Neural mechanisms distinguishing the neocortical EEG of C57BL/6 mice from that of DBA/2 mice.

C57BL/6 inbred mice lack the 1-5 sec bursts of 6-7 cps spindles characteristic of the neocortical EEG of DBA/2 mice during waking. C57BL/6 mice (1) may be unable to generate any synchronized cortical EEG activity, (2) may lack the thalamocortical circuitry required to generate these brief spindle episodes (BSEs), (3) may lack mechanisms that can activate this circuitry or (4) may possess a potent mechanism to suppress BSE initiation and generation. Possibilities 1 and 2 have been eliminated because C57BL/6 mice generate pentobarbital, rostropontine-induced and sleep spindles, and because certain C57BL/6 sleep spindles resembled the BSEs seen in DBA/2 mice. Possibilities 3 and 4 were examined in the experiments reported here. In DBA/2 mice, pentylenetetrazol activates BSEs at subconvulsant doses. In contrast, neither 20 nor 50 mg/kg, IP, pentylenetetrazol activated BSEs in C57BL/6 mice, although the higher dose provoked 4-5 cps slow waves and myoclonic jerks. In DBA/2 mice, the beta-noradrenergic antagonist propranolol has been reported to powerfully release BSEs. In C57BL/6 mice, 10 and 15 mg/kg propanolol weakly released BSEs; fewer than 3 per hour occurred. Hence neither possibilities 3 and 4 are sufficient in themselves to explain the lack of BSEs during waking in C57BL/6 mice. However, simultaneous administration of 10 mg/kg propranolol and 20 mg/kg pentylenetetrazol provoked numerous BSEs in C57BL/6 mice. This suggests that perhaps C57BL/6 mice, as compared to DBA/2 mice, possess both a more powerful noradrenergic mechanism to suppress spindles and a more weakly functioning mechanism to activate BSEs. Hence possibilities 3 and 4 may both be correct.(ABSTRACT TRUNCATED AT 250 WORDS)