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Licking microstructure in response to novel rewards, reward devaluation and dopamine antagonists: Possible role of D1 and D2 medium spiny neurons in the nucleus accumbens. | LitMetric

Licking microstructure in response to novel rewards, reward devaluation and dopamine antagonists: Possible role of D1 and D2 medium spiny neurons in the nucleus accumbens.

Neurosci Biobehav Rev

Dipartimento di Scienze Biomediche, Università di Sassari, Viale S. Pietro 43/b, Sassari 07100, Italy. Electronic address:

Published: October 2024

AI Article Synopsis

  • The text reanalyzes evidence on how dopamine D1 and D2-like antagonists affect licking microstructure, especially in relation to sugar intake and the role of nucleus accumbens (NAc) medium spiny neurons (MSNs).
  • D1 MSN activation is linked to increased licking bursts in response to new rewards, while D2 MSN activation is linked to smaller bursts and decreased licking when a reward's value is lowered.
  • Understanding these neural mechanisms can improve definitions of licking behavior and its relevance in studying motivation and eating disorders.

Article Abstract

Evidence on the effect of dopamine D1 and D2-like antagonists and of manipulations of reward value on licking microstructure is reanalysed considering recent findings on the role of nucleus accumbens (NAc) medium spiny neurons (MSNs) in the control of sugar intake. The results of this analysis suggest that D1 MSN activation, which is involved in the emission of licking bursts, might play a crucial role in response to novel rewards. D2 MSN activation, which results in reduction of burst size and suppression of licking, might mediate the response to reward devaluation. Elucidating the neural mechanisms underlying the licking response might lead to a better definition of its microstructural measures in behaviourally and psychologically meaningful functional terms. This could further support its use as a behavioural substrate in the study of the neural mechanisms of ingestive behaviour and motivation, as well as in animal models of pathological conditions such as eating disorders and obesity.

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Source
http://dx.doi.org/10.1016/j.neubiorev.2024.105861DOI Listing

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