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B-50 is a brain-specific phosphoprotein, the phosphorylation state of which may play a role in the regulation of (poly)phosphoinositide metabolism. Several kinases were tested for their ability to phosphorylate purified B-50 protein. Only calcium-activated, phospholipid-dependent protein kinase (kinase C) and B-50 protein kinase were able to use B-50 protein as a substrate. Furthermore, kinase C specifically phosphorylates B-50 when added to synaptic plasma membranes. We further characterized the sensitivity of kinase C and B-50 kinase to ACTH (and various fragments), phospholipids, chlorpromazine, and proteolytic activation. Since the sensitivities of both kinases were similar, we conclude that B-50 protein kinase is a calcium-dependent, phospholipid-stimulated protein kinase of the same type as kinase C.

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. The pontine parabrachial nucleus (PBN) has been implicated in regulating ingestion and contains opioids that promote feeding elsewhere in the brain. We tested the actions of the selective -opioid receptor (-OR) agonist [D-Ala 2 ,N-Me-Phe 4 ,Gly 5 -ol]enkephalin (DAMGO) in the PBN on feeding in male rats with free access to food. Infusing DAMGO (0.5-4.0 nmol/0.5 l) into the lateral parabrachial region (LPBN) increased food intake. The hyperphagic effect was anatomically specific to infusions within the LPBN, dose and time related, and selective for ingestion of chow compared with (nonnutritive) kaolin. The nonselective opioid antagonist naloxone (0.1-10.0 nmol intra-PBN) antagonized DAMGO-induced feeding, with complete blockade by 1.0 nmol and no effect on baseline. The highly selective -opioid antagonist D-Phe-Cys-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP; 1.0 nmol) also prevented this action of DAMGO, but the -antagonist nor-binaltorphimine did not. Naloxone and CTAP (10.0 nmol) decreased intake during scheduled feeding. Thus stimulating -ORs in the LPBN increases feeding, whereas antagonizing these sites inhibits feeding. Together, our results implicate -ORs in the LPBN in the normal regulation of food intake.feeding; hyperphagia; DAMGO; naloxone; CTAP STIMULATING ANY OF THE SUBTYPES of opioid receptors (ORs; , , ␦) or the related orphan receptor for nociceptin increases food intake in mammals (6,24,26,71,77). The orexigenic effects of these treatments are evident particularly in settings using preferred foods for the test diet (e.g., 39, 94, 95), although consumption of standard chow is also enhanced (9, 72). Conversely, drugs that block ORs reduce food intake (11,16,41,49). This hypophagia may occur especially under conditions when opioid pathways are highly activated (53). The data, therefore, suggest that opioid peptides play roles in the physiological control of feeding.The anatomic loci subserving opioidergic feeding are distributed widely throughout the brain. Attention has focused on the nucleus accumbens (NAC) and the rest of the ventral striatum as a critical region (9,72,94,95). Infusing opioid agonists into the ventral tegmental area of the midbrain, which projects onto the ventral striatum, also stimulates feeding (45, 67); this circuitry is consistent with the view assigning a broader role for opioids to support positive affect and appetitive reward (39, 70). Another (probably integrated) circuit is defined by observations that opioid stimulation of the paraventricular hypothalamic nucleus (21, 22) The parabrachial nucleus (PBN) of the pons has bidirectional communication with the PVN, central nucleus of the amygdala, and NTS (19,29,61,62). The multiple subnuclei of the PBN sort afferent input from second-order sensory neurons originating in the NTS and spinal cord (38,83) and distribute the information to rostral targets (19,36,37,68). This sensory processing includes neurotransmission underlying gustatory and visceral function and their convergence (8,30,38).It is logical, then, that the PBN has been imp...