment or adrenalectomy were observed on any of the neurochemical measures. The present results suggest that glucocorticoid (type II) receptor activation is required for induction of sensitization to the locomotor stimulatory effect of nicotine, whereas corticosteroids are not required for the expression of the behavioural sensitization once established. Provided that HVA levels and the DOPAC/dopamine quotient relatively well reflect the presynaptic dopamine activating effect of nicotine, it may be suggested that corticosteroid-related mechanisms associated with behavioural sensitization to nicotine are post- rather than presynaptically located in relation to mesolimbic dopamine neurons.

Adrenalectomy↗
PubMed1986

A computational frame to study social behaviour in animals.

This paper presents new methods and procedures for studying collective behaviour in rats. The animals are assumed to be indistinguishable one from another and the behaviour of the group is represented analysed and interpreted in terms of the temporal evolution of a finite state probabilistic automaton. The automaton states are defined by measures on the clustering degree considered as a social response variable. The electronic system developed to carry out the cluster analysis and the automatic control of the social behaviour in the experimental environment includes a multimicroprocessor interacting with a 'social box' in which, together with classical sensors and effectors, a phototransistor based position sensor is included. Preliminary experiments show the discriminative power of the cluster automaton concerning sexual differences and emotivity, as well as the extensive of a basic mechanism of clustering as a collective response to stress. Pharmacologically, the new experimental medium proposed in this paper may be used to detect a new range of products affecting social but not individual behaviour. Also, well-known products, which in normal doses produce no detectable modification of individual behaviour, might have detectable effects on the collective level. Be this as it may, the experimental environment described constitutes a further experimental facility for the analysis and control of animal behaviour.

Animals↗
PubMed1995

The health behaviour of northern Finnish men in adolescence and adulthood.

The aim of the study was to produce data about health behaviour among men born in Northern Finland in 1966. A particular concern was to find out how well health behaviour in adolescence predicts health behaviour in adulthood. The family questionnaire on health and development was submitted in 1980 when the subjects were 14 years of age. The response rate was 97%. The second questionnaire survey was carried out 10 years later with 2500 respondents. The final response rate was 60%. The results indicated that health behaviour in adolescence predicted health behaviour in adulthood as far as smoking and physical exercise were concerned. Over half (65%) of those who were non-smokers in their youth did not smoke as adults. Similarly the majority (71%) of those who had taken physical exercise at least once a week in their youth continued to do so in adulthood. Most of the subjects (85%) used alcohol in adulthood. A good family situation was connected with healthy habits. In the case of drinking, however, the subjects whose fathers belonged to social classes I-II used alcohol to a somewhat greater extent than others. It is important to conceive of health behaviour as an element connected with a person's life situation. Health research should be incorporated into cultural research and should have closer co-operation with other disciplines.

Adolescent↗
PubMed1987

Behavioural interactions involving D1 and D2 dopamine receptors in non-habituated mice.

The effects of SKF 38393 (D1-agonist) and SCH 23390 (D1-antagonist) were compared with those of haloperidol (D2 greater than D1-antagonist) and metoclopramide (D2-antagonist) in the absence or presence of apomorphine (D1/D2-agonist) and RU 24213 (D2 agonist) in non-habituated mice. The motor behaviour studied which was typical of the species included sniffing, grooming, rearing and locomotion. Apomorphine and RU 24213 induced frozen inactivity, in small doses and head-down sniffing, coupled with ponderous forward walking, in large doses, consistent with the stimulation of D2 receptors at pre- and postsynaptic sites, respectively. Neither SKF 38393 nor metoclopramide modified rearing or locomotion over a wide range of doses. SKF 38393 promoted sniffing and grooming, while metoclopramide suppressed this behaviour. Apart from increased grooming with SCH 23390 in small doses, both this drug and haloperidol dose-dependently decreased all motor activity. In combination studies, the D2 blockers reversed the effects of stimulation of D2 receptors and released normal behaviour, whereas SCH 23390 converted both the behavioural syndromes mediated by pre- and postsynaptic D2-receptors into severe inactivity (but not catalepsy). The drug SKF 38393 had the opposite effect and promoted motor responding in the presence of D2 stimulation, in doses that were otherwise ineffective by themselves. In this model, SCH 23390 modified behaviour mediated by D2-receptors in a different manner to the D2-receptor antagonists, haloperidol and metoclopramide, suggesting it may interact with a different population of D2-receptors, or with D1-receptors. These and earlier data can be interpreted to mean that both subclasses of the dopamine receptor have distinct and probably interdependent roles in the management of motor behaviour.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Can vasopressin alone act as an unconditioned stimulus to produce passive avoidance behaviour in rats in a typical memory experiment?

