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Neuropeptide Y (NPY) was injected directly Into the paraventricular nucleus of the hypothalamus (PVN) of satiated, brain-cannulated rats, and food and water intake were measured 0.5, 1, 2, 4, and 22 hr postinjection. NPY (24, 78, 235, 783, and 2351 pmol/0.3 pl) produced a large, dosedependent increase in food intake as well as a small increase in water intake. The latency to eat was about 10 min, with substantial feeding occurring in the first 30 min. At doses below 78 pmol, the eating generally occurred only within the first hour. At doses above 235 pmol, however, the subjects' food intake continued to increase such that by 4 hr postinjection they had consumed the equivalent of normal 22-hr intake, and 22 hr postinjection they had also eaten significantly more than control subjects. Previous studies have shown that norepinephrine injected into the PVN stimulates feeding through aadrenergic receptors. To investigate a possible interaction, subjects were given PVN injections of phentolamine (60 nmol) prior to injections of either NPY (78 pmol) or norepinephrine (20 nmol). Phentolamine pretreatment significantly decreased feeding elicited by norepinephrine without affecting feeding elicited by NPY. This suggests that NPY does not stimulate feeding through the release of endogenous norepinephrine. The powerful stimulation of feeding elicited by this neuropeptide suggests an important role for hypothalamic NPY, or a structurally related peptide, in the regulation of feeding behavior.Neuropeptide Y (NPY), a 36-amino acid member of the pancreatic polypeptide family, was discovered in porcine brain by Tatemoto et al. in 1982 (1, 2). Subsequently, the concentration of NPY in the brain was found to exceed the concentration of any other peptide (3). Our interest in a possible role for NPY in the control of feeding behavior was stimulat ed by the recent reports that it is colocalized with norepinephrine (NE) and epinephrine in brainstem catecholamine cell groups, which send afferent fibers to the paraventricular nucleus of the hypothalamus (PVN) (4, 5; however, see ref.32), and also by reports that it is found within numerous presynaptic terminals in the PVN (3, 6, 7). Experiments investigating brain mechanisms of feeding behavior have demonstrated that central injections of several putative neurotransmitters, including NE, y-aminobutyric acid, acetylcholine, and opiate agonists, can selectively stimulate feeding behavior (8-11). The most intensely studied of these is NE. It has been shown that PVN injection of exogenous NE, or drug-induced release of endogenous NE from brainstem catecholamine neurons that ascend to the PVN, elicits feeding behavior through stimulation of a2-adrenergic receptors (12-15). The feeding response appears to be mediated through the PVN, since this is the brain region that is most sensitive to NE and since NE-induced feeding is severely attenuated by PVN lesions (12, 16). A role for this system in natural (deprivation-induced) feeding was suggested by the findings that PVN a-adrenergic r...

The immune privileged nature of the CNS can make it vulnerable to chronic and latent infections. Little is known about the effects of lifelong brain infections, and thus inflammation, on the neurological health of the host. Toxoplasma gondii is a parasite that can infect any mammalian nucleated cell with average worldwide seroprevalence rates of 30%. Infection by Toxoplasma is characterized by the lifelong presence of parasitic cysts within neurons in the brain, requiring a competent immune system to prevent parasite reactivation and encephalitis. In the immunocompetent individual, Toxoplasma infection is largely asymptomatic, however many recent studies suggest a strong correlation with certain neurodegenerative and psychiatric disorders. Here, we demonstrate a significant reduction in the primary astrocytic glutamate transporter, GLT-1, following infection with Toxoplasma. Using microdialysis of the murine frontal cortex over the course of infection, a significant increase in extracellular concentrations of glutamate is observed. Consistent with glutamate dysregulation, analysis of neurons reveal changes in morphology including a reduction in dendritic spines, VGlut1 and NeuN immunoreactivity. Furthermore, behavioral testing and EEG recordings point to significant changes in neuronal output. Finally, these changes in neuronal connectivity are dependent on infection-induced downregulation of GLT-1 as treatment with the ß-lactam antibiotic ceftriaxone, rescues extracellular glutamate concentrations, neuronal pathology and function. Altogether, these data demonstrate that following an infection with T. gondii, the delicate regulation of glutamate by astrocytes is disrupted and accounts for a range of deficits observed in chronic infection.

Event DAS‐59122‐7 is a novel transgenic trait designed to protect the roots and yield potential of maize from the insect pest corn rootworm Diabrotica spp. (Col.: Chrysomelidae). The increased pest status of corn rootworm, exceptional efficacy of this trait, and anticipated increases in farm efficiency and grower and environmental safety will drive adoption of this trait. Strong grower acceptance of this trait highlights the importance of science‐based and practical resistance management strategies. A non‐diapause trait was introgressed into two laboratory colonies of Diabrotica virgifera virgifera collected from geographically distinct locations: Rochelle, IL and York, NE. Both colonies were divided and each reared on maize containing event DAS‐59122‐7 or its near isoline. Selected and unselected colonies were evaluated for phenotypic change in larval development, injury potential and survival to adulthood during 10 and 11 generations. The F1 generation of both selected colonies displayed increased larval development, survivorship and measurable, but economically insignificant increases in injury potential on DAS‐59122‐7 maize. Survival rates of 0.4 and 1.3% in F1 generations of both selected colonies corroborate field estimates of survival on DAS‐59122‐7 maize. Over later generations, total phenotypic variation declined gradually and irregularly. Despite the absence of random mating, the tolerance trait could not be fixed in either population after 10 or 11 generations of selection. An allele conferring major resistance to DAS‐59122‐7 was not identified in either selected colony. The assessment also concluded that major resistance gene(s) are rare in populations of D. v. virgifera in the United States, and that a minor trait(s) conferring a low level of survival on DAS‐59122‐7 maize was present. The tolerance trait identified in this study was considered minor with respect to its impact on DAS‐59122‐7 maize efficacy, and the role this trait may play in total effective refuge for major resistance genes with recessive inheritance is the basis of future work.

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Rats learned to self-administer d-amphetamine (10 micrograms/microliter) through a cannula implanted in the nucleus accumbens. They responded more frequently for 65 +/- 15 nl of amphetamine than for equal amounts of saline. When presented with two levers (one amphetamine, one blank) they responded more on the correct lever for amphetamine. They would also switch levers, when necessary, to maintain access to the drug. When half the usual drug intake was given automatically, animals reduced their response rate by half, thus self-regulating the total amount of amphetamine they received. In tests for leakage into the ventricles, eight rats that self-injected with an accumbens cannula showed response extinction when switched to a ventricular cannula. We conclude that amphetamine self-injected into the accumbens is a positive reinforcer. This localization of 'amphetamine reward' suggests that the nucleus accumbens contains a synaptic mechanism underlying amphetamine abuse and, perhaps, also natural reinforcement of behavior.

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