Brenowitz S, David J, Trussell L
Neuroscience Training Program, University of Wisconsin-Madison, 53706, USA.
Neuron. 1998 Jan;20(1):135-41. doi: 10.1016/s0896-6273(00)80441-9.
Activation of presynaptic inhibitory receptors or high-frequency synaptic stimulation normally inhibits excitatory synaptic transmission by reducing transmitter release. We have explored the interactions between these two pathways for reducing synaptic strength and found that for synapses stimulated at high rates, agonists of the GABA(B) receptor become excitatory and strengthen transmission. At an auditory glutamatergic synapse featuring strong synaptic depression, the GABA(B) agonist baclofen reduced by 90% postsynaptic currents elicited at low frequency. By contrast, synaptic currents elicited at high frequencies were 5-fold larger in baclofen and had a markedly increased likelihood of firing well-timed postsynaptic action potentials. Presynaptic GABA(B) receptors may thus regulate transmitter release to enable sustained transmission at higher stimulus frequencies, thereby extending the dynamic range of neural circuits.
突触前抑制性受体的激活或高频突触刺激通常通过减少递质释放来抑制兴奋性突触传递。我们探究了这两条降低突触强度的途径之间的相互作用，发现对于高频刺激的突触，GABA(B)受体激动剂会变为兴奋性并增强传递。在一个具有强烈突触抑制的听觉谷氨酸能突触处，GABA(B)激动剂巴氯芬使低频诱发的突触后电流降低了90%。相比之下，在巴氯芬存在时高频诱发的突触电流增大了5倍，并且引发适时突触后动作电位的可能性显著增加。因此，突触前GABA(B)受体可能调节递质释放，以在更高刺激频率下实现持续传递，从而扩展神经回路的动态范围。