The claim that vasopressin improves memory has been largely based on results obtained from shock avoidance experiments. In the majority of these studies, "memory" was defined operationally as the hesitation of a rat to enter the darkened compartment of a box in which it had once received an electric foot-shock. A single post-trial injection of arginine vasopressin (AVP) enhances such passive avoidance behaviour. In view of the recent demonstration that AVP has aversive effects, it was argued that vasopressin alone (without giving the rats foot-shock, prior to the peptide) might be a sufficient inhibitory stimulus to produce passive avoidance behaviour in a typical memory experiment. This hypothesis was tested in the present study. The results of these experiments indicate that a behaviourally active dose of AVP (10 micrograms/kg; s.c.) was a sufficient stimulus to produce passive avoidance behaviour in the rats. A small dose of AVP (1.25 micrograms/kg; s.c.) was without effect. However, AVP (10 microgram/kg) was only effective with repeated administration (Experiment 1). This result is in contrast with the post-trial effect of the peptide on inhibitory avoidance behaviour, which is obtained with just one injection in the normal single trial step-through experiment. However, it was found that if the rats were injected with AVP (10 micrograms/kg) and placed in the dark compartment of the apparatus for 20 min, thereby ensuring that the animals made the explicit connection between the aversive effects of the peptide and the dark environment, they displayed avoidance behaviour after a single trial (Experiment 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Behavioural and ECoG spectrum changes induced by intracerebral infusion of interferons and interleukin 2 in rats are antagonized by naloxone.

Rat interferon, alpha-interferon, interleukin 2 and recombinant interleukin-2 injected into the third cerebral ventricle produced typical behavioural sedation and/or sleep and ECoG synchronization in rats while beta-interferon produced no behavioural sleep or ECoG synchronization. A slight sedation was observed after the largest dose of beta-interferon only. During sleep induced by lymphokines, a dose-dependent increase in total voltage power as well as in the 0.5-3, 4-7 and 12-16 Hz frequent bands was observed. Much smaller doses were required to produce similar behavioural and ECoG spectrum effects after infusion of interferons and interleukin-2 into the locus coeruleus. No significant behavioural and ECoG changes were obtained after infusion of the same doses of interferons and interleukin-2 into other areas of the brain (caudate nucleus, dorsal hippocampus, substantia nigra pars compacta, ventromedial hypothalamus). The behavioural and ECoG effects of alpha-interferon, rat interferon and interleukin-2 were blocked in animals pretreated with naloxone. These results are consistent with the hypothesis that the behavioural and ECoG effects of these lymphokines are mediated at locus coeruleus level by stimulation of opiate receptors.

Animals↗
PubMed1991

Effects of the benzodiazepine receptor inverse agonist, DMCM, on the behaviour of mice: an ethopharmacological study.

Ethopharmacological procedures and a two-compartment black and white test box were used to examine behavioural effects produced by the benzodiazepine receptor inverse agonist, methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM), when given by intraperitoneal injection (0.4 and 1.0 mg/kg) to pair-housed adult CD1 male mice. Control mice received injections of the solvent. Behaviour in the light-dark box was examined at 30 min after the injection and behaviour during encounters with an untreated group-housed male, in a neutral cage, was then assessed by ethological procedures. In dominant mice, aggressive behaviour was significantly reduced and the ratio of flight, relative to aggression received, was significantly increased by DMCM at 0.4 mg/kg. At 1 mg/kg but not 0.4 mg/kg, DMCM decreased time spent by dominant mice in the light compartment of the test box. In both dominant and subordinate mice, flight was increased by DMCM at 1 mg/kg to a level close to statistical significance. Treatment with DMCM had no other detectable effect on the behaviour of subordinate animals. It is suggested that anxiogenic activity of this compound might induce a shift of agonistic behaviour from aggression to "fear-induced flight".

Aggression↗