Potassium channels represent one of the most functionally diverse families of neuronal ion channels, critically shaping membrane excitability, action potential kinetics, neurotransmitter release, and the restoration of resting membrane potential. This review summarizes current knowledge on the molecular architecture and functional specialization of major K⁺ channel classes in the nervous system, including voltage-gated (Kv), tandem-pore (K₂P), inwardly rectifying (Kir), and calcium-activated (KCa) channels. Particular emphasis is placed on the structural and functional properties of Kv1 family subunits, especially Kv1.2, their precise subcellular distribution (soma, dendrites, axon initial segment, presynaptic terminals), and their role in regulating action potential threshold, presynaptic Ca²⁺ entry, and neurotransmitter release. We discuss the mechanisms of hypoxic sensitivity of K⁺ channels and the consequences of oxygen deficiency for neuronal function. Hypoxia modulates the activity of multiple K⁺ channel types, leading either to hyperpolarization via KATP channel opening or to depolarization due to inhibition of Kv channels and subsequent Na⁺ accumulation. Dysregulation of Kv1.2 and related subunits during hypoxia and ischemia contributes to impaired Ca²⁺ homeostasis, enhanced neuronal excitability, glutamate-dependent excitotoxicity, and structural damage. The involvement of Kv channels in hypoxic pulmonary vasoconstriction and the downregulation of Kv1.2/Kv1.5 expression under chronic hypoxia in pulmonary artery smooth muscle cells are also highlighted. Finally, we describe the pathophysiological relevance of K⁺ channels in neurological disorders–including epilepsy, ischemic stroke, spinal cord injury, demyelinating diseases, and neurodegeneration– and outline therapeutic perspectives of pharmacological modulation of Kv, Kir, KCa, and K₂P channels in brain hypoxia and hypoxic-ischemic injury.