it has been known since the work of e. d. adrian ( adrian , 1950 ) that cognitive states can be associated with brain rhythms and that specific spectral content can be localized to specific areas of the brain . since then , there have been numerous studies linking a variety of cognitive tasks to more detailed data about brain rhythms and their interactions . however , a fundamental issue is still mysterious : what roles , if any , do rhythms play in cognition ? the first is that  function  is tightly tied to physiological and dynamical properties of a given rhythm , not just its frequency . the second is that the connection between rhythms and function can be better understood if the latter is construed in terms of  useful computation  rather than the end - product of that computation , such as attention , memory , learning , etc . for example , as discussed below , physiology matters to the creation and manipulation of cell assemblies ( harris et al . , different rhythms are associated with different underlying physiology , they can participate differently in the computation of cell assembly creation . as a second example , we consider interactions of different brain regions via oscillations ( fries , 2005 ) . as discussed more fully below , changes in the modulatory setting of the rhythms can change the flow of information through cortical circuits , again tying physiology to computation . by  cell assemblies  , we will mean subsets of pyramidal cells that fire approximately synchronously in a transient manner , whether or not those cells have recurrent excitatory connections . models show that gamma rhythms , especially the so - called  pyramidal - interneuron network gamma are especially good at creating cell assemblies ( olufsen et al . , 2003 ) . the ping rhythm is fundamentally an interaction between fast spiking ( fs ) interneurons and excitatory pyramidal cells . the zeroth order description of the mechanism is straightforward : the pyramidal cells excite the fs cells , which then inhibit both the pyramidal cells and themselves ; when the inhibition wears off , the pyramidal cells fire again . thus , the period of the gamma rhythm is tightly tied to the decay time of the inhibition , though it is also affected by the level of excitatory drive to the pyramidal cells . there is another kind of gamma rhythm that is important in function : the persistent gamma rhythm ( traub et al . , 2000 ) , which can be obtained in vitro by exposing neuronal networks to the neuromodulators kainate or carbachol . in this version of the gamma rhythm , pyramidal cells fire sparsely , and the rhythm is maintained by the fs cells , which fire on almost every cycle . persistent gamma requires noisy activation of the pyramidal cells , which is believed to be provided by ectopic spiking of pyramidal cells and amplification by an axonal plexus ( traub et al . inhibition is critical in both kinds of in vitro gamma ( whittington et al . , 2000 ) . the role of the inhibition in gamma rhythms was discovered in vitro , but has been corroborated in vivo ( atallah and scanziani , 2009 ; cardin et al . , 2009 ) . the physiology of ping provides an excellent setting for the creation and protection of cell assemblies . increased tonic input to a subset of pyramidal cells ( either not previously activated or participating in persistent gamma ) can create ( approximately ) synchronous firing in that subset in a ping rhythm , while other pyramidal cells in the network are suppressed ( figure 1 ) . models suggest that the essential reason for this competition is that the stronger input defines the firing rate of the inhibitory cells and entrains the target network ; the stronger input then arrives just before the next bout of inhibition , when the inhibition is lowest , while the weaker input , which excites its targets more slowly , arrives when inhibition is higher ( borgers et al . , 2005 , 2008 ) . we think of the persistent gamma as a background state in which further inputs can create a ping rhythm ( borgers et al . , 2005 ) . upper left : a cartoon representation of two interacting cell populations that generate a persistent gamma rhythm ; circles labeled  e  represent pyramidal cells and the two cell populations are reciprocally connected with excitatory ( green ) and inhibitory ( red ) synapses from each cell to all other cells . upper right : cartoon example of the spiking activity of the two cell populations during persistent gamma activity . each tick mark represents an action potential ( or spike ) of an e ( green ) or i ( red ) cell . in each cycle of the persistent gamma rhythm , when the inhibition decays sufficiently , one of the pyramidal cells generates another spike , and the rhythm continues . lower : increased depolarizing input to a subset of pyramidal cells ( yellow box on the left ) increases their spiking activity . the population gamma rhythm continues with the  driven  pyramidal cells ( yellow box on the right ) dominating the excitatory activity . it has been shown via modeling that the windowing of inhibition in the persistent gamma oscillation makes it easier for a weak input to create a cell assembly than if the same level of inhibition is more spread out in time ( borgers et al . , 2005 ) . another connection to attention is the ability of a coherent oscillatory source with a gamma frequency to create and lock to a gamma oscillation in the target network , locking out the effects of other input sources , even when the latter have somewhat greater amplitude ( borgers et al . , 2008 ) . the lock - out effect comes from the fact that the feed - forward inhibition produced by the more coherent input is active during the less coherent other input ; the importance of the gamma frequency input is that the frequency of the rhythm in the target is tied to the decay time of inhibition , and hence a gamma frequency input produces feed - forward inhibition at an optimal frequency to keep all but the most coherent input locked out . since attention is associated with more coherence in the gamma range in most reports ( tiitinen et al . , 1993 ; fries et al . , 2008 ; jung et al . , 2008 ; , 2010 ; but see chalk et al . , 2010 ) , it can bias competition in the input at a downstream structure . finally , results about firing rate changes associated with selective attention ( reynolds et al . , 1999 ) can be understood via changes in gamma - producing networks in response to cholinergic modulation ( borgers et al . . for other observations about gamma and attention , see buia and tiesinga ( 2006 ) and ardid et al . the physiology of the gamma rhythm supports the ability of the networks of excitatory and inhibitory neurons to produce gamma . however , the properties of this rhythm , including the tendency of cell assemblies to compete instead of cooperate , makes it difficult to use the ping rhythm to coordinate and manipulate multiple cell assemblies , as needed for some higher - order processing . we suggest below that other rhythms may play these roles , and how the specific physiological properties of other rhythms may contribute to that function . that other possible computations involving cell assemblies might be done with other rhythms is suggested by close study of the beta1 rhythm ( 15  hz ) in the rodent secondary somatosensory association cortex ( s2 ) ( roopun et al . , 2008 ) . this rhythm can appear in vivo after the stimulation that induces a gamma rhythm is over ( tallon - baudry et al . , 1999 ; haenschel et al . , 2000 ) . to mimic the basic features of this phenomenon in vitro , roopun et al . ( 2006 ) first produced a gamma rhythm in s2 evoked by a bath application of kainate ; subsequently , after 1  h , the kainate - mediated excitation is reduced using a kainate antagonist . in the initial , higher excitation regime , only the superficial layers produce the gamma ; the deep layer ( layer v ) produced a beta2 rhythm ( 25  hz ) . the gamma oscillation is the standard persistent gamma described above ; the beta2 oscillation is produced by intrinsic currents timed by the kinetics of the m - current ( a subthreshold potassium current modulated by muscarinic receptors ) and synchronized by gap junctions . when the kainate antagonist was added , the two independent rhythms both changed to the beta1 rhythm in a manner that was coordinated between the superficial and deep layers . this required some plasticity in the network , since an immediate removal of kainate did not produce the switch to beta1 . experiments and modeling have shown ( kramer et al . , 2008 ; roopun et al . , 2008 ) that the coordination between the layers is mediated by inhibitory rebound : excitation in layer v intrinsic bursting neurons ( ib cells ) excite superficial fs cells , which inhibit regular spiking ( rs ) superficial pyramidal cells , which respond by rebound and initiate a gamma cycle in the superficial layers . the spiking of the rs cells excites the low - threshold spiking interneurons ( lts cells ) , another population of inhibitory cells in the superficial layers , which inhibit the apical dendrites of the ib cells . the result is that the beta1 rhythm is a  concatenation  of one superficial layer gamma cycle followed by one deep layer beta2 cycle ; the period of the beta1 is indeed a sum of the periods of the gamma and beta2 ( figure 2 ) . thus , assemblies composed of superficial rs cells can co - exist with assemblies composed of deep layer ib cells , and fire at different times in the beta1 cycle . the fact that the beta1 operates through inhibitory rebound makes it possible for this rhythm to continue in the absence of continuing input , unlike the ping rhythm . ( a ) cross - correlogram showing stable phase relationship between layer 2/3 and layer 5 field potentials in association cortex ( s2 ) . when excitation is high , layer 2/3 generates a gamma rhythm ( c. 40  hz ) and layer 5 a beta2 rhythm ( c. 25  hz ) . reducing excitation then concatenates these two rhythms to generate a beta1 ( c. 15  hz ) frequency oscillation in both layers . ( b ) the asymmetric phase relationship seen for field potentials in ( a ) is also seen when comparing the timing of layer 2 units with layer 5 units . ( c ) intracellular recordings , relative to an on - going beta1 frequency field potential , show the sequence of outputs from different neurons . each beta1 period begins with a brief burst from layer 5 intrinsically bursting ( ib ) neurons . superficial regular spiking pyramids ( rs ) spike on the rebound of the resulting ipsp , triggering superficial low - threshold spiking interneurons ( lts ) to fire . ( d ) a cartoon representation of the important cell types in the beta1 rhythm . to the ping model in figure 1 , we add a population of low - threshold spiking ( lts ) interneurons and intrinsically bursting ( ib ) pyramidal cells . we note that the lts cells inhibit the ib cells , and that the ib cells form excitatory synapses onto all inhibitory cells . a cartoon rastergram is on the right . the beta1 rhythm results from a process of period concatenation . first , the ib cells spike ( 1 ) and cause the basket cells to spike ( 2 ) . the basket cells inhibit the superficial pyramidal cells ( 3 ) , which recover and spike after one gamma cycle . the superficial pyramidal cell spikes cause the basket and lts cells to spike ( 4 ) which inhibit the ib cells . the ib cells then recover and spike after one beta2 cycle ( interval indicated with beta2 label at bottom of this panel ) and the rhythm repeats . ( a  c ) adapted from roopun et al . ( 2008 ) . in hippocampus , where there is only a single pyramidal cell lamina , theta rhythms may work to both coordinate and separate cell assemblies formed within the gamma rhythm . for this we consider the nesting of gamma rhythms in the theta rhythm in the hippocampus ( bragin et al . , 1995 ) . the latter is believed to make use of the so - called oriens - lacunosum moleculare ( o - lm ) cell ( gillies et al . , 2002 ; goutagny et al . , 2009 ) , whose physiology has been studied ( saraga et al . , 2003 ; lawrence et al . it is known experimentally that a theta rhythm can be produced in purely inhibitory networks including the o - lm cells ( gillies et al . , 2002 ) , and modeling has suggested that the inhibitory interactions among o - lm cells alone do not produce a coherent theta rhythm because of the interaction of the inhibition with intrinsic currents in the o - lm cells , especially the mixed cation , hyperpolarization - activated , inward h - current ( rotstein et al . , 2005 ) . however , the interaction of the o - lm cells with fs cells can produce a coherent rhythm ( rotstein et al . , 2005 ) , with fast ipsps produced by the fs cells coordinated with the slow ipsps produced by the o - lm cells , as in ( gillies et al . , 2002 ) . when ampa transmission is not blocked , the ca1 network in vitro is capable of producing gamma , theta , or a nesting of the two ( gloveli et al . , 2005 ) , depending on how well the o - lm neuronal processes are preserved in the slice ( determined by the angle of cut during tissue preparation ) . modeling ( gloveli et al . , 2005 ; tort et al . , 2007 ) reveals that the nesting of the gamma in the theta rhythm can be explained from the o - lm  fs interneuronal interaction to form theta , and the overlapping network of pyramidal  fs cell interaction to form the gamma . the coordination of cell assemblies in the nesting of these rhythms depends on the underlying physiology . gamma rhythms can form in transverse slices , in which the o - lm axons project fairly locally . we considered multiple transverse slices (  modules  ) connected only by o - lm axons projecting to pyramidal cells of other modules . modeling using multiple compartment ( tort et al . , 2007 ) or single compartment ( kopell et al . , 2010 ) biophysical neurons showed that the o - lm input , with its long - lasting ipsps , can synchronize cell assemblies created by the pyramidal fs interaction in different modules ; for synchronization of subsets of pyramidal cells to happen , it is necessary that those subsets be involved in the gamma oscillation ( tort et al . . more recent work ( malerba , 2010 ) has shown that the phases of the gamma rhythm within the theta oscillation can depend on the connections within a module : if the synapses from the pyramidal cells to the o - lm cells are relatively stronger than those from the fs cells to the o - lm cells ( excitation - dominated or ed regime ) , the phases of the pyramidal cells cluster more highly than if the reverse is true ( inhibition - dominated or i d regime ) , leading to more coordination of cell assemblies ( figure 3a ) . modules in the ed regime can be well - synchronized if they are not too far apart in drive ( tort et al . , 2007 ) ; if they are sufficiently far apart in drive , separate cell assemblies co - exist ( figure 3b ) . there can be coordination of cell assemblies in the i d regime , but cell assemblies formed in the ed regime