Glutaminergic signaling in the caudate nucleus is required for behavioral sensitization to methylphenidate.
Animals
Attention Deficit Disorder with Hyperactivity
/ drug therapy
Behavior, Animal
/ drug effects
Caudate Nucleus
/ anatomy & histology
Central Nervous System Stimulants
/ administration & dosage
Dopamine
/ metabolism
Dopamine Agonists
/ administration & dosage
Dose-Response Relationship, Drug
Glutamic Acid
/ metabolism
Locomotion
/ drug effects
Male
Methylphenidate
/ administration & dosage
Motivation
/ drug effects
Rats
Rats, Sprague-Dawley
Reward
Caudate nucleus
Glutamate
Lesion
Methylphenidate
Sensitization
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:
09 2019
09 2019
Historique:
received:
11
02
2019
revised:
17
06
2019
accepted:
18
06
2019
pubmed:
23
6
2019
medline:
27
2
2020
entrez:
23
6
2019
Statut:
ppublish
Résumé
Methylphenidate (MPD) is a widely prescribed psychostimulant for the treatment of attention deficit hyperactivity disorder, and is growing in use as a recreational drug and academic enhancer. MPD acts on the reward/motive and motor circuits of the CNS to produce its effects on behavior. The caudate nucleus (CN) is known to be a part of these circuits, so a lesion study was designed to elucidate the role of the CN in response to acute and chronic MPD exposure. Five groups of n = 8 rats were used: control, sham CN lesions, non-specific electrolytic CN lesions, dopaminergic-specific (6-OHDA toxin) CN lesion, and glutaminergic-specific (ibotenic acid toxin) CN lesions. On experimental day (ED) 1, all groups received saline injections. On ED 2, surgeries took place, followed by a 5-day recovery period (ED 3-7). Groups then received six daily MPD 2.5 mg/kg injections (ED 9-14), then three days of washout with no injection (ED 15-17), followed by a re-challenge with the previous 2.5 mg/kg MPD dose (ED 18). Locomotive activity was recorded for 60 min after each injection by a computerized animal activity monitor. The electrolytic CN lesion group responded to the MPD acute and chronic exposures similarly to the control and sham groups, showing an increase in locomotive activity, i.e. sensitization. The dopaminergic-specific CN lesion group failed to respond to MPD exposure both acute and chronically. The glutaminergic-specific CN lesion group responded to MPD exposure acutely but failed to manifest chronic effects. This confirms the CN's dopaminergic system is necessary for MPD to manifest its acute and chronic effects on behavior, and demonstrates that the CN's glutaminergic system is necessary for the chronic effects of MPD such as sensitization. Thus, the dopaminergic and glutaminergic components of the CN play a significant role in differentially modulating the acute and chronic effects of MPD respectively.
Identifiants
pubmed: 31228508
pii: S0091-3057(19)30072-3
doi: 10.1016/j.pbb.2019.172737
pmc: PMC6692216
mid: NIHMS1533086
pii:
doi:
Substances chimiques
Central Nervous System Stimulants
0
Dopamine Agonists
0
Methylphenidate
207ZZ9QZ49
Glutamic Acid
3KX376GY7L
Dopamine
VTD58H1Z2X
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
172737Subventions
Organisme : NIDA NIH HHS
ID : R01 DA027222
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.
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