Catecholamine regulation of neocortical spindling in DBA/2 mice

The waking EEG of DBA/2 mice is punctuated by conspicuous bursts of high-amplitude, 6-7-cps spindles. Catecholamine depletion by 2.0 mg/kg, i.p., reserpine or 120 mg/kg, i.p., alpha-methyl-p-tyrosine increased the occurrence and duration of these brief spindle episodes (BSEs). This effect may reflect noradrenergic depletion because the beta-noradrenergic antagonist propranolol (10 mg/kg, i.p.) powerfully promoted BSE occurrence and increased BSE duration in freely-moving and midpontine-transected mice, whereas the dopamine antagonist haloperidol (2.0 mg/kg, i.p.) neither increased nor decreased BSE occurrence. The alpha-noradrenergic agonist clonidine (0.05 mg/kg, i.p.), which is known to inhibit noradrenergic neuronal firing as well as act at postsynaptic alpha receptors, also promoted BSE occurrence in transected mice. In addition, the dopamine agonist apomorphine (2.0 mg/kg, i.p.) increased BSE occurrence in freely-moving mice once the behavioral activation it produced subsided. These effects were blocked by 2.0 mg/kg haloperidol, i.p. The convulsant drug pentylenetetrazol, which is known to promote BSE occurrence at subconvulsant doses in DBA/2 mice, may activate BSEs, in part, by activating dopamine neurons: 2.0 mg/kg haloperidol, i.p., partially blocked the facilitation of BSEs by 20 mg/kg pentylenetetrazol, i.p., in midpontine DBA/2 mice. Thus, noradrenergic neurons may block spindle occurrence in DBA/2 mice whereas dopamine neurons may be one of several systems that can promote spindle occurrence.