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Scorching-hot muscle worship action! For these experiments, animals were handled for 3 days and habituated to the chamber (48 cm.times.38 cm.times.20 cm) on the day prior to the test session. At least five days after surgery, a single antisense oligonucleotide injection was diluted in water and delivered via a programmable infusion pump (Knopf) at a rate of 10 .mu.l/minute in a volume of 10 to 50 .mu.l. The oligomers were administered to mice by either intracerebroventricular (i.c.v.) injection or intrathecal injection. For one hour following the single injection of antisense oligonucleotide ICV or IT, animals were observed for behavioral side effects and scored for the severity of side effects on a scale of zero (no side effects) to 20 (convulsions resulting in euthanasia). Tau antisense oligonucleotide impact on spontaneous calcium oscillations in primary neurons is summarized in FIG. 4. See Murphy et al., J. Neurosci. As discussed in Example 2, the effect of therapeutic proteins on primary neuronal spontaneous calcium oscillations will be measured under two conditions, in the presence and absence of 1 mM MgCl.sub.2 as described previously (Murphy et. Antisense oligomer inhibition of spontaneous calcium oscillations mediated by either NMDA or AMPA was assessed in the presence or absence of 1 mM MgCl.sub.2 (representing 100% control in each case; FIG. 2). Addition of 25 .mu.M antisense oligomers (ASO) inhibited AMPA receptor but not NMDA receptor mediated oscillations (FIG. 2). ASOs, and other oligomers that behaved similarly, were shown to negatively impact central nervous system (CNS) network activity in vivo and electrophysiologic spontaneous neuronal activity in vitro (data not shown).



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