Emotion, Motivation And Drug Addiction
Emotion
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.
Motivation
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.
Drug addiction
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.
