Evidence of hypoglycemic anhedonia and modulation by bupropion in rats.
Anhedonia
/ drug effects
Animals
Antidepressive Agents, Second-Generation
/ administration & dosage
Appetitive Behavior
/ drug effects
Bupropion
/ administration & dosage
Deoxyglucose
/ adverse effects
Depression
/ complications
High Fructose Corn Syrup
/ administration & dosage
Hypoglycemia
/ chemically induced
Hypoglycemic Agents
/ adverse effects
Male
Rats
Rats, Sprague-Dawley
Reward
Self Administration
Taste
/ drug effects
2-deoxy-d-glucose
Anhedonia
Bupropion
Hypoglycemia
Self-administration
Journal
Pharmacology, biochemistry, and behavior
ISSN: 1873-5177
Titre abrégé: Pharmacol Biochem Behav
Pays: United States
ID NLM: 0367050
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
11
11
2020
revised:
17
01
2021
accepted:
18
01
2021
pubmed:
27
1
2021
medline:
15
9
2021
entrez:
26
1
2021
Statut:
ppublish
Résumé
Disorders characterized by dysfunction of glucose metabolism are often comorbid with depression. The current study investigated whether a hypoglycemic state caused by 2-deoxy-d-glucose (2-DG) can result in anhedonic behaviors responsive to stimulation of monoamine activity. In experiment 1, male Sprague-Dawley rats were tested for maintenance of intra-oral self-administration (IOSA) of a sweet solution after pre-treatment with 300 or 500 mg/kg 2-DG, a blocker of glucose metabolism. Experiment 2 determined whether exposure to an environment previously paired with the effects of 2-DG (0, 200 or 300 mg/kg) can influence IOSA, and whether 2-DG can modify taste reactivity to same sweet solution. Finally, experiment 3 examined whether 0 or 30 mg/kg bupropion, a monoamine-reuptake blocker, would attenuate the effect of 300 mg/kg 2-DG on IOSA and taste reactivity. It was found that 2-DG produced a sustained decrease in IOSA when animals were tested drug-free. This decrease in IOSA did not appear linked to place conditioning or to alterations in taste reactivity, and it was partially normalized by pre-treatment with bupropion. Taken together, these results in rats suggest that rapid hypoglycemia can induce an anhedonic state characterized by impaired consummatory responses to nutritional incentive stimuli and that can be alleviated by the antidepressant bupropion.
Sections du résumé
BACKGROUND
Disorders characterized by dysfunction of glucose metabolism are often comorbid with depression. The current study investigated whether a hypoglycemic state caused by 2-deoxy-d-glucose (2-DG) can result in anhedonic behaviors responsive to stimulation of monoamine activity.
METHODS
In experiment 1, male Sprague-Dawley rats were tested for maintenance of intra-oral self-administration (IOSA) of a sweet solution after pre-treatment with 300 or 500 mg/kg 2-DG, a blocker of glucose metabolism. Experiment 2 determined whether exposure to an environment previously paired with the effects of 2-DG (0, 200 or 300 mg/kg) can influence IOSA, and whether 2-DG can modify taste reactivity to same sweet solution. Finally, experiment 3 examined whether 0 or 30 mg/kg bupropion, a monoamine-reuptake blocker, would attenuate the effect of 300 mg/kg 2-DG on IOSA and taste reactivity.
RESULTS
It was found that 2-DG produced a sustained decrease in IOSA when animals were tested drug-free. This decrease in IOSA did not appear linked to place conditioning or to alterations in taste reactivity, and it was partially normalized by pre-treatment with bupropion.
CONCLUSIONS
Taken together, these results in rats suggest that rapid hypoglycemia can induce an anhedonic state characterized by impaired consummatory responses to nutritional incentive stimuli and that can be alleviated by the antidepressant bupropion.
Identifiants
pubmed: 33497714
pii: S0091-3057(21)00018-6
doi: 10.1016/j.pbb.2021.173120
pii:
doi:
Substances chimiques
Antidepressive Agents, Second-Generation
0
High Fructose Corn Syrup
0
Hypoglycemic Agents
0
Bupropion
01ZG3TPX31
Deoxyglucose
9G2MP84A8W
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
173120Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.