Although traditionally thought to act primarily in the spinal cord, emerging evidence support important inhibitory functions by glycinergic transmission in the brain. In the ventral pallidum (VP), glycinergic afferents from the brainstem make synapses onto cholinergic interneurons to regulate arousal. Notably, VP is comprised of a heterogeneous population of GABAergic neurons, of which those that express somatostatin (SOM+) comprise a significant group and have been implicated in the control of sleep and wakefulness directly inhibiting cholinergic, glutamatergic and parvalbumin neurons. Here, we investigate whether glycine may mediate inhibition onto SOM+ cells to control VP function and circuit communication. Using genetic, pharmacology, and electrophysiological approaches, we evaluated the inhibitory synaptic transmission onto somatostatin positive (SOM+) neurons in mice, approved bioethics act code CBC 55-2022. We found that in addition to GABAergic inputs, SOM+ neurons also receive functional glycinergic inputs, demonstrated by the presence of glycine-induced currents that are sensitive to the blockade by strychnine, a glycine receptor antagonist. Consistently, bath application of strychnine reduces both spontaneous and electrically evoked inhibitory postsynaptic currents (IPSCs) in SOM+ neurons. Moreover, inhibition of the glycinergic transporter (GlyT2) also reduces IPSCs recorded from SOM+ neurons, strongly suggesting the presence of functional glycinergic synapses in the VP. Interestingly, inhibitory synaptic transmission onto SOM+ neurons express activity-dependent changes of synaptic efficacy in the form of long-term depression and can be regulate by cannabinoid signaling in a CB1 receptor dependent manner. Whether these changes in synaptic efficacy could impact both glycinergic and GABAergic synaptic transmission is currently under investigation.