Leptin reduces GABA release from reticular thalamic nucleus

URBANO FJ; PERISSINOTTI PP; RIVERO ECHETO MC; GARCIA-RILL E ; BISAGNO V

Little Rock, AR

Congreso; American Society for Neurochemistry Annual Meeting; 2017

American Society for Neurochemistry

Leptin is an adipose-derived hormone that controls appetite and energy expenditure. Leptin receptors are expressed on ventrobasal (VB) and reticular thalamic (RTN) nuclei from embryonic stages, and leptin has been reported to inhibit pedunculopontine neurons. Here, we studied the effects of local application of leptin (2.5 microM) on synaptic transmission and action potential properties. We used whole-cell patch-clamp recordings of thalamocortical VB neurons from wildtype and leptin-deficient obese mice (ob/ob). Our results show that leptin (2.5 microM) reduced paired-pulse evoked GABA release onto VB neurons in wildtype mice, without affecting excitatory glutamate transmission. Effects of leptin (2.5 microM) were not observed in thalamocortical VB neurons from ob/ob mice. In addition, leptin (2.5 microM) reduced both frequency and amplitude of GABAergic miniature IPSPs, suggesting that leptin was able to modulate both pre- and postsynaptic sites of the RTN-VB GABAergic synapse. At the postsynaptic level, we observed a rapid and reversible reduction by leptin of the number of action potentials of VB neurons. Results described here are important for understanding the control of thalamocortical excitability by leptin and sleep dysregulation linked to obesity.