Instinctual Energies and Affective States

It now seems evident that there is considerable chemical coding of basic affective processes, and one major way to decode those controls is to detail the neural underpinnings of instinctual-emotional processes in the brains of other mammals. This project is just beginning. An urgent question for biological psychiatry is how affect is actually generated in the brain. So far we only have biogenic amine theories of affect, especially dopamine, norepinephrine, and serotonin based hypotheses, but those very general state-control processes help regulate practically all emotions nonspecifically. The emergence of the idea that distinct affective states are created, in part through various neuropeptide modulators contained in emotional systems that may all have glu-tamatergic transmission at their core (Panksepp, 1993, 1998a), provides an abundance of novel therapeutic ideas (Chapter 21).

So far, the question of how affect is actually generated by neural activities has only been addressed in theoretical terms. As noted at the outset of this chapter, there is a prevailing notion that it is produced, in some manner, by higher cerebral activities that mediate cognitive consciousness, for instance, by brain areas that mediate working memory (e.g., LeDoux, 1996) or in those that allow us to resymbolize events in terms of language (Rolls, 1999). Damasio (1996), with his "somatic marker" hypothesis, has entertained the classic James-Lange view that emotional experience arises from inputs to the somatosensory processing areas of the cortex.

We would advance the view that affect is an intrinsic aspect of the neurodynamics of the subcortically situated emotional systems of the brain that generate characteristic instinctual actions in response to various situations (largely social) that promote survival as well as various archetypal threats to survival. This last perspective has envisioned that the primitive dynamics of affect operate, in substantial part, through a primal neural representation of a neurodynamically created virtual body schema—a "core self" concentrated in the paramedian brainstem areas, such as the PAG, that are richly interconnected with higher limbic areas (Panksepp, 1998b). This theme has also been advanced by Damasio (1999). In addition, there are also various sensory affects (e.g., the pleasure and aversion of various tastes) that arise from brain mechanisms that encode the value of simple external stimuli that have consistently enhanced or diminished survival in the history of the species (Berridge and Robinson, 1998; Panksepp,

1998a). Considering the complexity of this important topic, it may well be that all of the above views will contribute substantially to an ultimate solution of how affective experience is created within the brain. Indeed, it is possible to envision how cortico-cognitive systems of the brain, which transmit information from the cortex to basal ganglia via descending glutamatergic systems, would also have neuropeptide codes that increase the duration of arousal in subcortical systems (for an example of such descending anxiogenic and dopamine modulating effects of CCK, see You et al., 1998).

However, a disparity remains between the animal and human work. The animal data has tended to emphasize emotional circuits quite low in the neuroaxis, while the human data, as already summarized, has typically emphasized the functions of higher limbic areas that are well connected to these lower circuits. Although subcortical areas of the mammalian brain contain various genetically ingrained operating systems for certain basic emotional instinctual responses, to appreciate the full complexity of human emotions, we must obviously focus on the role of higher cognitive processes—those unique mental complexities that have arisen from a massive cortical evolution in hominids. The full spectrum of human affective experience clearly requires hierarchical interactions between lower and higher brain zones as highlighted throughout this chapter. However, it is also important to emphasize how much affect can still be elaborated in the human brain after most of the higher limbic reaches of the brain have been severely damaged (Adolphs et al., 2003).

Getting to Know Anxiety

Getting to Know Anxiety

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