Abstract
A compelling body of evidence suggests that the worldwide obesity epidemic is underpinned by excessive sugar consumption, typified by the modern western diet. Furthermore, evidence is beginning to emerge of maladaptive changes in the mesolimbic reward pathway of the brain in relation to excess sugar consumption that highlights the importance of examining this neural circuitry in an attempt to understand and subsequently mitigate the associated morbidities with obesity. While the basolateral amygdala (BLA) has been shown to mediate the reinforcing properties of drugs of abuse, it has also been shown to play an important role in affective and motivated behaviours and has been shown to undergo maladaptive changes in response to drugs of abuse and stress. Given the overlap in neural circuitry affected by drugs of abuse and sucrose, we sought to examine the effect of short- and long-term binge-like sucrose consumption on the morphology of the BLA principal neurons using an intermittent-access two-bottle choice paradigm. We used Golgi-Cox staining to impregnate principal neurons from the BLA of short- (4 week) and long-term (12 week) sucrose consuming adolescent rats and compared these to age-matched water controls. Our results indicate possibly maladaptive changes to the dendritic architecture of BLA principal neurons, particularly on apical dendrites following long-term sucrose consumption. Specifically, our results show reduced total dendritic arbor length of BLA principal neurons following short- and long-term sucrose consumption. Additionally, we found that long-term binge-like sucrose consumption caused a significant reduction in the length and complexity of apical dendrites. Taken together, our results highlight the differences between short- and long-term binge-like sucrose consumption on BLA principal neuron morphology and are suggestive of a perturbation in the diverse synaptic inputs to these neurons.
Highlights
Increased sugar intake is considered one of the fundamental and principal factors of the current worldwide obesity epidemic [1]
Our results demonstrate the differences between short- and long-term binge-like sucrose consumption on basolateral amygdala (BLA) principal neuron morphology and are suggestive of an imbalance in the diverse inputs received by these neurons
Following short-term (4 weeks) sucrose consumption, the total dendritic arbor length of principal neurons in the BLA was decreased by 31% compared to water consuming controls (Water: 1928 ± 211 μm, n = 7; Sucrose 1337 ± 84 μm, n = 7, P = Ã0.0229, two-tailed unpaired Student’s t-test, Fig 2A, Table 1)
Summary
Increased sugar intake is considered one of the fundamental and principal factors of the current worldwide obesity epidemic [1]. Consumption of sugar and sweetened food in humans can cause cravings similar to those produced by addictive substances such as alcohol, nicotine or cocaine, primarily by activating the mesolimbic reward pathway [7]. There is evidence that suggests long-term consumption of highly palatable food can cause adaptations in the brain reward pathways, suggestive of an imbalance in the normal reward processing homeostasis [6, 16, 17]. While we have previously shown that medium spiny neurons in the NAc undergo morphological changes following long-term sucrose consumption [18], other studies have implicated the amygdala in incentive learning and motivational behaviors associated with the rewarding effects of addictive substances [19, 20]. In particular recent studies have highlighted the influence of the basolateral amygdala (BLA) to reward learning and the association with adaptive, goal-directed and emotional behavior [21]
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