A comparison of the effects of localized brain administration of catecholamine and protein synthesis inhibitors on memory processing.

Protein synthesis inhibitors disrupt biosynthetic processes thought to control the formation of long-term memory. While the agents used (i.e. puromycin, acetoxycycloheximide, cycloheximide and anisomycin) do not selectively inhibit the synthesis of any particular class of protein, it has generally been hypothesized or assumed that the critical proteins(s) is structural and necessary for modification and/or growth of synapses. Recent reports indicated that all of the protein synthesis inhibitors causing amnesia inhibited tyrosine hydroxylase activity. Tyrosine hydroxylase is needed for the conversion of tyrosine to dopamine (DA) and norpinephrine (NE); altering the level of this enzyme could affect catecholamine (CA) turnover. Since drugs known to inhibit CA synthesis cause amnesia, it is of considerable interest whether amnesia induced by protein synthesis inhibitors depends basically on inhibition of CA synthesis.