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This chapter reviews data from a range of disciplines and, in particular, the comparison of lesion effects with those of anti-anxiety drugs. It presents an essentially two-dimensional picture of the neurology of defense that matches the two ethological dimensions described in Chapter 2. Small defensive distances are dealt with by lower neural levels and large ones by higher neural levels following the hierarchy: periaqueductal gray; hypothalamus; amygdala/hippocampus; cingulate cortex; prefrontal cortex. Different streams within these levels control fear and anxiety, respectively.

This chapter shows that analgesia evoked from the periaqueductal grey matter (PAG) is best viewed as a component of one or more complex adaptive emotional coping responses. The PAG is organized functionally into four longitudinal columns of neurons. Two distinct forms of analgesia arise from activation specifically of the dorsolateral/lateral PAG columns or the ventrolateral PAG column. A long-acting, opioid-mediated analgesia is a component of a vlPAG-mediated passive coping or conservation-withdrawal reaction that promotes recovery and healing, typically as a response to extreme, inescapable physical stress, including traumatic injury. In contrast, a short-acting, non-opioid-mediated analgesia represents a component of a dlPAG- or lPAG-mediated active coping or defensive reaction to an escapable threat or stress, including acute pain. Anatomical data indicate that each PAG column lies embedded within a distinct forebrain circuit that includes select medial and orbital PFC, hypothalamic and amygdaloid areas.

Chapter 6 explores the neural mechanisms that regulate the decrease in anxiety and increase in maternal aggression that co-occur in postpartum mammals. Too much anxiety antagonizes maternal aggression. Therefore, postpartum anxiety reduction promotes maternal aggression. The neural circuitry of maternal aggression includes projections from the ventromedial nucleus of the hypothalamus to the periaqueductal gray and to other brainstem sites. Anxiety-related behaviors are mediated by corticotropin-releasing factor (CRF) neurons, and the projection of central nucleus of amygdala (CeA) CRF neurons to the dorsal bed nucleus of the stria terminalis is involved. Neural circuits are described to show how enhanced CRF release can depress maternal aggression. These circuits are typically downregulated in postpartum females, and oxytocin (OT) is involved. OT exerts anxiolytic effects and one mechanism of OT action is to depress the output of CeA.

Chapter 5 reviews the brain circuits that regulate maternal behavior in nonhuman mammals. The medial preoptic area (MPOA) is essential for both the onset and maintenance of maternal behavior. Hormones and oxytocin act on the MPOA to stimulate the onset of maternal behavior. The neurotransmitters contained within MPOA neurons that may regulate maternal behavior are described, as are several neural inputs to the MPOA that regulate its output. A defensive neural circuit that inhibits maternal behavior in most virgin female mammals is described. MPOA output stimulates maternal behavior by depressing the defensive circuit while also activating neural circuits that underpin maternal motivation. MPOA output to the mesolimbic dopamine system is essential for appetitive maternal responses, while its output to the periaqueductal gray regulates consummatory responses. Synaptic plasticity within the MPOA-to-mesolimbic DA circuit is involved in the development of an enduring mother–infant bond.