The brain undergoes constant activity fluctuations related to processes like learning, development, and sleep. Neuronal plasticity enables information storage relevant to those changes but also serves to regulate stable neuronal firing. Homeostatic plasticity mechanisms protect neurons from activity extremes that are associated with pathological conditions such as mood disorders, epilepsy, and dementia. Our aim is to assess how targeted human brain neurons and the synaptic connections between them adapt to prolonged elevation of activity. To assess plasticity, we perform whole-cell patch-clamp recordings of pyramidal neurons in layers 2/3 of acute human brain slices prepared from surgically resected tissue. Following recording, slices are incubated in aCSF supplemented with 8 mM potassium for over 18 hours before subsequently targeting the same set of neurons for repatching. We observe an increase of the action potential (AP) threshold of single neurons after prolonged whole network depolarization. Passive cellular properties are not affected by the treatment once the elevated potassium is washed out. We aim to assess the amplitude and frequency of spontaneous and miniature synaptic events given analogous experimental conditions. In conclusion, in line with previous research conducted in non-human, model organisms, prolonged network depolarization appears to decrease the intrinsic excitability of pyramidal neurons in layer 2/3 of the human temporopolar cortex.