GABAB receptors: modulation of thalamocortical dynamics and synaptic plasticity.

• GABA B -Rs can be pre or postsynaptic, inhibiting both excitatory and inhibitory neurons, and also decreasing excitation. • Activation of GABA B -Rs in the thalamus and cortex modulates emergent rhythms and synaptic plasticity. • In the thalamus, activation of GABA B -Rs switches the network from generating spindle waves to spike-and-wave cycles. • During cortical Up and Down states, GABA B -R blockade consistently elongates Up states and modifies the rhythmic cycle. • Blockade of GABA B -Rs increases regularity of the cycle and decreases the network complexity of causal interactions. GABA B -receptors (GABA B -Rs) are metabotropic, G protein-coupled receptors for the neurotransmitter GABA. Their activation induces slow inhibitory control of the neuronal excitability mediated by pre- and postsynaptic inhibition. Presynaptically GABA B -Rs reduce GABA and glutamate release inhibiting presynaptic Ca2+ channels in both inhibitory and excitatory synapses while postsynaptic GABA B -Rs induce robust slow hyperpolarization by the activation of K+ channels. GABA B -Rs are activated by non-synaptic or volume transmission, which requires high levels of GABA release, either by the simultaneous discharge of GABAergic interneurons or very intense discharges in the thalamus or by means of the activation of a neurogliaform interneurons in the cortex. The main receptor subunits GABA B 1a , GABA B 1b and GABA B 2 are strongly expressed in neurons and glial cells throughout the central nervous system and GABA B -R activation is related to many neuronal processes such as the modulation of rhythmic activity in several brain regions. In the thalamus, GABA B -Rs modulate the generation of the main thalamic rhythm, spindle waves. In the cerebral cortex, GABA B -Rs also modulate the most prominent emergent oscillatory activity—slow oscillations—as well as faster oscillations like gamma frequency. Further, recent studies evaluating the complexity expressed by the cortical network, a parameter associated with consciousness levels, have found that GABA B -Rs enhance this complexity, while their blockade decreases it. This review summarizes the current results on how the activation of GABA B -Rs affects the interchange of information between brain areas by controlling rhythmicity as well as synaptic plasticity. [ABSTRACT FROM AUTHOR]