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Effects of oral methylphenidate on prefrontal cortex‐associated neurocognitive deficits in the spontaneous hypertensive rat strain
Author(s) -
Kantak Kathleen M,
Harvey Roxann C,
Dembro Kimberly A,
Mutebi Michael M,
Singh Teghpal,
Kerstetter Kerry A,
Dwoskin Linda P,
Deschepper Christian F
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.906.1
Subject(s) - methylphenidate , neurocognitive , impulsivity , working memory , prefrontal cortex , attention deficit hyperactivity disorder , spontaneously hypertensive rat , psychology , medicine , neuroscience , cognition , psychiatry , blood pressure
Though several animal models of Attention Deficit Hyperactivity Disorder (ADHD) exist, the spontaneous hypertensive rat (SHR) model is most frequently used. SHR display the same core behavioral symptoms as individuals with ADHD (hyperactivity, inattention, impulsivity), and also show extradimensional set‐shifting and non‐spatial working memory deficits that are unrelated to hypertension. The objective here was to determine if treatment with methylphenidate could prevent these deficits in the SHR. Extradimensional set‐shifting was assessed using the Attentional Set‐Shift Task and non‐spatial working memory was assessed using the Odor Delayed Win‐Shift Task. The SHR and several comparator rat strains were administered either methylphenidate at a clinically relevant dose (1.5 mg/kg), route (oral) and pretreatment time (30 min), vehicle, or were left untreated. Results demonstrated that treating the SHR with low‐dose oral methylphenidate prevented working memory and set‐shifting deficits that were observed in untreated SHR, and eliminated strain differences in both tasks. The findings provide further evidence that the SHR is a valid model for studying neurocognitive deficits associated with ADHD. Moreover, the current behavioral approach is appropriate to assess novel medications that target neurocognitive deficits associated with ADHD. Supported by SBE‐0354378, RO1 DA11716 and P50 DA05312.