Cerebellar D1DR-expressing neurons modulate the frontal cortex during timing tasks.

Converging lines of evidence suggest that the cerebellum plays an integral role in cognitive function through its interactions with association cortices like the medial frontal cortex (MFC). It is unknown precisely how the cerebellum influences the frontal cortex and what type of information is reciprocally relayed between these two regions. A subset of neurons in the cerebellar dentate nuclei, or the homologous lateral cerebellar nuclei (LCN) in rodents, express D1 dopamine receptors (D1DRs) and may play a role in cognitive processes. We investigated how pharmacologically blocking LCN D1DRs influences performance in an interval timing task and impacts neuronal activity in the frontal cortex. Interval timing requires executive processes such as working memory, attention, and planning and is known to rely on both the frontal cortex and cerebellum. In our interval timing task, male rats indicated their estimates of the passage of a period of several seconds by making lever presses for a water reward. We have shown that a cue-evoked burst of low-frequency activity in the MFC initiates ramping activity (i.e., monotonic increases or decreases of firing rate over time) in single MFC neurons. These patterns of activity are associated with successful interval timing performance. Here we explored how blocking right LCN D1DRs with the D1DR antagonist SCH23390 influences timing performance and neural activity in the contralateral (left) MFC. Our results indicate that blocking LCN D1DRs impaired some measures of interval timing performance. Additionally, ramping activity of MFC single units was significantly attenuated. These data provide insight into how catecholamines in the LCN may drive MFC neuronal dynamics to influence cognitive function.

The left temporal pole is a convergence region mediating the relation between names and semantic knowledge for unique entities: Further evidence from a "recognition-from-name" study in neurological patients.

Prior research has implicated the left temporal pole (LTP) as a critical region for naming semantically unique items, including famous faces, landmarks, and musical melodies. Most studies have used a confrontation naming paradigm, where a participant is presented with a stimulus and asked to retrieve its name. We have proposed previously that the LTP functions as a two-way, bidirectional convergence region brokering between conceptual knowledge and proper names for unique entities. Under this hypothesis, damage to the LTP should result in a "two way" impairment: (1) defective proper name retrieval when presented with a unique stimulus (as shown in prior work); and (2) defective concept retrieval when presented with a proper name. Here, we directly tested the second prediction using a "recognition-from-name" paradigm. Participants were patients with LTP damage, brain-damaged comparisons with damage outside the LTP, and healthy comparisons. Participants were presented with names of famous persons (e.g., "Marilyn Monroe"), landmarks (e.g., "Leaning Tower of Pisa"), or melodies (e.g., "Rudolph the Red-Nosed Reindeer") and were asked to provide conceptual knowledge about each. We found that individuals with damage to the LTP were significantly impaired at conceptual knowledge retrieval when given names of famous people and landmarks (but this finding did not hold for melodies). This outcome supports the theory that the LTP is a bidirectional convergence region for proper naming, but suggests that melody retrieval may rely on processes different from those supported by the LTP.

Musical anhedonia after focal brain damage.

People listen to music because it is pleasurable. However, there are individual differences in the reward value of music. At the extreme low end of this continuum, individuals who derive no pleasure from music are said to have 'musical anhedonia.' Cases of acquired musical anhedonia following focal brain damage are rare, with only a handful having been reported in the scientific literature. Here, we surveyed a large sample of patients with focal brain damage to identify the frequency, specificity, and neural correlates of acquired musical anhedonia. Participants completed the Musical anhedonia Questionnaire and the Barcelona Music Reward Questionnaire (Mas-Herrero et al., 2013) to assess changes in musical enjoyment and reward following brain injury. Neuroanatomical data were analyzed with a proportional MAP-3 method to create voxelwise lesion proportion difference maps. No clear or consistent neuroanatomical correlates of musical anhedonia were identified. One patient with damage to the right-hemisphere putamen and internal capsule displayed specific and severe acquired musical anhedonia. These findings indicate that acquired musical anhedonia is very uncommon, a result which is consistent with the fact that only a small number of such cases have been reported in the literature. This rarity could have positive implications for the therapeutic potentialities of music in patients with severe neurological disorders.