Sr2+-dependent asynchronous evoked transmission at rat striatal inhibitory synapsesin vitro

Postsynaptic receptor occupancy during evoked transmission at striatal GABAergic synapses in vitro.

The effect of benzodiazepines (BZs) on GABA(A)-ergic synaptic responses depends on the control receptor occupancy: the BZ-induced enhancement of receptor affinity can lead to greater peak amplitudes of quantal responses only when, under normal conditions, receptors are not fully saturated at peak. Based on this fact, receptor occupancy at the peak of spontaneous miniature inhibitory postsynapti...

Inhibitory Transmission Mediated by Asynchronous Transmitter Release

At fast CNS synapses, the role of asynchronous release following initial synchronous release is poorly understood. We examined the contribution of asynchronous release to GABAergic transmission in the cochlear nucleus across a 40-fold range of electrical stimulus frequencies. Whereas quantal release was highly synchronized at low frequencies, it was largely continuous and desynchronized at high...

Dopamine-dependent tuning of striatal inhibitory synaptogenesis.

Dopaminergic projections to the striatum, crucial for the correct functioning of this brain region in adulthood, are known to be established early in development, but their role is currently uncharacterized. We demonstrate here that dopamine, by activating D(1)- and/or D(2)-dopamine receptors, decreases the number of functional GABAergic synapses formed between the embryonic precursors of the m...

Dopaminergic Modulation of Striatal Inhibitory Transmission and Long-Term Plasticity

Dopamine (DA) modulates glutamatergic synaptic transmission and its plasticity in the striatum; however it is not well known how DA modulates long-term plasticity of striatal GABAergic inhibitory synapses. This work focused on the analysis of both dopaminergic modulation of inhibitory synapses and the synaptic plasticity established between GABAergic afferents to medium spiny neurons (MSNs). Ou...

Inhibitory Synaptic Transmission in Striatal Neurons after Transient Cerebral Ischemia