Emotion, Motivation And Drug Addiction
Initial attempts to understand the brain bases of emotions focused on the limbic system (see Chapter 45), with the amygdala as the key component in the system thought to be central to emotional processing. The evidence to support such an association has already been discussed in part (in Chapter 45), but it is also worth mentioning the Klüver–Bucy syndrome. This condition is seen with bilateral amygdala damage and is characterized by, among other phenomena, an apparent absence of the normal fear response and by marked placidity.
In addition, functional neuroimaging studies in humans have been consistent with animal studies, implicating the amygdala in the processing of emotional stimuli and, notably, in fear conditioning (wherein a previously neutral stimulus can, through association with an unpleasant outcome, produce a fear response when presented alone). It is proposed that the amygdala is the critical site in which: the necessary associations between the stimuli are formed using a process akin to the long-term potentiation (LTP) seen in the hippocampus (see Chapter 45); and the origin of the broad series of phenomena that constitute a fear response through its efferent projections.
Emotions are potentially useful in that they are allied with, and perhaps consist of, behavioural responses. They may be critical in helping us choose between competing behavioural possibilities and to guide behaviours that maximize rewarding and minimize punishing outcomes. The relationship between emotion and motivation is therefore an important one. In this respect, the dopamine systems, most notably the mesolimbic system (see also Chapters 19 and 58), which has connections with the amygdala, appear critical. A series of hypotheses have been put forward concerning the dopaminergic contribution to motivation.
· Hedonia hypothesis: whilst dopamine has been thought to be critical to the experience of pleasure. There is increasing evidence against this view.
· Learning hypothesis: dopamine is critical to learning the relationship between stimuli and rewards. Dopamine acts as a ‘teaching signal’ for stimuli that predict rewards and thus is the origin of behaviour that makes the reward manifest.
· Activation hypothesis: dopamine is required for the actual engagement in work that must be done to obtain the reward. It is important for both the attentional and the locomotor components of the work involved in reward-seeking and consumption.
· Incentive salience: dopamine is important in imbuing certain stimuli with motivational or incentive properties.
It would be simplistic to express motivational processes solely in terms of the input of the mesolimbic dopamine system to the amygdala but it is nevertheless a useful model by which to explain drug addiction.
In addition to the motivational properties of specific stimuli, in many circumstances we must consider motivational states that appear stimulus independent. Feeding behaviours, for example, arise not solely from the motivational properties of foods (sight, smell, taste) but also from a drive state (hunger) dependent on a number of homeostatic factors, for example endocrine signals (levels of insulin, and of the hormones leptin and ghrelin which, respectively, reduce and promote feeding behaviour) acting predominantly through the hypothalamus (see Chapter 11). A comprehensive description of a motivational state would require several levels of description together with an understanding of the interactions inherent in the state; for example, the extent to which motivational properties of stimuli themselves influence, and/or are influenced by, the drive state of the individual. An additional, important concern is when individuals are motivated towards behaviours that are at odds with their homeostatic requirements and consequently detrimental to health, as is the case with addictive behaviours.
Using some recreational drugs can be rewarding, but the evidence is that addictive behaviours (and associated withdrawal phenomena) are determined by how the brain adapts in response to repeated drug administration rather than as a direct result of the fact that drugs may be intensely pleasurable. Conversely, although the reward properties of the drug are insufficient to explain addictive behaviours, it is simplistic, too, to consider addiction solely as behaviours aimed towards avoiding withdrawal symptoms. In addition to considering addiction in terms of the pursuit of pleasurable states (drug-induced euphoria) or the avoidance of withdrawal states (an array of physical and psychological symptoms which may actually be produced simply by a stimulus or environment that has become associated with previous withdrawal), we must also take into account what may be considered a markedly augmented state of motivation to taking the drug – referred to as craving. Important in this respect is the fact that a craving may be precipitated by a drug-related stimulus or environment long after the individual has recovered from the withdrawal symptoms.
Other important phenomena that need to be explained are tolerance (a requirement for increased frequency and/or dose of the drug with repeated usage) and sensitization (in contrast to tolerance effects, some of the consequences of the drug may actually increase with repeated ingestion). Interestingly, neither tolerance nor sensitization are explicable in purely pharmacological terms because both phenomena also show certain features suggesting that they are conditioned responses. One view that has been put forward to account for the simultaneous occurrence of tolerance and sensitization is that while the pleasurable effects of the drug diminish with repeated administration (leading to tolerance), the drug and related environments and paraphernalia become, over time, more likely to capture attention and to precipitate the associated behaviours (sensitization).
While the neurobiological basis of drug addiction is still not fully understood, there is increasing evidence that it involves mesolimbic dopamine systems and genetic susceptibilities, which may in turn affect the normal functioning of this pharmacological system. An example of this is the recent recognition that some patients with Parkinson’s disease develop abnormal behaviours with their dopaminergic therapies–the so-called dopamine dysregulation syndrome which can involve pathological gambling and hypersexuality.