Gamma-band Synchronization & Cortical Columns
Gamma-band synchronization has been an area of interest as a psychophysical hypothesis in perceptual binding since the late 1980’s (Fries, 2009) We recently suggested an alternative interpretation as to how this is involved in higher cortical processes (Moss, Hunter, Shah, & Havens, 2012). The literature we cited suggests early in development that thalamic gamma oscillations allow the formation of columns in the primary sensory cortex. This pattern then progresses across the cortex. Our suggestion is that the column is the binary unit involved in all cortical processing and memory storage. The rate of cell-firing frequency in the gamma range is involved in the dynamic formation of columns in which only the outermost neurons are synchronized. This allows column-sized (0.4 to 1.0 mm) information bits in which only a fraction of the neurons of the column are committed to that bit. Overlapping columns are believed to exist based on several studies we cited, and this is believed to allow for the necessary large volume requirement to be the cortical bit.
The theorized process of new and relevant stimulus input would go something like this. Once sensory information arrives at the cortex, the primary sensory cortical columns activate. Where efferent activity crosses is the location a new column forms, with the new column also reflecting the gamma frequency. Each posterior sensory column has a corresponding frontal action column which forms. In new association memories this leads to activation of the medial temporal lobe columns which project to the hippocampus. The hippocampal cells are activated and serve as the pacemakers for a hippocampo-thalamo-cortico-hippocampo circuit with gamma-frequency oscillations generated on the background of theta oscillations. We reviewed one study that showed a greater area of cortical activation happens at the low frequency while the gamma frequency activity activates column sized areas. GABA was implicated as the neurotransmitter involved in limiting the column-sized spread of activity at the gamma frequency range. The maintenance of activity in any given circuit of columns allows the strengthening of synaptic connections among the columns involved a new memory. Thus, instead of the current predominant view that association memories are first “stored” in the hippocampus and later somehow transferred to other locations such as the cortex, this theory says the columns originally involved in processing are the same as those involved in the memory and hippocampal activity is critical in facilitating the cortical memory. It seems likely that there are other frequency-to-size cortical tissue activation patterns as well. For example, beta activity has been shown (Wróbel, 2000) to be involved with attention. This may indicate a cortical area involving a large number of columns has increased activity such that when the expected stimulus occurs, the involved columns are primed to respond faster.
Being a clinician, I always think at an application level. If what we have suggested is accurate there can be implications for a better understanding of disorders. For instance, involvement of the hippocampus is seen early in the course of Alzheimer’s disease. As mentioned, we proposed that memories are stored at the cortical level, but the hippocampus acts in the role of starter and pacemaker in a circuit that goes from the hippocampus to the thalamus to the cortex and back to the hippocampus. By maintaining the activity in the circuit, the synaptic connections among columns are strengthened which is the definition of memory formation. Hippocampal neurons set the pattern in the circuit. If disrupted or damaged, then the hippocampal neurons may lack the ability to maintain the gamma frequency firing rate which would prevent the cortical columns from forming the associated memory. Interestingly, the cholinesterase inhibitors used in the treatment of early Alzheimer’s increase the availability of acetylcholine (ACh) at the cortical level. An action of ACh is to increase the ease with which cortical neurons fire (Krnjević, Pumain, & Renaud, 1971), which increases cell firing rates. By increasing the firing rates, this can feasibly allow dynamic formation of columns once again with the clinical finding of improved memory.
In relation to schizophrenia, it has been suggested that there is a fundamental disturbance throughout the cortex in neuronal connectivity and communication (Phillips & Silverstein, 2003). The poor coordination view has been supported by the fact that in schizophrenia there are various forms of reduced stimulus organization (e.g., memory and thought organization). There are multiple circuits of columns within each hemisphere and poor coordination among these circuits might be the level at which the cognitive coordination breaks down. For example, failure of frontal action columns’ control in coordinating other frontal and posterior columns, or the failure to form associative memory columns in the temporal cortex, may leave the circuits of columns in distal cortical areas unconnected or in conflict. This could feasibly lead to thought disorganization in which different perceptions result from simultaneous activation of separate circuits with poor coordination of which is in control.
At the receptor level, glutamatergic NMDARs are voltage dependent and it seems these are likely those involved at the gamma frequency range associated with dynamic column formation. The theory can also explain that sleep-dependent memory consolidation happens as a function of the activation of cortical column circuits via thalamic activation which allows the strengthening of the columnar synaptic connections and would be reflected in higher frequency EEG patterns. These are just a few of the possibilities that the columnar-based Dimensional Systems Model suggests in relation to an applied Clinical Biopsychological Model.
Fries, P. (2009). Neuronal gamma-band synchronization as a fundamental process in cortical computation. Annual Review of Neuroscience, 32, 209–224. doi: 10.1146/annurev.neuro.051508.13560
Krnjević, K., Pumain, R., & Renaud, L. (1971). The mechanism of excitation by acetylcholine in the cerebral cortex. The Journal of physiology, 215(1), 247-268.
Moss, R. A., Hunter, B. P., Shah, D., & Havens, T. (2012). A theory of hemispheric specialization based on cortical columns. Journal of Mind and Behavior, 33, 141-172.
Moss, R. A. (2006). Of bits and logic: Cortical columns in learning and memory. The Journal of Mind and Behavior, 27, 215-246.
Phillips, W. A., & Silverstein, S. M. (2003). Impaired cognitive coordination in schizophrenia: Convergence of neurobiological and psychological perspectives. Behavioral and Brain Sciences, 23, 65-138.