Striatal depth EEG reveals postsynaptic activity of striatal neurons following dopamine receptor stimulation and...

This paper demonstrates a technique for measuring depth electroencephalographic (EEG) recordings from the freely moving mouse. This technique minimizes electrical artifact associated with gross movements by amplifying the current of the EEG signal directly at permanently indwelling electrodes. Stable EEG signals, with high signal-to-noise ratios, can be obtained from these animals while their movement inside the testing cage remains relatively unrestricted. We used this technique to examine the effects of dopamine (DA) receptor agonist and antagonist treatments on depth EEG signals generated within the striatum. Baseline measures of spontaneous striatal EEG activity were obtained prior to drug administration and post-drug measures of striatal activity were subsequently obtained. Apomorphine treatment resulted in desynchronization of striatal EEG signals while haloperidol or sulpiride treatment induced slow wave synchronization. Fast Fourier analysis of EEG signals revealed that DA agonist and antagonist treatment altered spontaneous striatal EEG activity in an opposite manner--relative to baseline signals, apomorphine attenuated low frequency components and augmented higher frequency components of the signal while haloperidol augmented low frequency components and attenuated higher frequency components of the signal. Moreover, mice pretreated with unilateral intracerebral injections of sulpiride and subsequently administered systemic apomorphine simultaneously demonstrated EEG synchronization on the side ipsilateral to the injection of sulpiride and EEG desynchronization on the contralateral side. The population of neurons examined in the medial striatum appear to have the properties of being excitatory to DA agonist stimulation and show decreased activity following DA antagonist treatment. These results suggest that striatal EEG activity may be used as measure of postsynaptic activity of dopaminergic neurons.