The γ isoform of protein kinase C (PKCγ), which is concentrated in a specific class of interneurons within inner lamina II (IIi) of the spinal dorsal horn and medullary dorsal horn (MDH), is known to be involved in the development of mechanical allodynia, a widespread and intractable symptom of inflammatory or neuropathic pain. However, although genetic and pharmacological impairment of PKCγ were shown to prevent mechanical allodynia in animal models of pain, after nerve injury or reduced inhibition, the functional consequences of PKCγ activation alone on mechanical sensitivity are still unknown. Using behavioural and anatomical approaches in the rat MDH, we tested whether PKCγ activation in naive animals is sufficient for the establishment of mechanical allodynia. Intracisternal injection of the phorbol ester, 12,13‐dibutyrate concomitantly induced static as well as dynamic facial mechanical allodynia. Monitoring neuronal activity within the MDH with phospho‐extracellular signal‐regulated kinases 1 and 2 immunoreactivity revealed that activation of both lamina I–outer lamina II and IIi–outer lamina III neurons, including lamina IIi PKCγ‐expressing interneurons, was associated with the manifestation of mechanical allodynia. Phorbol ester, 12,13‐dibutyrate‐induced mechanical allodynia and associated neuronal activations were all prevented by inhibiting selectively segmental PKCγ with KIG31‐1. Our findings suggest that PKCγ activation, without any other experimental manipulation, is sufficient for the development of static and dynamic mechanical allodynia. Lamina IIi PKCγ interneurons have been shown to be directly activated by low‐threshold mechanical inputs carried by myelinated afferents. Thus, the level of PKCγ activation within PKCγ interneurons might gate the transmission of innocuous mechanical inputs to lamina I, nociceptive output neurons, thus turning touch into pain. Combining intracisternal injection of both phorbol ester and a specific antagonist to the γ isoform of PKC reveals that PKCγ activation within the medullary dorsal horn leads to facial static and dynamic mechanical allodynia in naïve rats. Thus, the level of PKCγ activation within the inner lamina II PKCγ interneurons that receive innocuous mechanical inputs, might gate the transmission of such inputs to lamina I, nociceptive output neurons, and thus the transformation of touch into pain.