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Development of sensory gamma oscillations and cross-frequency coupling from childhood to early adulthood.

ABSTRACT: Given the importance of gamma oscillations in normal and disturbed cognition, there has been growing interest in their developmental trajectory. In the current study, age-related changes in sensory cortical gamma were studied using the auditory steady-state response (ASSR), indexing cortical activity entrained to a periodic auditory stimulus. A large sample (n = 188) aged 8-22 years had electroencephalography recording of ASSR during 20-, 30-, and 40-Hz click trains, analyzed for evoked amplitude, phase-locking factor (PLF) and cross-frequency coupling (CFC) with lower frequency oscillations. Both 40-Hz evoked power and PLF increased monotonically from 8 through 16 years, and subsequently decreased toward ages 20-22 years. CFC followed a similar pattern, with strongest age-related modulation of 40-Hz amplitude by the phase of delta oscillations. In contrast, the evoked power, PLF and CFC for the 20- and 30-Hz stimulation were distinct from the 40-Hz condition, with flat or decreasing profiles from childhood to early adulthood. The inverted U-shaped developmental trajectory of gamma oscillations may be consistent with interacting maturational processes-such as increasing fast GABA inhibition that enhances gamma activity and synaptic pruning that decreases gamma activity-that may continue from childhood through to adulthood.

SUBMITTER: Cho RY

PROVIDER: S-EPMC4428298 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature

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Development of sensory gamma oscillations and cross-frequency coupling from childhood to early adulthood.

Cho Raymond Y RY Walker Christopher P CP Polizzotto Nicola R NR Wozny Thomas A TA Fissell Catherine C Chen Chi-Ming A CM Lewis David A DA

Cerebral cortex (New York, N.Y. : 1991) 20131210 6

Given the importance of gamma oscillations in normal and disturbed cognition, there has been growing interest in their developmental trajectory. In the current study, age-related changes in sensory cortical gamma were studied using the auditory steady-state response (ASSR), indexing cortical activity entrained to a periodic auditory stimulus. A large sample (n = 188) aged 8-22 years had electroencephalography recording of ASSR during 20-, 30-, and 40-Hz click trains, analyzed for evoked amplitud ...[more]

PMID: 24334917

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Project description:Introduction: Treatment-resistant depression, post-traumatic stress disorder, chronic pain, and L-DOPA-induced dyskinesia in Parkinson's disease are characterized by hypersynchronous neural oscillations. Sub-anesthetic ketamine is effective at treating these conditions, and this may relate to ketamine's capacity to reorganize oscillatory activity throughout the brain. For example, a single ketamine injection increases gamma (?40 Hz) and high-frequency oscillations (HFOs, 120-160 Hz) in the cortex, hippocampus, and striatum. While the effects of single injections have been investigated, clinical ketamine treatments can involve 5-h up to 3-day sub-anesthetic infusions. Little is known about the effects of such prolonged exposure on neural synchrony. We hypothesized that hours-long exposure entrains circuits that generate HFOs so that HFOs become sustained after ketamine's direct effects on receptors subside. Methods: Local-field recordings were acquired from motor cortex (M1), striatum, and hippocampus of behaving rats (n = 8), and neural responses were measured while rats received 5 ketamine injections (20 mg/kg, i.p., every 2 h, 10-h exposure). In a second experiment, the same animals received injections of D1-receptor antagonist (SCH-23390, 1 mg/kg, i.p.) prior to ketamine injection to determine if D1 receptors were involved in producing HFOs. Results: Although HFOs remained stable throughout extended ketamine exposure, broad-band high-frequency activity (40-140 Hz) in the hippocampus and delta-HFO cross-frequency coupling (CFC) in dorsal striatum increased with the duration of exposure. Furthermore, while ketamine-triggered HFOs were not affected by D1 receptor blockade, ketamine-associated gamma in motor cortex was suppressed, suggesting involvement of D1 receptors in ketamine-mediated gamma activity in motor cortex. Conclusion: Prolonged ketamine exposure does not enhance HFOs in corticostriatal circuits, but, instead, enhances coordination between low and high frequencies in the striatum and reduces synchrony in the hippocampus. Increased striatal CFC may facilitate spike-timing dependent plasticity, resulting in lasting changes in motor activity. In contrast, the observed wide-band high-frequency "noise" in the hippocampus suggests that ketamine disrupts action-potential timing and reorganizes connectivity in this region. Differential restructuring of corticostriatal and limbic circuits may contribute to ketamine's clinical benefits.

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Dataset Information

Development of sensory gamma oscillations and cross-frequency coupling from childhood to early adulthood.

Publications

Development of sensory gamma oscillations and cross-frequency coupling from childhood to early adulthood.

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