Anesthesia reduces discharge rates in the human pallidum without changing the discharge rate ratio between pallidal segments
Eur J Neurosci. 2016-10-13; 44(11): 2909-2913
DOI: 10.1111/ejn.13417
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Castrioto A(1)(2)(3), Marmor O(4), Deffains M(4)(5), Willner D(6), Linetsky
E(7), Bergman H(4)(5), Israel Z(8), Eitan R(5), Arkadir D(7).
Author information:
(1)Grenoble Institut des Neurosciences (GIN), University of Grenoble Alpes,
Grenoble, France.
(2)Inserm U1216, Grenoble, France.
(3)Movement Disorders Unit, Neurology Department, CHU de Grenoble, Grenoble,
France.
(4)Department of Medical Neurobiology, Hadassah-Hebrew University Medical
Center, Jerusalem, Israel.
(5)Edmond and Lily Safra Centre for Brain Research, The Hebrew University,
Jerusalem, Israel.
(6)Department of Anesthesiology, Hadassah-Hebrew University Medical Center,
Jerusalem, Israel.
(7)Department of Neurology, Hadassah-Hebrew University Medical Center,
Jerusalem, 91120, Israel.
(8)Department of Neurosurgery, Center for Functional and Restorative
Neurosurgery, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
Classical rate models of basal ganglia circuitry associate discharge rate of the
globus pallidus external and internal segments (GPe, GPi respectively) solely
with dopaminergic state and predict an inverse ratio between the discharge rates
of the two pallidal segments. In contrast, the effects of other rate modulators
such as general anesthesia (GA) on this ratio have been ignored. To respond to
this need, we recorded the neuronal activity in the GPe and GPi in awake and
anesthetized human patients with dystonia (57 and 53 trajectories respectively)
and in awake patients with Parkinson’s disease (PD, 16 trajectories) undergoing
deep brain stimulation procedures. This triad enabled us to dissociate pallidal
discharge ratio from general discharge modulation. An automatic offline spike
detection and isolation quality system was used to select 1560 highly isolated
units for analysis. The mean discharge rate in the GPi of awake PD patients was
dramatically higher than in awake dystonia patients although the firing rate in
the GPe was similar. Firing rates in dystonic patients under anesthesia were
lower in both nuclei. Surprisingly, in all three groups, GPe firing rates were
correlated with firing rates in the ipsilateral GPi. Thus, the firing rate ratio
of ipsilateral GPi/GPe pairs was similar in awake and anesthetized patients with
dystonia and significantly higher in PD. We suggest that pallidal activity is
modulated by at least two independent processes: dopaminergic state which
changes the GPi/GPe firing rate ratio, and anesthesia which modulates firing
rates in both pallidal nuclei without changing the ratio between their firing
rates.
© 2016 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.