do not easily coordinate with those in the i d regime , providing a mechanism to separate cell assemblies ( figure 3c ) . we note that there is a similar dichotomy in firing patterns of pyramidal cells in hippocampal slices ( senior et al . , 2008 ) . these computational results suggest an alternative to the idea of sequential gamma slots within a theta cycle , each corresponding to a separate cell assembly ( jensen and lisman , 1996 ) . instead , the cell assemblies can be separated , while each one participates in multiple gamma cycles within a theta cycle . top , a module in the excitation - dominated ( ed ) regime ; red crosses mark the pyramidal cell spikes . the black diamonds mark the o - lm spikes at zero theta phase in all panels . bottom , a single module in inhibition dominated ( i d ) regime ; light blue crosses mark the pyramidal cell spikes . ( b ) two coupled modules , in identical ed regimes , receiving different gamma drives . the spike phases on top are for the pyramidal cell of the module that receives stronger gamma drive . the two cell assemblies do not synchronize ( tort et al . , 2007 ) . ( c ) two coupled modules , receiving identical gamma drive , in different excitation regimes . the red crosses mark activity of the module in ed regime , the light blue marks report activity of the module in i d regime . the theta phases of the gamma spikes in the i d regime do not cluster , so the two gamma signals in the two different modules have the same frequency but have different theta phases . the physiology of concatenated gamma and beta2 rhythms ( see different rhythms allow temporal segregation of multiple assemblies ) has important consequences for the formation and manipulation of cell assemblies in the context of the beta1 rhythm ( kopell et al . , 2009 ) . for example , if a subset of superficial pyramidal cells already participating in the beta1 rhythm is given more input , those cells can form a gamma - frequency cell assembly nesting inside the beta1 rhythm , without affecting the deep - layer cell assemblies ( figure 4a ) . thus , there are cell assemblies existing simultaneously that code for past and current input : the past is represented by the cell assemblies formed in the beta1 oscillation , and the present by the cell assembly nesting inside the superficial layer beta1 assembly . if two such subsets are given different amounts of input , they can form synchronizing assemblies with reduced competition ( figure 4b ) when compared to ping ( borgers et al . , 2005 , 2008 ) . thus , the beta1 rhythm is , in principle , suitable for higher - order processing in which it is necessary to compare new and old information , or put together information arriving from different modalities ( tallon - baudry et al . , 2001 ; weiss et al . , 2005 ; models suggest that the beta1 rhythm also allows assemblies of deep layer cells firing at beta1 to build up over time as more input becomes available ( kopell et al . , 2009 ) , useful for tasks in which information must be temporally integrated before a decision can be made ( donner et al . , 2009 ) . we note that these roles for beta band oscillations are consistent with the suggestion ( engel and fries , 2010 ) that beta is a frequency useful for holding in place certain signals ; indeed , the beta1 rhythm discussed above persists by virtue of interacting inhibitory rebound , without need for further input . we suggest here that the beta1 oscillations can also be used to manipulate the signals that have been held in place , to facilitate further processing . ( a ) increased depolarization of a subset of superficial pyramidal cells ( yellow box on the left ) produces a gamma rhythm nested in the beta1 activity . the depolarized pyramidal cells , which are connected by all - to - all excitatory synapses , receive enough excitation to generate two bouts of spikes : once after recovering from basket cell input ( matching figure 1 ) and a second time before receiving basket cell input ( yellow shaded regions on the right ) . ( b ) different levels of excitation to subsets of superficial pyramidal cells still produces gamma activity nested in beta1 . a population of superficial pyramidal cells , with all - to - all excitatory synapses , receives two levels of increased input , one stronger ( yellow ) and the other weaker ( blue ) . the subset receiving larger input ( shaded yellow on the right ) tends to spike more , while the subset receiving weaker input ( shaded blue ) continues to spike , unlike in ping . the interaction of different substructures of the brain depends on both the dynamics in the different regions and how they react to neuromodulators . the first of these concerns coordination between hippocampal ca3/ca1 and the entorhinal cortex ( ec ) . it has been shown ( middleton et al . , 2008 ) that the ec is capable of two physiologically different gamma rhythms . in normal acsf , with some kainate - mediated activation , the ec produces a persistent gamma rhythm , using