[Abstract Title]. - Society for Neuroscience

1 IBDML, CNRS UMR6216, Marseille, France; 2 Lab. de Neurobiologie de la Cognition, CNRS
UMR6155, Marseille, France; 3 IBDML, CNRS, Marseille, France
Abstract: High-frequency stimulation (HFS) of the subthalamic nucleus (STN) is, to date, one
of the most efficient treatments for the symptoms of Parkinson‟s disease (PD). However, despite
its efficacy, the consequences of STN HFS on the circuitry and the neuronal activity within the
basal ganglia (BG) are still a matter of debate. In parkinsonian rats, it has been demonstrated in
vitro that the output neurons of the striatum show an increased spontaneous synaptic activity
mediated by glutamate, and that such hyperactivity is reversed by chronic (5 days) STN HFS,
which also ameliorates akinesia. However, since slice recordings do not allow the preservation of
the BG circuitry, an in vivo approach is necessary to fully evaluate the consequences of this
treatment on striatal neurons. For this reason, we have performed a parallel electrophysiological
study from freely moving rats undergoing chronic STN HFS, both control and parkinsonian (6-
OHDA lesion). Interestingly, also in vivo recordings showed a marked decrease of striatal
neurons activity, in terms of spike frequency, triggered by STN HFS. Moreover, while in non
stimulated rats we recorded a mixed tonic/burst spike mode, most of the residual spikes in
stimulated animals occurred within bursts. Overall, these data show that STN HFS inhibits both
glutamate synaptic transmission and spike activity of striatal neurons, confirming that the
striatum is deeply involved in the pathophysiological mechanisms of PD and that its function is
strongly affected by STN HFS.
Disclosures: P. Gubellini, None; P.P. Salin , None; C. Baunez, None; S. Lardeux, None; D.
Paleressompoulle, None.
Poster
247. Parkinson's Disease Interventions: Animal and Clinical Models
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 247.5/R12
Topic: C.02.d. Therapies
Support: FRST NZ postdoctoral fellowship
Title: Ghrelin promotes nigrostriatal dopamine function and protects dopamine cells in a mouse
model of Parkinson‟s disease
Authors: *Z. B. ANDREWS 1 , D. ERION 2 , R. BEILER 3 , J. ELSWORTH 4 , R. ROTH 4 , T. L.
HORVATH 1 ;
1 OB/GYN, 2 Intrnl. Med., 3 Comparative Med., 4 Psychiatry, Yale Univ., New Haven, CT