D1-class dopamine receptor involvement in the behavioral recovery from prefrontal cortical injury

• Published in: Behavioural brain research Vol. 72; no. 1-2; pp. 39 - 48
• Main Authors: VARGO, J. M, BROMBERG, B. B, BEST, P. J, CORWIN, J. V, MARSHALL, J. F
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Science 14.12.1995
• Subjects: Animals; Behavior, Animal - physiology; Behavioral psychophysiology; Benzazepines - metabolism; Benzazepines - pharmacology; Biological and medical sciences; Caudate Nucleus - metabolism; Dopamine Antagonists - metabolism; Dopamine Antagonists - pharmacology; Functional Laterality - physiology; Fundamental and applied biological sciences. Psychology; Membranes - metabolism; Neostriatum - metabolism; Neurotransmission and behavior; Prefrontal Cortex - injuries; Prefrontal Cortex - metabolism; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Putamen - metabolism; Rats; Receptors, Dopamine D1 - antagonists & inhibitors; Receptors, Dopamine D1 - drug effects; Receptors, Dopamine D1 - physiology; Rat; Rodentia; Central nervous system; D1 Dopamine receptor; Basal ganglion; Corpus striatum; Prefrontal cortex; Recovery; Vertebrata; Visual stimulus; Mammalia; Acoustic stimulus; Animal; Plasticity; Sensorial perception; Lesion; Mechanical stimulus; Laterality; Brain (vertebrata); Neglect of space exploration
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/0166-4328(95)00028-3

Following unilateral aspiration of the left medial agranular cortex (AGm) region of prefrontal cortex, rats demonstrate contralateral neglect, characterized by a failure to orient to visual, tactile and auditory stimuli presented on the contralateral body side. While dopamine (DA) has been implicated in cortical neglect and its recovery, this study specifically examined D1-class DA receptors for their involvement in spontaneous recovery from neglect caused by AGm ablation. In the first experiment, left AGm-ablated rats demonstrated severe neglect of contralateral stimuli of each modality which spontaneously recovered over a period of several weeks. Recovered rats were given 7.0 micrograms/kg (s.c.) of the D1-selective antagonist SCH 23390. SCH 23390 reinstated severe neglect of contralateral stimuli, yet had no effect on orientation to ipsilateral stimuli. The same dose had no effect on the orientation behavior of controls. In a second experiment, D1 receptor characteristics were quantified via binding of [3H]SCH 23390 to tissue homogenates of the caudate-putamen of recovered AGm-ablated rats. Numbers and affinities of striatal D1 receptors of rats with unilateral AGm ablations did not differ between hemispheres or from values obtained from lesioned controls. Considered together, these findings indicate that recovery from neglect produced by cortical injury is associated with an increased dependence on D1-class receptor-mediated events, and that this increased dependence is unlikely to be mediated through changes in D1-class receptor numbers or affinities within caudate-putamen.