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A bottom-up approach to emulating emotions is expounded in this thesis. This is intended to be useful in research where a phenomenon is to be emulated but the nature of it can not easily be defined. This approach not only advocates emulating the underlying mechanisms that are proposed to give rise to emotion in natural agents, but also advocates applying an open-mind as to what the phenomenon actually is. There is evidence to suggest that neuromodulation is inherently responsible for giving rise to emotions in natural agents and that emotions consequently modulate the behaviour of the agent. The functionality provided by neuromodulation, when applied to agents with self-organising biologically plausible neural networks, is isolated and studied. In research efforts such as this the definition should emerge from the evidence rather than postulate that the definition, derived from limited information, is correct and should be implemented. An implementation of a working definition only tells us that the definition can be implemented. It does not tell us whether that working definition is itself correct and matches the phenomenon in the real world. If this model of emotions was assumed to be true and implemented in an agent, there would be a danger of precluding implementations that could offer alternative theories as to the relevance of neuromodulation to emotions. By isolating and studying different mechanisms such as neuromodulation that are thought to give rise to emotions, theories can arise as to what emotions are and the functionality that they provide. The application of this approach concludes with a theory as to how some emotions can operate via the use of neuromodulators. The theory is explained using the concepts of dynamical systems, free-energy and entropy.

Play fighting is common in juvenile mammals as a peri-pubertal form of agonistic behavior preceding adult aggressive behavior. In golden hamsters, play fighting peaks in early puberty around postnatal day 35 (P-35), and gradually matures into adult aggression in late puberty. Though extensively studied, the neural mechanisms underlying play fighting remains poorly understood. My dissertation focuses on identifying the neural circuitry and neural transmitter systems that mediate this behavior in juvenile golden hamsters. Based on behavioral similarities between the offensive components of play fighting and adult aggression, I predicted that the neural circuitries mediating both behaviors shared common components. This possibility was tested by quantifying the immunolabeling of c-Fos expression in juvenile hamsters after the consummation of play fighting. In support of my hypothesis, I found that areas previously associated with offensive aggression in adult hamsters, including the ventrolateral hypothalamus (VLH), the posterior dorsal part of the medial amygdala (MePD), and the bed nucleus of the stria terminalis (BST), also showed enhanced c-Fos expression after play fighting, which supported my hypothesis. Vasopressin (AVP) facilitates aggression in adult hamsters. Therefore, I hypothesized that AVP also activates play fighting. To test my hypothesis, juvenile male golden hamsters were tested for play fighting after they received central microinjections of an AVP V1A-receptor antagonist into the anterior hypothalamus (AH). Also, immunocytochemistry was performed to identify possible AVP neurons associated with this behavior. I found that the AVP antagonist selectively inhibited the attack components of play fighting in experimental animals. In addition, AVP cells in the nucleus circularis (NC) and the medial division of the supraoptic nucleus (mSON), which were associated with offensive aggression, also showed increased c-Fos activity after play fighting. Together, these results show that AVP facilitates offensive behaviors throughout hamster development, from play fighting in juveniles to aggression in adults. A recent study shows that oral administration of a CRH receptor antagonist inhibits aggression in adult hamsters. Therefore, I predicted that CRH plays a similar role in play fighting. To test my prediction, juvenile hamsters were tested for play fighting after central microinjections of a CRH receptor antagonist. I found that microinjections of the CRH receptor antagonist within the lateral septum (LS) resulted in an inhibition of several aspects of play fighting. The possible source of CRH affecting the behavior was tested through combined immunocytochemistry to CRH and c-Fos. I found CRH neurons in the diagonal band of Broca (DBB), an area with extensive connections with the LS, were particularly activated in association with play fighting. In conclusion, I find that shared neural elements participating in the “vertebrate social behavior neural network” are associated with both aggression and play fighting in hamsters. This circuitry is activated before the onset of puberty and is affected by rising levels of steroid hormones during the developmental period leading to adult behaviors. Within the circuitry, vasopressin release in the AH appears to control the activation of play fighting attacks. In contrast, CRH release in the LS affects a broader range of aspects of play fighting, including not just consummatory aspects of the behavior, but apparently also appetitive components in the form of contact duration. / text