Search Results

This chapter argues that spontaneously occurring brain rhythms during slow wave sleep (SWS) produce plastic changes in thalamic and neocortical neurons. It discusses the role played by augmenting responses elicited by stimuli at 10 Hz, which are the experimental model of sleep spindles, in producing plastic changes in neuronal properties through the rhythmic repetition of spike-bursts and spike-trains fired by thalamic and cortical neurons.

In patients with tinnitus, structural and functional brain imaging combined with electro- and magnetoencephalograms have suggested correlations between aspects of tinnitus and brain functioning. Participating brain regions are among others in the auditory cortex, in the limbic system and in the cerebellum. Spontaneous EEG and MEG points to a reduction of alpha-band activity and an increase in delta- and gamma-band activity. The strength of the latter appears to correlate well with tinnitus loudness, whereas that of the alpha- and delta-band relates more to the level of annoyance caused by the tinnitus. The clear changes in spontaneous synchrony in the MEG activity between different neocortical areas in tinnitus patients also suggest wide involvement of brain areas in this disorder.

In humans with tinnitus, changes in the synchrony between neural activity recorded with scalp electrodes are found. This suggests that large-scale cortical networks show higher synchrony in the gamma band and reduced synchrony in the alpha band. At the level of local circuits in cat auditory cortex increased spike firing synchrony is observed in conjunction with increased spontaneous firing rates. Such local synchrony could facilitate synchronous activity along fiber tracts connecting widely spaced cortical areas and hence result in more efficient information transfer. Tinnitus could thus be the consequence of the formation of a large-scale neural assembly in cortex that is especially pronounced during silence, but can be disrupted by external sound and may be modifiable by attention.

The functional role of neural synchrony is reflected in cortical tonotopic map reorganization and in the emergence of pathological phenomena such as autism, schizophrenia and epilepsy. First of all experimenter-centered and subject-centered views of neural activity will be contrasted; this argues against the use of stimulus-correction procedures of cross-correlograms and favors the use of a correction procedure based on neural activity without reference to stimulus timing. Within a cortical column neurons fired synchronously with on average about 6% of their spikes in a 1 ms bin and occasionally showing 30% or more of such coincident spikes. For electrode separations exceeding 200 µm the average peak correlation strength only occasionally reached 3%. The experimental evidence for coincidence of neural activity, neural correlation and neural synchrony shows that horizontal fibers activity can induce strong neural correlations. Cortico-cortical connections for a large part connect cell groups with characteristic frequencies differing by more than one octave. Such neurons have generally non-overlapping receptive fields but still can have sizeable peak cross-correlations. Correlated neural activity and heterotopic neural interconnections are presented as the substrates for cortical reorganization. The macroscopic appearance of brain rhythms in the gamma frequency range, which have been linked to cognition, are due to synchronized spiking of inhibitory interneurons. The gamma cycle could thus implement of a temporal coding scheme that enables fast processing and flexible routing of activity, supporting fast selection and binding of distributed responses. This links cortical reorganization with synchrony changes potentially underlying temporal processing deficits in neurological disorders.

Synchronization of oscillatory responses in the beta- and gamma-band is involved in a variety of cognitive functions, such as perceptual grouping, attention-dependent stimulus selection, working memory, and perceptual awareness. Here, we review evidence that autism (ASD), schizophrenia and epilepsy show temporal processing deficits that are associated with abnormal neural synchronization. There are close correlations between abnormalities in neuronal synchronization and cognitive dysfunctions, emphasizing the importance of temporal coordination. ASD is a developmental disability that affects social behavior and language acquisition. Current theories and experimental data converge on the notion that dysfunctional integrative mechanisms in autism may be the result of reduced neural synchronization. There is also consistent evidence that neural synchrony in the β‎- and γ‎-frequency ranges is impaired in patients with schizophrenia. The cognitive abnormalities in schizophrenic patients include fragmented perception, erroneous binding of features, deficits in attention, impaired working memory, delusions, and hallucinations. Synchronization of oscillatory activity in the beta- and gamma-band frequency range is associated with cognitive functions that are disturbed in schizophrenia patients. Epilepsy is a common and diverse set of chronic neurological disorders characterized by seizures. Seizures may not only be a consequence of heightened neuronal excitability such as results from an imbalance between excitatory and inhibitory mechanisms. Alterations of the mechanisms that support the oscillatory patterning and the synchronization of neuronal activity appear to be equally important. Both the reduced synchronization preceding some forms of epileptic activity and the enhanced synchronization associated with seizures proper go along with the disturbance of cognitive functions. There are suggestive genetic links between schizophrenia and epilepsy, between schizophrenia and dyslexia via magnocellular deficits, and between autism and SLI through impaired language.