The role of the medial prefrontal cortex in the play fighting of rats.

Although decorticated rats are able to engage in play, their play is abnormal in three ways. First, decorticates do not display the normal, age-related shifts in defensive strategies during development. Second, decorticates do not modify their defensive tactics in response to the social identity of their partners. Third, decorticates display a global shift in defensive tactics from more complex to less complex strategies. It has been shown that lesions of the motor cortex (MC) selectively produce the abnormal developmental effects on play, and that lesions of the orbitofrontal cortex (OFC) selectively produce the deficits in behavioral discrimination between social partners. In the current set of experiments, we demonstrate that lesions of the medial prefrontal cortex (mPFC) produce the shift from more complex to less complex defensive tactics, while leaving intact the age-related and partner-related modulation of defensive strategies. Thus, we have evidence for a triple dissociation of function between the MC, the OFC, and the mPFC with respect to social play behavior.

The modulation of play fighting in rats: role of the motor cortex.

The cortex is not necessary for rats to engage in play fighting, but it is necessary for them to modify their pattern of play fighting in different contexts. Two experiments were conducted to determine the role of the motor cortex (MC). Rats with bilateral ablations of the MC performed on Postnatal Day 10 failed to show the normally present age-related modulation in defense but were able to modulate defense with different social partners. This latter finding was confirmed in rats given ablations as adults, in which responses to social status could be monitored before and after brain damage. It appears that different forms of cortical modulation of play fighting involve different cortical circuits.

The effects of orbital frontal cortex damage on the modulation of defensive responses by rats in playful and nonplayful social contexts.

In a series of 3 experiments on rats, 2 hypotheses were tested: (a) that damage to the orbital frontal cortex (OFC) would alter the socially relevant context for executing defensive responses but not their performance and (b) that damage done to the OFC in early infancy would produce more deficits in social behavior than similar damage occurring in adulthood. Bilateral or unilateral OFC damage in adult males did not impair their ability to defend themselves during play fighting and when protecting their food but did impair their ability to modify the pattern of defense in response to different partners. Rats that sustained bilateral damage at 3 days of age not only had deficits in partner-related modulation of defense but also exhibited hyperactivity in their play. The findings thus supported the proposed hypotheses.

Neonatal and pubertal, but not adult, ovarian steroids are necessary for the development of female-typical patterns of dodging to protect a food item.

Rats protect food by dodging horizontally away from a conspecific. Females and males use different movement and stepping patterns to execute a dodge. An unresolved question is whether exposure to ovarian steroids in females is necessary for the development of the female-typical pattern. Females ovariectomized neonatally and prior to puberty use a combination of male and female tactics. Pregnant females, however, use a female-typical pattern of dodging, suggesting that the patterns used by prepubertal ovariectomized females are not due to their increase in body mass. Thus, the contribution of ovarian steroids to the development of female-typical patterns of behavior needs to be studied further at both a behavioral and neural level with regard to the organization of movement.

Manipulation of gonadal hormones in neonatal rats alters the morphological response of cortical neurons to brain injury in adulthood.

The authors examined the effects of sex and neonatal hormones on the response of pyramidal cells (Layer III, parietal cortex) to injury of the medial frontal cortex in the adult rat. At birth, males were gonadectomized (GDX) or sham-operated. Females were given testosterone (T) or oil injections. In adulthood, rats that had been left intact at birth were GDX, and they then received bilateral medial frontal cortex lesions or sham surgery. Rats not exposed to T at birth exhibited losses of dendritic arbor (males GDX at birth) or dendritic spine density (oil-treated females). Compensation after cortical injury is dependent on the rat's sex and history of exposure to gonadal steroids.