Dopaminergic activation[edit]
Two main frontal areas have been implicated in the dream process. The first involves the deep white matter of the
frontal lobes (just above the eyes). The main systems at work here involve the mesolimbic and mesocortical dopaminergic pathways. There are connecting fibres that run between frontal and
limbic structures. A dopaminergic pathway runs from the
ventral tegmental area, ascends through the lateral
hypothalamus, various basal forebrain areas (nucleus basalis, stria terminalis, shell of nucleus accumbens) and terminates in the
amygdala,
anterior cingulate gyrus and frontal cortex.
Damage to the dopaminergic pathway results in a loss of dreaming. Furthermore, chemical stimulation of the pathway (with L-DOPA for example) increases the frequency and vividness of dreams without affecting REM sleep.[10] It is interesting to note that the mesolimbic and mesocortical pathways are considered the seeking areas or the motivational command centers of the brain. Damage not only results in the loss of dreams but also of motivated behaviour.[6] Transection or inhibition of the dopamine pathway also reduces some positive symptoms of
schizophrenia, many of which have been likened to dream-like states. Drugs that block the system have anti-psychotic effects but also reduce excessive and vivid dreaming.
[10] Further evidence that dreaming can occur independently of REM sleep is found in the occurrence of nocturnal
seizures during NREM that often present themselves as nightmares. Activation here is seen in the
temporal lobe, again a forebrain area.
[6][10]
The evidence of the involvement of mesolimbic and mesocortical dopaminergic pathways suggests that dreaming occurs when a motivational component is activated. Only when this pathway is removed do dreams cease to occur. This system can be activated by mechanisms of REM sleep but can also occur independently during NREM stages of sleep.
