Bottom-up gamma maintenance in various disorders

Abstract

Maintained gamma band activity is a key element of higher brain function, participating in perception, executive function, and memory. The pedunculopontine nucleus (PPN), as part of the reticular activating system (RAS), is a major source of the "bottom-up" flow of gamma activity to higher regions. However, interruption of gamma band activity is associated with a number of neurological and psychiatric disorders. This review will focus on the role of the PPN in activating higher regions to induce arousal and descending pathways to modulate posture and locomotion. As such, PPN deep brain stimulation (DBS) can not only help regulate arousal and stepping, but continuous application may help maintain necessary levels of gamma band activity for a host of other brain processes. We will explore the potential future applications of PPN DBS for a number of disorders that are characterized by disturbances in gamma band maintenance.

Aberrant Sensory Gating of the Primary Somatosensory Cortex Contributes to the Motor Circuit Dysfunction in Paroxysmal Kinesigenic Dyskinesia

“…Brain oscillations at different frequencies detected via MEG represent the neural networking of various brain functions. Oscillations in the gamma frequency band (30 to 100 Hz) are driven by “bottom-up” brain processing which involves the activation of lower brain centers by sensory events such that the information moves to higher centers to promote perception ( 2 , 3 ). The role of synchronized gamma oscillations in sensory gating, binding of information from various regions into a united whole, has been recognized as an important mechanism of automatic cortical inhibition ( 4 , 5 ).…”

Local and Relayed Effects of Deep Brain Stimulation of the Pedunculopontine Nucleus

“…This agent is therefore effective in increasing coherence through increased coupling, especially at higher frequencies of activity due to the decrease in GABAergic tone. As such, it represents a potential adjunct to the treatment of neurological and psychiatric disorders that manifest decreases or dysregulation in gamma band activity [45]. Issue 4.…”

“…Moreover, the gamma band activity generated at the level of the cortex manifests coherence in the EEG across distant cortical sites during waking, but not during REM sleep. That is, gamma band activity during waking is different than gamma band activity during REM sleep (see review in [45]).…”

“…The proteins modulated normally by gamma band oscillations that were blocked by TSA were related to intracellular calcium regulation, namely, calcineurin (a calcium- and calmodulin-dependent phosphatase), neuronal nitric oxide synthase (enzyme found in PPN cholinergic neurons at high levels), and neuronal calcium sensor protein-1 (over expressed in schizophrenia and bipolar disorder, and modulates gamma oscillations) [41,45]. Issue 9.…”

“…This calls into question the interpretation of behavioral assays, for example, measures of sleep–wake rhythms, anxiety, fear, or depression tests, mainly because of the long latency between optic stimulation and the behavioral change. Thirdly, stimulation to induce locomotion, as described above, typically has a latency of ~1 s; however, optogenetic stimulation normally takes 10–20 s to induce an effect [45]. These abnormally long latencies to generate a behavior sheds doubt on the assessment of whether an animal falls sleep or awakens in direct response to optogenetic stimulation.…”