Neuronal activity in the striatum of the genetically hypertensive rat, a putative animal model of attention-deficit hyperactivity disorder
TL;DRAbstract
The striatum is a forebrain nucleus required for the acquisition of appetitive reinforcement. Striatal structure and gross activation is abnormal in attention-deficit hyperactivity disorder (ADHD), a condition in which reinforcement-obtaining behaviour is altered, but it is currently unknown whether it is accompanied by abnormal striatal processing and output, or how the stimulant drugs used to treat ADHD modifies striatal neuron activity in disorder sufferers. This was addressed by recording pre- and post-amphetamine (AMPH) striatal single-unit activity from freely-moving genetically hypertensive (GH) rats, a putative animal model of ADHD, both as they rested, and during a contextually-signalled classical conditioning task. The isolation and characterisation of neuronal subtypes revealed that putative fast-spiking (pFS) interneuron activity was upregulated in resting GH rats, compared to the control Wistar (WI) strain. AMPH increased the activity of these cells in resting WI rats, but
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The striatum is a forebrain nucleus required for the acquisition of appetitive reinforcement. Striatal structure and gross activation is abnormal in attention-deficit hyperactivity disorder (ADHD), a condition in which reinforcement-obtaining behaviour is altered, but it is currently unknown whether it is accompanied by abnormal striatal processing and output, or how the stimulant drugs used to treat ADHD modifies striatal neuron activity in disorder sufferers. This was addressed by recording pre- and post-amphetamine (AMPH) striatal single-unit activity from freely-moving genetically hypertensive (GH) rats, a putative animal model of ADHD, both as they rested, and during a contextually-signalled classical conditioning task. The isolation and characterisation of neuronal subtypes revealed that putative fast-spiking (pFS) interneuron activity was upregulated in resting GH rats, compared to the control Wistar (WI) strain. AMPH increased the activity of these cells in resting WI rats, but
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