The Declarative/Procedural Model of Pinker, Ullman and colleagues claims that the basal ganglia are part of a fronto-striatal procedural memory system which applies grammatical rules to combine morphemes (the smallest meaningful units in language) into complex words (e.g. talk-ed, talk-ing). We tested this claim b y investigating whether striatal damage or loss of its dopaminergic innervation is reliably associated with selective regular past tense deficits in patients wi th subcortical cerebrovascular damage, Parkinson’s disease or Huntington’s dis ease.We focused on past tense morphology since this allows us to contrast the re gular past tense (jump-jumped), which is rulebased,with the irregular past tens e (sleep-slept), which is not We used elicitation and priming tasks to test pat ients’ability to comprehend and produce inflected forms. We found no evidence o f a consistent association between striatal dysfunction and selective impairment of regular past tensemorphology, suggesting that the basal ganglia are not esse ntial for processing the regular past tense as a sequence of morphemes, either i n comprehension or production, in contrast to the claims of the Declarative/Proc edural Model. All patient groups showed normal activation of semantic and morpho logical representations in comprehension, despite difficulties suppressing seman tically appropriate alternatives when trying to inflect novel verbs. This is con sistent with previous reports that striatal dysfunction spares automatic activat ion of linguistic information, but disrupts later language processes that requir e inhibition of competing alternatives. The Declarative / Procedural Model of Pinker, Ullman and colleagues claims that the basal ganglia are part of a fronto-striatal procedural memory system that applies grammatical rules to combine morphemes (the smallest meaningful units in language) into complex words (eg talk-ed, talk-ing). We tested this claim by investigating whether striatal damage or loss of its dopaminergic innervation is reliably associated with selective past past tense deficits in patients wi th subcortical cerebrovascular damage, Parkinson’s disease or Huntington’s dis ease. We focused on past tense morphology since this allows us to contrast the re gular past tense (jump-jumped), which is rulebased, with the irregular past tens e (sleep-slept), which is not We used elicitation and priming tasks to test pat ients’ability to comprehend and produce inflected forms. We found no evidence of a consistent association between striatal dysfunction and selective impairment of regular past tensemorphology, suggestin g that the basal ganglia are not esse ntial for processing the regular past tense as a sequence of morphemes, either in comprehension or production, in contrast to the claims of the Declarative / Proc edural Model. All patient groups showed normal activation of semantic and morpho This is con sistent with previous reports that striatal dysfunction spares automatic activat ion of linguistic information, but disrupts later language processes that requir e inhibition of competing alternatives.