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Funding Information: We are especially thankful to Rob G. Bijlsma who generously shared with us his extensive dataset from the Sahel region. We are also thankful to Afan Ajang, Linn M. Bjørvik, Tamuka Chapata, Wouter van Dongen, Patrick Guay, Lenka Harmáčková, Lukasz Jankowiak, Jan van der Kamp, Lennox Kirao, Jakub Kosicki, Philista Malaki, Pretty Maoko, John Mchetto, Grayson Mwakalebe, Organisation for Tropical Studies (South Africa), Diogo Samia, Trine Hay Setsaas, Libor Vaicenbacher and Leo Zwarts for their help with data collection. MW is thankful to Allison Piper, and a Deakin University Faculty of Science, Engineering and the Built Environment National and International Research Collaboration Grant in Kenya and BEACH (Beach Ecology and Conservation Hub; Venus Bay) in Australia. In Kenya, field data collection was approved by National Commission for Science Technology and Innovation no. NACOSTI/P14/4653/660 to M.W. and P.M. and no. NACOSTI/P18/52438/25493 to MW, Kenya Wildlife Service no KWS/BRP/5001 to M.W. A Rocha Kenya and the National Museum of Kenya supported and helped conduct fieldwork in Kenya. In South Africa, the University of Cape Town Science Faculty Animal Ethics Committee (2015/V11/SC) to S.J.C., Northern Cape Department of Environment and Nature Conservation (FAUNA 1489/2015) to P.P. In Brazil, we worked on private lands where no permits were required. In Australia, research was approved by the Deakin University (B32/2012, B11/2015, B10/2018), the Charles Darwin University Animal Ethics (A11013), the Macquarie University Animal Research Committee (99021), the Queensland Parks and Wildlife Service (#FA/000379/00/SA), and the Northern Territory Parks and Wildlife (41035 and 55233). This study was financially supported by the DSI-NRF Centre of Excellence at the FitzPatrick Institute of African Ornithology, University of Cape Town (grant to S.J.C.), The Leventis Foundation through the A.P. Leventis Ornithological Research Institute, Jos Nigeria (grant to B.D.A.B.), by a fellowship of the Fulbright (Slovakia) programme to P.M. for a visit to the University of California, Los Angeles. Animal tolerance towards humans can be a key factor facilitating wildlife–human coexistence, yet traits predicting its direction and magnitude across tropical animals are poorly known. Using 10,249 observations for 842 bird species inhabiting open tropical ecosystems in Africa, South America, and Australia, we find that avian tolerance towards humans was lower (i.e., escape distance was longer) in rural rather than urban populations and in populations exposed to lower human disturbance (measured as human footprint index). In addition, larger species and species with larger clutches and enhanced flight ability are less tolerant to human approaches and escape distances increase when birds were approached during the wet season compared to the dry season and from longer starting distances. Identification of key factors affecting animal tolerance towards humans across large spatial and taxonomic scales may help us to better understand and predict the patterns of species distributions in the Anthropocene.

IT has been suggested that the opiate addict gets pleasure both from the physiological effects of the drug and from the complex of environmental stimuli associated with obtaining and administering the drug. These latter stimuli achieve their control over behaviour by a conditioning process and can therefore, in theoretical terms, be considered as conditional stimuli in the Pavlovian sense. Wilder1 proposes that the repeated occurrence of certain exteroceptive stimuli which accompany the interoceptive stimulation induced by the opiate, results in conditioning of the environment to the drug state.

The affinities of olanzapine, clozapine, haloperidol, and four potential antipsychotics were compared on binding to the neuronal receptors of a number of neurotransmitters. In both rat tissues and cell lines transfected with human receptors olanzapine had high affinity for dopamine D1, D2, D4, serotonin (5HT)2A, 5HT2C, 5HT3, alpha 1-adrenergic, histamine H1, and five muscarinic receptor subtypes. Olanzapine had lower affinity for alpha 2-adrenergic receptors and relatively low affinity for 5HT1 subtypes, GABAA, beta-adrenergic receptors, and benzodiazepine binding sites. The receptor binding affinities for olanzapine was quite similar in tissues from rat and human brain. The binding profile of olanzapine was comparable to the atypical antipsychotic clozapine, while the binding profiles for haloperidol, resperidone, remoxipride, Org 5222, and seroquel were substantially different from that of clozapine. The receptor binding profile of olanzapine is consistent with the antidopaminergic, antiserotonergic, and antimuscarinic activity observed in animal models and predicts atypical antipsychotic activity in man.

