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Rodents spontaneously run on wheels, but what underlies variation within and between species is unknown. This study used Fos immunoreactivity to compare brain activity in mice selectively bred for high wheel running (S) versus control (C) mice. Mice ran for 6 days, but on Day 7, half the mice were prevented from running. A strong positive correlation was found between running distance and Fos in the dentate gyrus of C runners that was lost in S runners. In mice prevented from running, Fos was higher in S than in C in the lateral hypothalamus, medial frontal cortex, and striatum. Results implicate specific brain regions in motivation to run and others in control of the intensity of the locomotor behavior itself.Voluntary wheel running is one of the most widely studied behaviors in laboratory rodents, yet the underlying cause of variation in this behavior is not known (Sherwin, 1998). Recently, it has been proposed that wheel running is naturally rewarding and addictive

Lactating females that fiercely protect offspring exhibit decreased fear and anxiety. The authors tested whether decreased corticotropin-releasing factor (CRF), an activator of fear and anxiety, plays a functional role in maternal aggression. Intracerebroventricular (icv) injections of CRF (1.0 and 0.2 microg, but not 0.02 microg) significantly inhibited maternal aggression but not other maternal behaviors. The CRF antagonist D-Phe-CRF(12-41) had no effect. Maternal aggression and icv CRF (0.2 microg) induced Fos in 11 of the same regions, including the lateral and medial septum, the bed nucleus of the stria terminalis, the medial and central amygdala, the periaqueductal gray, the dorsal raphe, and the locus coeruleus. These findings suggest that decreased CRF is necessary for maternal aggression and may act by altering brain activity in response to an intruder.

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In insects, the shedding of the old cuticle at the end of a molt involves a stereotyped sequence of distinct behaviors. Our studies on the isolated nervous system of Manduca sexta show that the peptides ecdysis-triggering hormone (ETH) and crustacean cardioactive peptide (CCAP) elicit the first two motor behaviors, the pre-ecdysis and ecdysis behaviors, respectively. Exposing isolated abdominal ganglia to ETH resulted in the generation of sustained pre-ecdysis bursts. By contrast, exposing the entire isolated CNS to ETH resulted in the sequential appearance of pre-ecdysis and ecdysis motor outputs. Previous research has shown that ETH activates neurons within the brain that then release eclosion hormone within the CNS. The latter elevates cGMP levels within and increases the excitability of a group of neurons containing CCAP. In our experiments, the ETH-induced onset of ecdysis bursts was always associated with a rise in intracellular cGMP within these CCAP neurons. We also found that CCAP immunoreactivity decreases centrally during normal ecdysis. Isolated, desheathed abdominal ganglia responded to CCAP by generating rhythmical ecdysis bursts. These ecdysis motor bursts persisted as long as CCAP was present and could be reinduced by successive application of the peptide. CCAP exposure also actively terminated preecdysis bursts from the abdominal CNS, even in the continued presence of ETH. Thus, the sequential performance of the two behaviors arises from one modulator activating the first behavior and also initiating the release of the second modulator. The second modulator then turns off the first behavior while activating the second. Key words: CCAP; ecdysis; pre-ecdysis; ecdysis triggering hormone; eclosion hormone; cGMPNeuromodulators (such as monoamines and neuropeptides) activate, alter, and create behavioral motor outputs from the nervous system. A major research question has been how these neuromodulators produce their distinct motor outputs. The most detailed work regarding this question has examined the stomatogastric ganglion of decapod crustaceans. In the absence of modulators, this ganglion shows a basal level of activity (Moulins and Cournil, 1982). Diverse neuromodulatory inputs, however, cause the emergence of functional neural circuits that generate discrete behaviors by altering the cellular (e.g., intrinsic excitability) (Flamm and Harris-Warrick, 1986) and synaptic properties (e.g., increased strength of electrical coupling) (Johnson et al., 1993) of neurons within the ganglion (Simmers et al., 1995). The effect of neuromodulators on behavioral motor programs is also evident at the level of the whole animal. For example, octopamine activates flight in insects (Sombati and Hoyle, 1984), dopamine triggers walking in decerebrate cats (Grillner and Zangger, 1979), and serotonin elicits swimming in nudibranchs (McClellan et al., 1994) and aggressive posturing in lobsters (Kravitz, 1988).Many behaviors, however, do not occur in isolation but occur as part of a behavioral sequence with distinct phas...