3.5.1 Appetite, hunger and thirst

The Neural Circuits Involved in Appetite, Hunger and Thirst, Including Disturbance in Eating Disorders, Mood Disorders and Medication Side Effects

Appetite, hunger and thirst:

Appetite, hunger, and thirst are complex processes that are regulated by several neural circuits in the brain. Some of the key brain regions involved in the regulation of these processes include the hypothalamus, the amygdala, and the mesolimbic dopamine system.

The hypothalamus is a region of the brain that plays a key role in the regulation of appetite, hunger, and thirst. It contains several nuclei that are involved in the control of these processes, including the arcuate nucleus, the paraventricular nucleus, and the lateral hypothalamic area. These nuclei receive input from various sources, such as the gastrointestinal tract, the bloodstream, and other organs, and respond by releasing hormones that modulate appetite, hunger, and thirst.

The amygdala is another brain region that is involved in the control of appetite, hunger, and thirst. It is a part of the limbic system and is involved in the regulation of emotions and motivation. Activation of the amygdala has been linked to increased food intake, particularly in response to palatable or high-fat foods, and to increased thirst in response to negative emotions or stressful situations.

The mesolimbic dopamine system, which includes the ventral tegmental area and the nucleus accumbens, is a key pathway in the brain’s reward system. Activation of this pathway has been linked to increased food intake and the pleasure associated with eating.

Overall, the neural circuits involved in appetite, hunger, and thirst are complex and involve the interaction of multiple brain regions and pathways. Disruptions in these circuits can contribute to disordered eating behaviours and disturbances in fluid balance and hydration status (Power, 2009).

Eating disorders:

Eating disorders are complex conditions that are characterized by abnormal eating behaviours and attitudes towards food. These behaviours and attitudes are thought to be influenced by a combination of genetic, environmental, and psychological factors, as well as disruptions in neural circuits in the brain.

Some of the key brain regions involved in the development and maintenance of eating disorders include the prefrontal cortex, the amygdala, and the mesolimbic dopamine system.

The prefrontal cortex is a brain region that is involved in decision-making, impulse control, and emotional regulation. Dysfunction in this region has been linked to disordered eating behaviours and impaired ability to regulate food intake.

The amygdala is a brain region that is involved in the regulation of emotions and motivation. Activation of the amygdala has been linked to increased food intake, and to increased reward and pleasure associated with eating. Dysfunction in the amygdala has been linked to disordered eating behaviours, such as binge eating and bulimia nervosa.

The mesolimbic dopamine system, which includes the ventral tegmental area and the nucleus accumbens, is a key pathway in the brain’s reward system. Activation of this pathway has been linked to increased food intake and the pleasure associated with eating. Dysfunction in this pathway has been linked to disordered eating behaviours, such as binge eating and food addiction.

Overall, the neural circuits involved in eating disorders are complex and involve the interaction of multiple brain regions and pathways. Further research is needed to fully understand the neural basis of eating disorders and to develop effective treatments (Kaye, 2009).

Mood disorders:

Mood disorders, such as depression and bipolar disorder, are complex conditions that are characterized by disturbances in mood and emotion. These disturbances are thought to be influenced by a combination of genetic, environmental, and psychological factors, as well as disruptions in neural circuits in the brain.

Some of the key brain regions involved in the development and maintenance of mood disorders include the prefrontal cortex, the amygdala, the hippocampus, and the basal ganglia.

The prefrontal cortex is a brain region that is involved in decision-making, impulse control, and emotional regulation. Dysfunction in this region has been linked to symptoms of depression and other mood disorders, such as difficulty making decisions and controlling emotions.

The amygdala is a brain region that is involved in the regulation of emotions and the processing of emotional information. Dysfunction in the amygdala has been linked to symptoms of depression, such as negative emotion and anhedonia (loss of pleasure).

The hippocampus is a brain region that is involved in the regulation of emotions and the consolidation of memories. Decreased volume and function of the hippocampus have been observed in individuals with mood disorders, particularly depression.

The basal ganglia are a group of structures in the brain that are involved in the regulation of movement and emotion. Dysfunction in the basal ganglia has been linked to symptoms of mood disorders, such as changes in activity levels and motivation.

Overall, the neural circuits involved in mood disorders are complex and involve the interaction of multiple brain regions and pathways. Further research is needed to fully understand the neural basis of mood disorders and to develop effective treatments (Shepherd, 2004).

Medication side-effects:

Medications can have various side effects that may be due to disruptions in neural circuits in the brain. The specific side effects of the medication will depend on the medication and the brain regions and pathways that it affects.

For example, some medications that act on the brain’s neurotransmitter systems, such as antidepressants and antipsychotics, may cause side effects such as drowsiness, dizziness, and changes in appetite and weight. These side effects may be due to the medication’s effects on brain regions and pathways involved in the regulation of sleep, appetite, and mood.

References:
(1) Kaye, W. H., & Fudge, J. L. (2009). Neurobiology of anorexia nervosa and bulimia nervosa. Physiology & behavior, 97(5), 599-606.

(2) Power, M. L., & Schulkin, J. (2009). The neuroendocrinology of appetite: A review. Physiology & Behaviour, 97(5), 561-572.

(3) Shepherd, G. M. (2004). The synapse: structure, function, and plasticity. The Journal of Physiology, 561(1), 1-9.