The beneficial effects of hypothermia have long been known in non-traditional medicine but it is only in the past few decades that studies on the neuroprotective effects of hypothermia in hypoxic-ischemic brain injury have begun. Different mechanisms have been put forward to explain hypothermic neuroprotection including reduction of the excessive release of the excitatory amino acid neurotransmitter, glutamate. Recent experiments have questioned the key role of this neurotoxin in hypoxic-ischemic neuropathogenesis. In contrast, a mediatory role for another neurotransmitter, glycine in the neuroprotective effects of hypothermia has become more attractive, along with an indication of its role in the pathogenesis of ischemic neuronal damage. Thus, on the basis of reviewing relevant literature the hypothesis of a glycine-related mechanism of hypothermic neuroprotection in ischemia-induced neuronal injury has been put forward.