Abstract
The basal ganglia (BG) are a group of interconnected nuclei which play a pivotal part in limbic, associative, and motor functions. This role is mirrored by the wide range of motor and behavioral abnormalities directly resulting from dysfunction of the BG. Studies of normal behavior have found that BG neurons tend to phasically modulate their activity in relation to different behavioral events. In the normal BG, this modulation is highly specific, with each neuron related only to a small subset of behavioral events depending on specific combinations of movement parameters and context. In many pathological conditions involving BG dysfunction and motor abnormalities, this neuronal specificity is lost. Loss of specificity (LOS) manifests in neuronal activity related to a larger spectrum of events and consequently a large overlap of movement-related activation patterns between different neurons. We review the existing evidence for LOS in BG-related movement disorders, the possible neural mechanisms underlying LOS, its effects on frequently used measures of neuronal activity and its relation to theoretical models of the BG. The prevalence of LOS in a many BG-related disorders suggests that neuronal specificity may represent a key feature of normal information processing in the BG system. Thus, the concept of neuronal specificity may underlie a unifying conceptual framework for the BG role in normal and abnormal motor control.
Highlights
We have shown that during the expression of motor tics, Loss of specificity (LOS) was accompanied by an altered increase/decrease ratio of globus pallidus internus (GPi) movement-related activity compared to this ratio in intact animals, with phasic rate decreases becoming more frequent (McCairn et al, 2009)
Summary Neuronal specificity emerges as a key feature of information processing in the normal basal ganglia (BG)
Loss of specificity of neuronal encoding is a main feature in BG dysfunction
Summary
Reviewed by: Peter Redgrave, University of Sheffield, UK Thomas Wichmann, Emory University, USA. Animal models and anecdotal findings in human patients confirmed that localized dysfunctions (inactivation or disinhibition) of different parts of the BG could directly induce behavioral abnormalities similar to the symptoms observed in these disorders (Martin and Alcock, 1934; Crossman et al, 1988; Hamada and DeLong, 1992; Grabli et al, 2004; Desmurget and Turner, 2008; McCairn et al, 2009; Bronfeld et al, 2010). One physiological phenomenon is common to many BG-related disorders: neuronal loss of specificity (LOS) In many of these pathological conditions, individual BG neurons lose their characteristic selective movement-related activity profiles and instead display similar activity modulations related to a broader range of behavioral events (Figure 1). Recording of neuronal activity from the BG of human PD patients has recently become possible due to the use of
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