Skip to main content
. Author manuscript; available in PMC: 2013 Oct 4.
Published in final edited form as: Neuron. 2012 Oct 4;76(1):192–208. doi: 10.1016/j.neuron.2012.09.026

Figure 3. NPS / NPSR circuitry potentially impacting addiction-related behaviors.

Figure 3

NPS is expressed in about 500 cells located between the Peri-LC (locus coeruleus), the lateral parabrachial nucleus and the principal sensory trigeminal nucleus, where it is largely co-expressed with Glu and CRF, respectively. NPS cells project (red arrows) to three main target clusters: the hypothalamus (HYP; grey), which regulates, basic physiological functions such as feeding and arousal; the thalamus (light brown), which integrates somatosensory imputs, as well as endocrine and autonomic responses; and a third cluster (light blue) composed of the Subiculum (SUB), Basolateral Amygdala (BLA) and Lateral Entorhinal Cortex (LEnt), involved in emotional memory. The thalamus sends non-NPS projections (black arrows) to several brain regions, including central amygdala (CeA) and bed nucleus of the stria terminalis (BNST), that are involved in emotional aspects of stress responses. The CeA as well as the nucleus accumbens (NAC) also receive heavy non-NPS projection from the basolateral amygdala (BLA) and cortical areas (not depicted in this schematic) that integrate cognitive function with emotional stress and reward processing. NPS neurotransmission is located upstream of these pathways, and can therefore have complex effects on drug seeking and taking, that impact both negatively and positively reinforced aspects of these behaviors.