Adenosine modulates the excitability of layer II stellate neurons in entorhinal cortex through A1 receptors

Abstract

Stellate neurons in layer II entorhinal cortex (EC) provide the main output from the EC to the hippocampus. It is believed that adenosine plays a crucial role in neuronal excitability and synaptic transmission in the CNS, however, the function of adenosine in the EC is still elusive. Here, the data reported showed that adenosine hyperpolarized stellate neurons in a concentration-dependent manner, accompanied by a decrease in firing frequency. This effect corresponded to the inhibition of the hyperpolarization-activated, cation nonselective (HCN) channels. Surprisingly, the adenosine-induced inhibition was blocked by 3 μM 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective A(1) receptor antagonists, but not by 10 μM 3,7-dimethyl-1-propargylxanthine (DMPX), a selective A(2) receptor antagonists, indicating that activation of adenosine A(1) receptors were responsible for the direct inhibition. In addition, adenosine reduced the frequency but not the amplitude of miniature EPSCs and IPSCs, suggesting that the global depression of glutamatergic and GABAergic transmission is mediated by a decrease in glutamate and GABA release, respectively. Again the presynaptic site of action was mediated by adenosine A(1) receptors. Furthermore, inhibition of spontaneous glutamate and GABA release by adenosine A(1) receptor activation was mediated by voltage-dependent Ca(2+) channels and extracellular Ca(2+) . Therefore, these findings revealed direct and indirect mechanisms by which activation of adenosine A(1) receptors on the cell bodies of stellate neurons and on the presynaptic terminals could regulate the excitability of these neurons.

Short-term sleep deprivation disrupts the molecular composition of ionotropic glutamate receptors in entorhinal cortex and impairs the rat spatial reference memory

“…The present study for the first time, to the best of our knowledge, symmetrically investigated the influence of short-term SD on the AMPAR and NMDAR subunit expression in the EC, which is the 'hub' between neocortex and hippocampus and serves a vital role in spatial cognition [16,18,22,35,36]. We found 4h SD differently affected the AMPAR subunit surface expression primarily via influencing their membrane trafficking.…”

Caffeine inhibits hypothalamic A1R to excite oxytocin neuron and ameliorate dietary obesity in mice

“…3i–k), which is in agreement with the neuronal inhibitory function of this receptor. Indeed, previous studies displayed that agonist-mediated activation of A 1 R decreased the neuronal activities in the dorsal root ganglia34, lateral horn35, entorhinal cortex36, whereas caffeine could facilitate the release of glutamate from neurons in the cerebral cortex37. Furthermore, overexpression of A 1 R in the PVN, but not Arc or DMH neurons significantly attenuated caffeine’s effect on energy metabolism (Fig.…”

Effects of Interface Pressure Distribution on Human Sleep Quality

“…Our previous studies have also demonstrated that short-term sleep deprivation influences the excitability of neurons in the prefrontal cortex [32]. Moreover, adenosine, the intrinsic sleep-promoting factor, plays a role in the regulation of neuronal excitability in the entorhinal cortex [33], a brain region involved in learning and memory [34], [35]. Because slow wave sleep is beneficial for the consolidation of declarative memories [36], [37], our results imply that the regulation of pressure distribution may be effective in improving the performance of subjects in tasks related to declarative memory, though behavioral studies have not yet been conducted.…”