Final answer:
Facilitation in the secondary neurons of the pain pathway can lower their firing threshold, leading to non-painful stimuli becoming painful. This process is involved with hyperalgesia and is associated with complex nociceptive pathways that project to the thalamus and hypothalamus in the brain.
Step-by-step explanation:
Facilitation can extend to the secondary neurons in the pain pathway by lowering their threshold for firing. This means that the neurons will be more easily activated, whereby normally non-painful stimuli can be perceived as painful. This state of heightened sensitivity is often referred to as hyperalgesia. When a larger than normal stimulus depolarizes a neuron above its threshold, it may trigger an action potential in a postsynaptic neuron.
The nociceptive pathways involved in the processing of pain signals are complex, involving not only the projection to the thalamus but also direct pathways to the hypothalamus, which is involved in autonomic nervous system responses—modulating the cardiovascular and neuroendocrine functions. Furthermore, the intensity of a stimulus is coded in the rate at which action potentials are fired by sensory receptors, which in combination with the number of receptors activated, dictates how intense pain is perceived.