a subnetwork of pyramidal cells and fs cells ( cunningham et al . , 2003 ) . these fs cells , predominantly located in layer 2 , require nmda currents to be active ( jones and buhl , 1993 ) ; addition of an nmda - receptor blocker eliminates these cells from the network . this uncovers a different gamma rhythm , with a lower frequency ( 2535  hz ) , created from a subnetwork of pyramidal cells and another kind of interneuron , called a  goblet cell  ( middleton et al . , 2008 ) . the nmda - receptor blockade changes the subset of interneurons that dominates the full network , and thereby determines the frequency generated by the local circuit . functional implications of this mechanism make use of observations concerning the frequencies of neural rhythms in ca3 and ca1 : in the same acsf that produces the higher frequency gamma rhythm , the natural frequency of the active ca3 local circuit in hippocampus is very similar to that of the nmda - blocked gamma , while the frequency of ca1 local circuits is very similar to the normal higher frequency of persistent gamma in ec . models have shown that , when a phasic input ( driver ) to an oscillator ( target ) has approximately the same frequency as that oscillator , the two can phase - lock , creating coherent oscillations at which the relative phases of the input and output stay constant ( kopell and ermentrout , 2002 ) . although networks need not behave like single oscillators , the results for the single oscillators suggest that the higher frequency , nmda receptor - dependent gamma rhythm in medial ec ( mec ) can drive that of ca1 , and the slower , nmda receptor - independent gamma rhythm can drive that of the ca3 . for single oscillators , if the frequencies are too different , it takes a much larger drive to lock phasic inputs to the target region 's intrinsic frequency , if at all ; in the absence of locking , the relative phases of the driver and target change cycle by cycle , implying that the effects of the driver on the target are also not reproducible cycle by cycle . thus , modulation of the nmda drive to ec during gamma rhythm generation may serve to change the path of information flow from ec through the hippocampal circuit ; the two physiologically different gamma rhythms support different pathways for processing ( figure 5 ) . a more recent report shows a similar phenomenon in vivo ( colgin et al . , 2009 ) . ( a ) medial entorhinal cortex ( mec ) generates two different frequencies of gamma rhythm depending on the degree of nmda receptor - mediated excitation present . in control conditions a c. 40  hz gamma rhythm is mediated by activity in layer 2 basket cells . in the absence of nmda receptor - mediated excitation the reduction in this source of phasic inhibition allows a second type of interneuron ( layer 3 goblet cells ) to become active , mediating a lower frequency ( c. 30  hz ) gamma rhythm . examples of reconstructed interneurons of both types and 1  s epochs of intracellularly recorded activity during local gamma rhythm generation are shown . ( b ) the two gamma rhythms in mec have modal peak frequencies which correspond to the main resonant frequency of either the hippocampal ca1 or ca3 subnetworks during gamma generation . spectra show that , in control conditions ( nmda present ) , mec frequency matches that of area ca1 . in the absence of nmda drive mec frequency matches that of area ca3 . in addition to the possibility of choosing the direction of information flow from a single source , it is possible for different rhythm mechanisms to dictate the direction of information between pairs of sources . however , in some cases there is a clear directionality to this communication ( e.g. , supp et al . . using an in vitro model of dynamical interactions between association cortex and primary auditory cortex ( roopun et al . , 2010 ) it is possible to see how different mechanisms underlying the same frequency of local network rhythm may impart directionality in communication . we have discussed above the mechanism underlying gamma and beta2 frequency rhythms in s2 ( an association area in rodent ) . in adjacent primary auditory cortex ( a1 ) an almost spectrally identical pair of frequencies is also generated in superficial and deep layers but by a very different physiological and dynamical mechanism . while glutamatergic excitation generates only a superficial gamma rhythm in a1 , the presence of cholinergic excitation reproduces the gamma / beta2 rhythms seen in adjacent s2 . this differential response to mode of excitation is even more marked when considering the converse : cholinergic drive alone , while generating gamma / beta2 in a1 , produces no rhythm generation in s2 . in auditory cortex the cholinergic beta2 rhythm is highly sensitive to blockade of gabaergic and glutamatergic fast synaptic neurotransmission , whereas the glutamate receptor driven s2 beta2 rhythm is almost completely inert to such manipulations ( roopun et al . , 2010 ) . this differential