Neurocircuitry of Impulsive-compulsive Disorders

Neurocircuitry of Impulsive-compulsive Disorders

Neurocircuitry of Impulsive-compulsive Disorders 150 150 Peter

Neurocircuitry of Impulsive-compulsive Disorders

1. Discuss the neurocircuitry of impulsive-compulsive disorders. For this discussion, address how an impulsive act can become a compulsive act.
2. Compare and contrast obesity as an impulsive-compulsive disorder and impulsive-compulsive disorders of behavior.
3. Compare and contrast nicotine and alcohol addictions. For this discussion, emphasize the mechanism of action, receptors and any pathways involved.

Sample Paper

Discuss the Neurocircuitry of Impulsive-compulsive Disorders

Impulsivity is defined as the inability to prevent initiation of action and is attributed to regulation by the ventral striatum, the ventromedial prefrontal cortex, the thalamus, and the anterior cingulate cortex. Impulsivity specifically is a predisposition that causes individuals to respond to external and internal stimuli without considering the negative consequences of their actions. Compulsivity is the inability to stop ongoing actions based on the dorsal striatum, orbitofrontal cortex, and thalamus. Compulsivity is the tendency to repetitively act in a habitual way to prevent a perceived negative consequence that leads to functional impairment (Zorrilla & Koob, 2019).

Cortical-Striatal circuits mainly deal with the regulation of compulsive and impulsive disorders through neurotransmitters modulation, and although the circuits controlling the impulsivity and compulsivity are neuroanatomically separate, they intercommunicate. The ventral striatum initiates impulsive actions in the impulsive circuit while the anterior cingulate cortex and ventromedial prefrontal cortex produce suppressive actions towards impulsive behavior. In the compulsive circuit, the dorsal striatum initiates and drives the compulsive actions while the orbitofrontal cortex produces an inhibitory effect against the behavior. Hyperactivity within striatal components and hypoactivity within the prefrontal components lead to impulsive or compulsive disorders. Behaviors that start as impulsive in the ventral loop can progress to the dorsal loop due to neuroplasticity and neuroadaptation, eventually becoming compulsive. This is facilitated by other regulatory mechanisms, including the amygdala, which regulates reward conditioning, and the hippocampus, which regulates memory (Fineberg et al., 2017).

Compare and Contrast Obesity as an Impulsive-Compulsive Disorder

Obesity can be classified as an impulsive-compulsive disorder. However, not all forms of obesity can be caused by genetic and lifestyle factors; only those that are due to excessive appetite for food controlled by the reward circuitry are classified as an impulsive-compulsive disorder. The neurobiological basis of eating is linked to the hypothalamus, which regulates the appetite-stimulating pathway. This pathway is mediated by neuropeptide Y and agouti-related protein. Peptide pro-opiomelanocortin is broken into α-melanocyte-stimulating hormone and functions to suppress appetite. The release of agouti-related protein and neuropeptide Y stimulates the melanocortin 4 receptors, which increases appetite for food and compels the individual to eat. The protein suppressing pathway releases pro-opiomelanocortin, which is then broken down to α-melanocyte-stimulating hormone, responsible for binding to melanocortin-4 receptors resulting in suppression of appetite. Obesity, therefore, can result from hyperactivity of the appetite-stimulating pathway or hypoactivity of the appetite-suppressing pathway, which compels the individuals to eat more and gain more weight (Boswell et al., 2021).

Compare and Contrast Nicotine and Alcohol Addictions

Nicotine addiction is linked to the nicotinic cholinergic receptors in reward circuits in the ventral tegmental area and is attributed to the increased release of dopamine into the nucleus accumbens. There are two types of nicotinic receptors, including α4βand α7subtype. Nicotine acts on α4β2-nicotinic postsynaptic receptors found on dopamine neurons, stimulating dopamine release into the nucleus accumbens. It also acts on α7-nicotinic presynaptic receptors, stimulating glutamate release and, consequently, dopamine release in the nucleus accumbens. It has also been shown to numb α4β2 postsynaptic receptors reducing the presence of GABA neurotransmission, which disinhibits mesolimbic dopamine neurons resulting in increased release of dopamine into the nucleus accumbens (Hayes et al., 2020).

Alcohol addiction affects various pathways in the brain, including the dopamine pathway; alcohol consumption or anticipation of alcohol stimulates the release of higher dopamine levels into the nucleus accumbens, creating a rewarding experience and causing people to seek alcohol. It also acts on the GABA and glutamate pathways. GABA is an essential neuro-inhibitor, and alcohol acts by causing inhibition at GABA synapses. Alcohol acts at GABA synapses to increase GABA release by blocking presynaptic GABAB receptors and stimulating postsynaptic GABAA receptors, commonly the δ subtype. It also acts on the glutamate pathway, where it inhibits the release of glutamate by blocking presynaptic metabotropic glutamate receptors (mGluRs) and presynaptic voltage-sensitive calcium channels (VSCCs) (Hayes et al., 2020).



Boswell, R. G., Potenza, M. N., & Grilo, C. M. (2021). The neurobiology of binge-eating disorder compared with obesity: implications for differential therapeutics. Clinical therapeutics43(1), 50-69.

Fineberg, N., Gillan, C., Vaghi, M., Apergis-Schoute, A., Chamberlain, S., Banca, P., … & Reid, J. (2017). 41. Neurocognition of Compulsive-Impulsive Disorders. Biological Psychiatry81(10), S17-S18.

Hayes, A., Herlinger, K., Paterson, L., & Lingford-Hughes, A. (2020). The neurobiology of substance use and addiction: evidence from neuroimaging and relevance to treatment. BJPsych Advances26(6), 367-378.

Zorrilla, E. P., & Koob, G. F. (2019). Impulsivity derived from the dark side: Neurocircuits that contribute to negative urgency. Frontiers in behavioral neuroscience13, 136.