Abstract
Beta frequency oscillations (10–35 Hz) in motor regions of cerebral cortex play an important role in stabilising and suppressing unwanted movements, and become intensified during the pathological akinesia of Parkinson's Disease. We have used a cortical slice preparation of rat brain, combined with concurrent intracellular and field recordings from the primary motor cortex (M1), to explore the cellular basis of the persistent beta frequency (27–30 Hz) oscillations manifest in local field potentials (LFP) in layers II and V of M1 produced by continuous perfusion of kainic acid (100 nM) and carbachol (5 µM). Spontaneous depolarizing GABA-ergic IPSPs in layer V cells, intracellularly dialyzed with KCl and IEM1460 (to block glutamatergic EPSCs), were recorded at −80 mV. IPSPs showed a highly significant (P< 0.01) beta frequency component, which was highly significantly coherent with both the Layer II and V LFP oscillation (which were in antiphase to each other). Both IPSPs and the LFP beta oscillations were abolished by the GABAA antagonist bicuculline. Layer V cells at rest fired spontaneous action potentials at sub-beta frequencies (mean of 7.1+1.2 Hz; n = 27) which were phase-locked to the layer V LFP beta oscillation, preceding the peak of the LFP beta oscillation by some 20 ms. We propose that M1 beta oscillations, in common with other oscillations in other brain regions, can arise from synchronous hyperpolarization of pyramidal cells driven by synaptic inputs from a GABA-ergic interneuronal network (or networks) entrained by recurrent excitation derived from pyramidal cells. This mechanism plays an important role in both the physiology and pathophysiology of control of voluntary movement generation.
Highlights
Beta oscillations (15–35 Hz) are a characteristic feature of neuronal network activity in primary motor cortex (M1) and such activity has been suggested to reflect an idling state of cortex, which prevails in the absence of appropriate sensory input [1]
These data indicate that whilst spiking frequency is much lower than local field potential (LFP) beta frequency in deep layers of M1, such activity is strongly phase locked to the LFP, almost certainly dictated by the characteristics of the bicuculline-sensitive beta frequency inhibitory postsynaptic potentials (IPSPs) described above
In our previous study [11], it was shown that phasic inhibitory and phasic/tonic excitatory synaptic inputs were required for persistent beta oscillations in M1 layer V coronal slices in vitro
Summary
Beta oscillations (15–35 Hz) are a characteristic feature of neuronal network activity in primary motor cortex (M1) and such activity has been suggested to reflect an idling state of cortex, which prevails in the absence of appropriate sensory input [1]. We have described a pharmacological approach to obtain persistent oscillations in slices of rat M1 [11] and showed that this region will generate synchronous network oscillations preferentially at beta frequency These oscillations were found to be generated in deep layers and dependent upon fast synaptic inhibition mediated by GABAA receptors. A contribution from NMDA receptors and GABAB receptors was evident, while electrical coupling of the neuronal network by gap junctions appears necessary for robust rhythmogenesis These features, including the involvement of glutamate and GABA synaptic drive and direct electrical coupling, are common to many types of oscillatory activity in hippocampus, entorhinal cortex and somatosensory cortex [12,13,14,15,16]
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