The ability of glycogen, the depot into which excess glucose is stored in mammals, to act as a source of rapidly available energy substrate, has been exploited by several organs for both general and local advantage. The liver, expressing the highest concentration of glycogen maintains systemic normoglycemia ensuring the brain receives a supply of glucose in excess of demand. However the brain also contains glycogen, although its role is more specialized. Brain glycogen is located exclusively in astrocytes in the adult, with the exception of pathological conditions, thus in order to benefit neurons, and energy conduit (lactate) is trafficked inter-cellularly. Such a complex scheme requires cell type specific expression of a variety of metabolic enzymes and transporters. Glycogen supports neural elements during withdrawal of glucose, but once the limited buffer of glycogen is exhausted neural function fails and irreversible injury ensues. Under physiological conditions glycogen acts to provide supplemental substrates when ambient glucose is unable to support function during increased energy demand. Glycogen also supports learning and memory where it provides lactate to neurons during the conditioning phase of in vitro long-term potentiation (LTP), an experimental correlate of learning. Inhibiting the breakdown of glycogen or intercellular transport of lactate in in vivo rat models inhibits the retention of memory. Our current understanding of the importance of brain glycogen is expanding to encompass roles that are fundamental to higher brain function.

Altered performance monitoring is implicated in obsessive-compulsive disorder (OCD), Gilles de la Tourette syndrome (GTS), attention-deficit/hyperactivity disorder (ADHD) and autism. We conducted a systematic review and meta-analysis of electrophysiological correlates of performance monitoring (error-related negativity, ERN; error positivity, Pe; feedback-related negativity, FRN; feedback-P3) in individuals with OCD, GTS, ADHD or autism compared to control participants, or associations between correlates and symptoms/traits of these conditions. Meta-analyses on 97 studies (5890 participants) showed increased ERN in OCD (Hedge's g=0.

Altered performance monitoring is implicated in obsessive-compulsive disorder (OCD), Gilles de la Tourette syndrome (GTS), attention-deficit/hyperactivity disorder (ADHD) and autism. We conducted a systematic review and meta-analysis of electrophysiological correlates of performance monitoring (error-related negativity, ERN; error positivity, Pe; feedback-related negativity, FRN; feedback-P3) in individuals with OCD, GTS, ADHD or autism compared to control participants, or associations between correlates and symptoms/traits of these conditions. Meta-analyses on 97 studies (5890 participants) showed increased ERN in OCD (Hedge’s g=0.54[CIs:0.44,0.65]) and GTS (g=0.99[CIs:0.05,1.93]). OCD also showed increased Pe (g=0.51[CIs:0.21,0.81]) and FRN (g=0.50[CIs:0.26,0.73]). ADHD and autism showed reduced ERN (ADHD: g=-0.47[CIs:-0.67,-0.26]; autism: g=-0.61[CIs:-1.10,-0.13]). ADHD also showed reduced Pe (g=-0.50[CIs:-0.69,-0.32]). Implications of these findings in terms of shared and distinct performance monitoring alterations across these neurodevelopmental conditions are discussed.