FIGURE 10. Induction ofc-Fos in the cerebral cortex of an NMA-treated rat. 
(A) Diestrus female rats show strong induction ofc-Fos in the 
somatomotor cortex following subconvulsive doses of NMA. (B) 
Similar treatment of lactating rats fails to induce c-Fos in the 
cerebral cortex. The patterns of c-Fos expression appeared to 
mirror the behavioral effects of NMA. 
pulses of 40 mg/kg NMA were administered at 10-minute intervals. Ninety 
minutes following the last dose of NMA, the rats were anesthetized and 
perfused for localization of c-Fos. In the diestrus rats, administration of NMA 
elicited signs of hyperactivity, but no seizures. In contrast, administration of 
NMA to lactating rats did not induce behavioral changes. Examination of c-Fos 
revealed marked induction of c-Fos in neurons throughout the neural axis of the 
diestrus rats, whereas the same treatment of lactating rats did not induce c-Fos 
immunoreactivity. Examples of c-Fos staining within the neocortex of a diestrus 
and lactating rat treated with NMA are shown in figure 10. Initial studies 
exploring the recovery of excitability in lactating rats reveal that both the 
suckling stimulus as well as progesterone participate in the dampening of NMA 
responsiveness (Abbud et al. 1991). These studies not only provide another 
example of IEG products as effective tools for studying neuronal activation but 
also illustrate the importance of the animal’s endocrine state in determining the 
effects of drugs on the nervous system. 
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