Presynaptic GABAB receptors inhibit synaptic inputs to rat subthalamic neurons

• Published in: Neuroscience 2001-12, Vol.108 (3), p.431-436
• Main Authors: Shen, K.-Z, Johnson, S.W
• Format: Article
• Language: English
• Subjects: baclofen; Biological and medical sciences; Central nervous system; Electrophysiology; Fundamental and applied biological sciences. Psychology; GABA; glutamate; subthalamic nucleus; synaptic transmission; Vertebrates: nervous system and sense organs
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/S0306-4522(01)00424-9

Effects of baclofen on synaptic transmission were studied in rat subthalamic neurons using whole-cell patch clamp recording from brain slices. Focal electrical stimulation of the brain slice evoked GABAergic inhibitory postsynaptic currents and glutamatergic excitatory postsynaptic currents. Baclofen reduced the amplitude of evoked inhibitory postsynaptic currents in a concentration-dependent manner with an IC50 of 0.6±0.2 μM. Evoked excitatory postsynaptic currents were also reduced by baclofen concentration-dependently (IC50 of 1.6±0.2 μM), but baclofen was more potent at reducing the GABAA receptor inhibitory postsynaptic currents. The GABAB receptor antagonist CGP 35348 blocked these inhibitory effects of baclofen on evoked inhibitory and excitatory postsynaptic currents. Baclofen increased the paired-pulse ratios of evoked inhibitory and excitatory postsynaptic currents. Furthermore, baclofen reduced the frequency of spontaneous miniature excitatory postsynaptic currents, but had no effect on their amplitude. These results provide evidence for presence of presynaptic GABAB receptors that modulate both GABA and glutamate release from afferent terminals in the subthalamus.