Role of the caudate nucleus in recovery from neonatal mediofrontal cortex lesions in the rat

Abstract

Ablation of medial prefrontal cortex impairs spatial discrimination learning in adult but not in neonatally lesioned rats. Orbital prefrontal cortex and adjacent convexity neocortex need not be left intact to observe this sparing of function. This study examined the possibility that the caudate nucleus, remaining intact after early medial prefrontal cortex lesions, might be involved in the observed behavioral sparing. Neonatal rats given combined lesions of the medial prefrontal cortex and head of the caudate nucleus were compared to age/litter-matched sham-operated controls on spatial alternation and place response acquisition and "reversal" tests. The results show that the performance of these neonatally lesioned subjects was deficient on both tests. The discussion centers on possible recovery mechanisms in rats given prefrontothalamic system damage early in life.

Spatial discrimination reversal learning in weanling rats is impaired by striatal administration of an NMDA-receptor antagonist

“…These findings are very similar to the data seen after early mPFC lesions on delayed response, SDA, and spatial reversals, when rats lesioned as infants are tested as adults (Kolb and Nonneman 1978;Nonneman and Corwin 1981). Combined mPFC and CN lesions in neonatal rats (P7) severely impaired SDA performance in a T-maze and place acquisition and reversal in a water maze, when rats are tested as adults (Vicedomini et al 1984). These data suggest that the CN in developing rats is critical for spatial learning, and when damaged can increase response perseveration during adult reversal performance.…”

“…Similar results have been found after lesions of the hippocampus, mPFC, and mediodorsal thalamus (Divac 1971;Kolb et al 1974;Nonneman et al 1974;Kolb 1977), suggesting that there may be anatomical links between these structures and the striatum that are relevant to spatial reversal learning. The literature regarding the ontogeny of learning and memory functions within the striatum is sparse and is confined to rats tested as adults following neonatal lesions (Vicedomini et al 1982(Vicedomini et al , 1984. As mentioned previously in text, neonatal lesions (P8-P10) did not impair SDA performance, but juvenile (P25-P27) and adult (P150-P160) lesions severely impaired SDA performance in adulthood (Vicedomini et al 1982).…”

Influence of the mesocortical dopaminergic system on activity, food hoarding, social-agonistic behavior, and spatial delayed alternation in male rats.

“…Ablation or destruction of the orbital prefrontal cortex results in increased activity (de Bruin, van Oyen, & van de Poll, 1983; Kolb & Whishaw, 1981; Nonneman & Corwin, 1981), increased shock-induced aggression (Kolb & Nonneman, 1974) and aggression in dyadic encounters (de Bruin et al, 1983), perseverative tendencies on a differential reinforcement for low rates of responding scheme (Kolb, Nonneman, & Singh, 1974), and disturbed bar-pressing extinction (Kolb et al, 1974). Lesions of the medial prefrontal cortex give rise to, for example, a disturbance in spatial delayed alternation (Corwin, Nonneman, & Goodlett, 1981; Corwin, Vicedomini, Nonneman, & Valentino, 1982; Kolb et al, 1974; Nonneman & Corwin, 1981; Ono, Nishino, Fukuda, Sasaki, & Nishyo, 1984; Thomas & Brito, 1980; Vicedomini, Corwin, & Nonneman, 1982; Vicedomini, Isaac, & Nonneman, 1984; Wikmark, Divac, & Weiss, 1973) and a disruption of food-hoarding behavior (Kolb, 1974; Kolb & Whishaw, 1981; Nonneman & Corwin, 1981; Nonneman & Kolb, 1979; Stamm, 1954). Behavioral changes following lesions of the prefrontal cortex have been reviewed by de Bruin (1981) and Kolb (1984).…”

Ontogeny of PFC-related behaviours is sensitive to a single non-invasive dose of methamphetamine in neonatal gerbils (Meriones unguiculatus)

“…It has been argued that after early disturbance of brain development, sparing of function depends on plasticity of maturing neurons which may be able to realize structural correlates of species-specific behaviours in more than just one way (Kolb and Whishaw, 1989;Vicedomini et al, 1982Vicedomini et al, , 1984. There are a number of reports that mechanical lesioning of the adult PFC may result in acute hyperactivity and impairment on delayed alternation (De Bruin et al, 1983;Bubser and Schmidt, 1990;Verin et al, 1993;De Brabander et al, 1993), whereas PFC-related behaviours were insensitive to neonatal lesioning (Freeman and Stanton, 1992;De Brabander et al, 1992;Carter et al, 1995).…”