Brain function in relation to behaviour and training of the performance horse: managing stereotypy from a neural and genetic stand point
Dr Andrew Hemmings, Royal Agricultural College, Cirencester GL7 6JS
1.0 Introduction
According to the current definition behavioural stereotypy serves no apparent purpose, and instead may be attributed to factors such as neural dysfunction or the repetitive deployment of an innate behavioural response. However, due to the massive impact on time budget, and the apparent high motivation towards performance, it has been suggested that stereotypy may have some form of functional consequence for the animal; in particular stereotypies may function as a coping mechanism employed in a stressful or sub-optimal environment. This issue is highly relevant to the welfare of the performance horse as equine stereotypies are often physically prevented through the application of invasive surgery, or through devices such as the crib-strap or anti-weave bar. If these behaviours do serve as a coping response, then physical prevention will leave the animal at risk from the deleterious effects of stress.
2.0 Brain mechanisms underlying the stereotypic response
Stereotypic behaviours have been described as frustrated goal directed (appetitive) strategies performed in the context of consummatory denial (McBride and Hemmings 2009). Brain centres responsible for reward of appetitive behaviour encompass structures of the midbrain such as the ventral tegmental area (VTA), whose nerve terminals release dopamine which binds to receptors on a forebrain region known as the nucleus accumbens (NA). Indeed, the binding of dopamine to its NA receptor would appear to be a pre-requisite for the pleasure associated with appetitive behaviour. Moreover, dopamine activity in the NA is also linked with the arrival of stressors associated with stereotypy development. And thus, due to the strong links with stereotypy our studies focussed on the NA and associated areas. Initial experiments involved radio-ligand binding protocols to quantify dopamine receptor (D1 & D2) density and affinity. The first study revealed a significant proliferation of dopamine receptors on the nucleus accumbens of cribbers versus controls (McBride and Hemmings 2005).
Similar studies using stereotypy rodents, would suggest that this type of receptor proliferation occurs as a result of repeated stress, only in those animals genetically pre-disposed to stereotypy. The effect of these changes include sensitisation of reward generation, such that behaviours which previously yielded only low levels of pleasure, increase in reward potential following stress. In a similar vein, humans subjected to chronic stressors often experience increased motivation to perform reward behaviours (i.e. alcohol consumption), and in this context such behaviours attain increased pleasure potential. And thus, stress induced receptor proliferation within the NA of the stereotypy horse, would endow mildly rewarding appetitive behaviour with increased reward potential. In the context of the Hughes and Duncan (1988) model of motivation, a confined horse deprived of forage, would become engaged in appetitive behaviour directed at feeding (i.e. grasping at objects with the teeth). Due to the mild reward potential of appetitive behaviour this grasping would be sustained. Over time, the stress associated with repeated behavioural frustration would induce NA receptor proliferation in those animals with a genetic pre-disposition, thereby increasing reward potential of the appetitive response. This would ensure the behaviour continues in repetitive ‘stereotypic’ fashion, finally becoming recognisable as crib-biting.
3.0 Conclusion
Evidence has been presented to suggest that equine stereotypy is the vestige of a highly motivated appetitive behaviour performed in the context of consummatory denial. Stress induced reward sensitisation ensures that the behaviour is performed repeatedly, in a stereotypic manner. However, if the rodent model is an indicator of horse physiology this sensitisation event only occurs in animals with a certain genetic pre-disposition. And thus, with the recent publication of the Equine Genome, studies can now proceed with the identification of the genes responsible, such that genetic screening could be instigated in breeding pairs and progeny. Unfortunately, the proliferation of dopamine receptors responsible for sensitisation appears permanent, meaning that stereotypy development is difficult to reverse. Predisposed animals should therefore have minimal contact with stressors known to cause stereotypy (feed restriction, social isolation, restricted movement). In management terms, this can prove difficult, especially if competition demands necessitate stabling. However, by pin-pointing motivational characteristics, the stressors most likely to induce stereotypy can be identified and subsequently minimised. For example, animals with high levels of feeding motivation will become stressed and maybe sensitised if denied forage. Such individuals should therefore be supplied with adlib hay. Conversely, a fit exercise motivated individual will need regular turn-out to ensure low levels of stress. Finally, in animals which do develop stereotypy, self-stimulation derived from these behaviours may promote coping in a stressful environment, and thus physical prevention is not advised.
4.0 References
Hughes, B. O. & Duncan, I. J. H. (1988) The notion of ethological need models of motivation and animal welfare. Animal Behaviour, 36, 1696-1707
McBride, S.D and Hemmings, A (2009) A neurologic perspective of equine stereotypy. Journal of Equine Veterinary Science. 29, 10-16
McBride, S.D. and Hemmings, A.J. (2005). Altered mesoaccumbens and nigro-striatal dopamine physiology is associated with stereotypy development in a non-rodent species. Behavioural Brain Research, 159, 113-118