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In their impressive target paper, Douglas Watt and Jaak Panksepp aim to consider the “psychological properties of the brain and its adaptive mandates” in the pathophysiology of depression. They argue that depression is “fundamentally connected to social attachment,” the neurobiology of which they consider to be related to the separation-distress mechanism. In this commentary I do not want to go into the neurochemical and neuroanatomical details of their impressive hypothesis but will briefly focus on one particular aspect of the brain's input. I want to raise the question for the kind of coding mechanisms that must be presupposed by the brain in order to link its intrinsic activity and the brain's input to the stimulus-induced activity. In doing so, I will briefly indicate how an abnormally altered brain's input may yield the kind of changes observed in depression.
How is it possible that the brain's internal separation-distress mechanisms can impact stimulus-induced activity? This occurs only if the neurobiological underpinnings of the brain's internal separation-distress mechanisms modulate and impact stimulus-induced activity in an abnormal way. In these circumstances, withdrawal from the social environment, together with the consecutive increased self-focus that is one of the hallmarks of depression, are generated. Hence, we must presuppose that the pathologically altered separation-distress system apparently decreases stimulus-induced neural-activity changes from the environment. The question I want to raise here concerns the kind of neural coding that must be presupposed in order for the brain (and its input) to have such disastrous effects on stimulus-induced activity. How must the brain code its neural-activity changes in order, first, to link its own input to the intrinsic activity and, second, to link the stimulus-induced activity to the environment?
Watt & Panksepp seem to remain unclear about the exact mechanisms of the interaction between the organism's s