RT Journal Article
SR Electronic
T1 Contributions of calcium-dependent and calcium-independent mechanisms to presynaptic inhibition at a cerebellar synapse
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1623
OP 1633
DO 10.1523/JNEUROSCI.16-05-01623.1996
VO 16
IS 5
A1 JS Dittman
A1 WG Regehr
YR 1996
UL http://www.jneurosci.org/content/16/5/1623.abstract
AB Activation of either adenosine A1 receptors or GABAB receptors inhibits many excitatory synapses in the mammalian brain. However, the extent to which different mechanisms contribute to such synaptic modulation is unclear. We examined the manner in which activation of adenosine A1 receptors and GABAB receptors modulates synaptic strength at the granule cell to Purkinje cell synapse in rat cerebellar slices. Optical determination of presynaptic calcium influx revealed that presynaptic calcium channels were modulated by 2-chloroadenosine (2CA) and baclofen, agonists of the adenosine A1 receptor and the GABAB receptor, respectively. 2CA and baclofen differentially affected three classes of calcium channels without altering the shape of the presynaptic volley, suggesting that changes in presynaptic waveform do not contribute significantly to synaptic modulation. 2CA affected neither the amplitude nor the frequency of spontaneous miniature postsynaptic currents, whereas baclofen reduced the frequency by approximately 40% without affecting the amplitude. In addition, 2CA and baclofen do not change either fiber excitability or presynaptic residual calcium. Taken together, our data indicate that activation of the adenosine A1 receptor reduces synaptic strength by modulating presynaptic calcium channels. Baclofen modulates presynaptic calcium channels as well but also affects release processes downstream from calcium entry.