Olanzapine (LY170053, 2-methyl-4-(4-methyl-1-piperazinyl)-10H-thieno[2,3-b][1,5] benzodiazepine) is a novel "atypical" antipsychotic agent with 5-hydroxytryptamine2.dopamine D1/D2 antagonist activity and anticholinergic properties. In behavioral studies, olanzapine (1.25-10 mg/kg, p.o.) antagonizes apomorphine-induced climbing behavior in mice, demonstrating that the compound possesses D1/D2 antagonist activity in vivo. Olanzapine (0.3-20 mg/kg, p.o.) antagonizes 5-hydroxytryptophan-induced head twitches in mice at doses much lower than those required to block the climbing response, confirming that in vivo, the compound is a more potent 5-hydroxytryptamine2 antagonist than dopamine antagonist. Olanzapine (2.5-10 mg/kg, p.o.) also antagonized oxotremorine-induced tremor in mice. In a conditioned avoidance paradigm in rats, olanzapine inhibits the avoidance response with an ED50 of 4.7 mg/kg p.o; however, unlike other antipsychotic agents, catalepsy is only observed at much higher doses (ED50 39.4 mg/kg, p.o.). These data would suggest that the compound will be less likely to produce undesirable extrapyramidal symptoms. Unlike "typical" antipsychotics, olanzapine (1.25-5 mg/kg p.o.) increases responding during the conflict component of a modified Geller Seifter test, demonstrating that the compound may also possess anxiolytic activity. In another series of experiments, olanzapine (1.25 mg/kg, i.p.) produced clozapine-appropriate responding in a drug discrimination model in which animals had been trained to discriminate clozapine (5 mg/kg, i.p.) from vehicle. On the basis of these results, it would therefore be predicted that olanzapine will have an atypical profile and will be less likely to induce undesirable extrapyramidal symptoms than currently available drugs.

Animals were trained on a three-component multiple schedule comprising variable interval reward, time out and conflict (reward plus punishment). Following training, dose response-functions of a number of psychoactive compounds were studied particularly with respect to their actions on the two low rate behaviours. Thus, during time out no specific effects were observed following morphine, amino-oxyacetic acid, caffeine or para-chlorophenylalanine (PCPA), although amphetamine, chlordiazepoxide (CDP) and diazepam (DZP) produced dose dependent changes in lever pressing rate. During conflict, however, significant attenuation of suppressed responding was only observed following administration of the benzodiazepines (CDP and DZP) and PCPA. These increases with CDP and DZP were quantitatively larger than those observed during time out. These results suggest that the benzodiazepines have specific effects on behavioural processes involved in punishment and that these actions are mediated by changes in 5-HT functional activity.

Aniamls were administered increasing doses of morphine for 16 days. During withdrawal they were challenged with an apomorphine ester or lergotrile. These dopamine agonists produced quantitatively different effects on behaviour. The results suggest that chronic morphine administration leads to dopamine supersensitivity which may be anatomically distinct in origin.

The effects of chlordiazepoxide (CDP) on emergence behavior was examined in socially reared and isolation reared rats. It was found that low doses of CDP decreased the emergence times of isolated animals but had little effect on the emergence of social animals. At higher doses the drug retarded emergence in all groups but there were no differential effects. The results do not support claims that rearing conditions influence the susceptability of rats to CNS depressants, rather they suggest that particular levels of CDP selectively influence "emotional" behavior.

Di-isobutyryl apomorphine (5 mg/kg i.p.) and lergotrile (5 mg/kg i.p.) produce long lasting turning behaviour in rats with 6-hydroxydopamine lesions at the level of the substantia nigra. Haloperidol (1.5 and 3.0 mg/kg p.o.) blocks the rotational behaviour due to the apomorphine ester but has no effect on lergotrile turning. Clozapine (10 and 20 mg/kg p.o.) blocks the lergotrile turning but stimulates the rotational behaviour produced by the apomorphine ester. The results support the concept of two anatomically separate dopamine receptors and their relevance to the study of antipsychotic activity is discussed.

PUNISHMENT is defined as the presentation of a noxious stimulus and results in the suppression of behaviour. This suppressive effect of punishment is seen clearly in conflict situations where the organism is encouraged to respond and then is punished for doing so. Brain 5-hydroxytryptamine (5-HT) systems have been implicated in the processes associated with the response to punishment. We show here that selective neurotoxin lesions to the 5-HT forebrain pathways reverse the suppressive effects of punishment, as do minor tranquillisers, supporting the view that 5-HT has a central role in conflict behaviour and in the effect of minor tranquillisers on such behaviour.

Ten London pigeons were trained on a schedule which allowed concurrent measurement of motor and exteroceptive sensory changes. The task involved a conditional colour discrimination contingent upon the completion of a fixed interval schedule of responding. As a preliminary pharmacological study the effects of the benzodiazepines, chlordiazepoxide and flurazepam were investigated. Both drugs enhanced perseverative responding (after completion of the FI), and to a variable degree responding during the FI, although there was no evidence for an increase in responding during the inter-trial-intervals. On the other hand, no marked changes in discrimination performance were observed. It is concluded that the most significant effects of these benzodiazepines are on motor mechanisms.