sensitivity to synaptic input for two spectrally identical rhythms results in highly directed coherence estimates favoring information flow from layer 5 of s2 to layer 5 of a1 via long - range cortico - cortical synaptic connections  ( figure 6 ) . ( a ) cross - correlogram showing a highly stable phase relationship between association cortex ( s2 ) and primary auditory cortex ( a1 ) when both generate beta2 frequency ( c. 25  hz ) oscillations driven by kainate in the presence of cholinergic neuromodulation . ( b ) while the beta2 frequency rhythms in each area are spectrally the same , the mechanisms underlying them at the local network level are not . s2 beta2 rhythms are almost completely resistant to blockade of fast glutamatergic ( sym = sym2206 , 20  m ) or gabaergic ( gabazine , 500  nm ) synaptic transmission , whereas the same frequency generated by a1 requires both these components of synaptic transmission . the resulting combination of a rhythm dependent on chemical synaptic activity and one resistant to it results in highly significant partial directed coherence estimates ( granger scores ) within the beta2 frequency band : the relatively synaptically inert s2 beta2 rhythm is able to dominate over the synaptically labile a1 beta2 rhythm . note that in both regions , the accompanying superficial layer gamma rhythm is abolished by synaptic blockade and that , for the gamma rhythm , interactions are bi - directional . more subtle changes in directionality of interactions are seen for the coexistent gamma rhythms in superficial layers . with kainate receptor - mediated drive alone , however , there is a small but robust difference in frequency of a few hz , with s2 gamma being faster than a1 gamma . this results in a coherence estimate directed in favor of s2 influencing a1 ( roopun et al . , 2010 ) . when both kainate and cholinergic drive are present , the additional drive from cholinergic receptors increases the frequency of a1 gamma selectively , and gamma frequencies match . in this situation directionality is lost and information flow , at gamma frequencies , is mutual ( figure 6 ) . it is not clear if any of the dynamical mechanisms described above are pertinent to the physiology of other rhythms , such as the alpha rhythm or delta rhythm , both of which support nesting with other rhythms ( palva and palva , 2007 ; schroeder and lakatos , 2009 ) . the gamma / theta nesting appears to depend on the overlap of cell types participating in the related rhythms . we do not know enough about the physiology of the alpha or delta rhythm to understand the mechanisms of nesting or cell assembly formation . as in other frequency bands , there are likely to be multiple mechanisms that produce the rhythms . for the gustatory cortex ( tort et al . , 2010 ) , there are ( at least ) two different rhythms in the alpha band associated with different temporal stages of the taste process , plus another associated with lack of engagement in the task . they lie in different sub - bands of the alpha range , and may have different mechanisms . it has been suggested that some kinds of alpha - band rhythms may be a product of single - cell dynamics in the lgn ( lorincz et al . , 2008 ) while others may be network phenomena involving both the neocortex and the thalamus ( lopes da silva et al . , 1980 ; contreras et al . , 1996 ) the recent enthusiasm for measuring cross - frequency coupling ( bruns and eckhorn , 2004 ; lakatos et al . , 2005 ; canolty et al . , 2006 ; jensen and colgin , 2007 ; tort et al . , 2008 , 2009 ) has begun to reveal the subtlety of the relationship between function and rhythms . these studies demonstrate that the sub - bands within the theta , gamma and very high frequency bands used to communicate between brain structures vary for different pairs of structures ( tort et al . , 2008 ) , and that the strength of the coupling can change in the course of a task . the discovery of such structure lends further weight to the hypothesis that rhythms are functionally important , and that subtle differences among rhythms in both frequency and physiology may provide important clues to function . we suggest here that diverse rhythms , or variations of a rhythm , can support different components of a cognitive act , with multiple rhythms potentially playing multiple roles . the authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest .
this essay discusses the relationship between the physiology of rhythms and potential functional roles . 
 we focus on how the biophysics underlying different rhythms can give rise to different abilities of a network to form and manipulate cell assemblies . 
 we also discuss how changes in the modulatory setting of the rhythms can change the flow of information through cortical circuits , again tying physiology to computation . 
 we suggest that diverse rhythms , or variations of a rhythm , can support different components of a cognitive act , with multiple rhythms potentially playing multiple roles .