Intake inhibition by NPY: role of appetitive ingestive behavior and aversion

Intraventricular infusion of neuropeptide Y (NPY) decreases the amount female rats ingest during intraoral infusion (consummatory behavior) of a 1-M solution of sucrose at a rate of 0.5 ml/min and simultaneously increases the number of times the rats visit a bottle filled with sucrose (appetitive behavior). In this study, we investigated if the suppression of consummatory behavior was dependent upon the increase of appetitive behavior. The shift from consummatory to appetitive ingestive behavior was attenuated by adding 3-mM quinine HCl (QHCl) to the sucrose solution in the bottle. However, the intraoral intake of the sucrose solution was still decreased in NPY-treated rats. NPY did not modify taste reactivity as measured by aversive responses during continuous intraoral infusion of sucrose or ingestive and aversive responses to brief intraoral infusion of sucrose (0, 0.3 or 1 M) or QHCl (0, 0.3 or 3 mM). NPY stimulated visits to a bottle and intake from the bottle and inhibited sexual behavior in male rats but had no effect on the sexual behavior in the absence of a bottle. The visits and the intake were suppressed, but sexual behavior was not activated by adding QHCl (3 mM) to the solution in the bottle. Obstructing appetitive ingestive behavior, therefore, does not indiscriminately facilitate consummatory behavior. Male rats showed aversive or ingestive behavior and sexual behavior simultaneously during intraoral infusion of QHCl or condensed milk. It is suggested that NPY decreases intraoral intake and increases appetitive ingestive behavior via partially separable mechanisms that are independent of taste aversion.     

Hindbrain catecholamine neurons control multiple glucoregulatory responses

Reduced brain glucose availability evokes an integrated constellation of responses that protect and restore the brain's glucose supply. These include increased food intake, adrenal medullary secretion, corticosterone secretion and suppression of estrous cycles. Our research has focused on mechanisms and neural circuitry underlying these systemic glucoregulatory responses. Using microinjection techniques, we found that localized glucoprivation of hindbrain but not hypothalamic sites, elicited key glucoregulatory responses, indicating that glucoreceptor cells controlling these responses are located in the hindbrain. Selective destruction of hindbrain catecholamine neurons using the retrogradely transported immunotoxin, anti-dopamine beta-hydroxylase conjugated to saporin (DSAP), revealed that spinally-projecting epinephrine (E) or norepinephrine (NE) neurons are required for the adrenal medullary response to glucoprivation, while E/NE neurons with hypothalamic projections are required for feeding, corticosterone and reproductive responses. We also found that E/NE neurons are required for both consummatory and appetitive phases of glucoprivic feeding, suggesting that multilevel collateral projections of these neurons coordinate various components of the behavioral response. Epinephrine or NE neurons co-expressing neuropeptide Y (NPY) may be the neuronal phenotype required for glucoprivic feeding: they increase NPY mRNA expression in response to glucoprivation and are nearly eliminated by DSAP injections that abolish glucoprivic feeding. In contrast, lesion of arcuate nucleus NPY neurons, using the toxin, NPY-saporin, does not impair glucoprivic feeding or hyperglycemic responses. Thus, hindbrain E/NE neurons orchestrate multiple concurrent glucoregulatory responses. Specific catecholamine phenotypes may mediate the individual components of the overall response. Glucoreceptive control of these neurons resides within the hindbrain.     

Hindbrain catecholamine neurons mediate consummatory responses to glucoprivation

Previous work using the retrogradely transported immunotoxin, saporin (SAP) conjugated to a monoclonal antibody against dopamine-beta-hydroxylase (DBH; DSAP), to selectively lesion norepinephrine (NE) and epinephrine (E) neurons projecting to the medial hypothalamus, demonstrated the essential role of these neurons for appetitive ingestive responses to glucoprivation. Here, we again utilized this lesion to assess the importance of these same neurons for the consummatory phase of glucoprivic feeding. To test consummatory responses, milk was infused intraorally through a chronic cheek fistula until rejected. Appetitive responses were tested in the same rats using pelleted food. Feeding responses to insulin-induced hypoglycemia, 2-deoxy-D-glucose (2DG)-induced blockade of glucose utilization, mercaptoacetate (MA)-induced blockade of fatty acid oxidation, 0.9% saline, and 18-h food deprivation were assessed. Unlike unconjugated SAP controls, the DSAP rats did not increase their food intake in response to glucoprivic challenges in either the pelleted food or the intraoral feeding tests. However, the DSAP rats did not differ from SAPs in their ingestive responses to food deprivation and blockade of fatty acid oxidation. The selective impairment of glucoprivic feeding responses indicates that DSAP did not impair the underlying circuitry required for either appetitive or consummatory ingestive responding but eliminated the mechanism for control of this circuitry specifically by glucoprivation. Results suggest that both appetitive and consummatory responses to glucoprivation are controlled and coordinated by multilevel terminations of the same catecholamine neurons.     

Effects of sibutramine on the appetitive and consummatory aspects of feeding in non-human primates

This study examined how sibutramine (0.06-4.0 mg/kg, i.m.), a clinically effective weight-loss medication which increases extracellular serotonin and norepinephrine levels, affected the appetitive and consummatory aspects of feeding of non-human primates. The effects were compared to the effects of the positive control dexfenfluramine (2.0-6.0 mg/kg, p.o.), which primarily increases extracellular serotonin levels. Baboons had access to food 24 h each day, but they had to complete a two-phase operant procedure in order to eat. Responding on one lever during a 30-min appetitive phase was required before animals could start a consumption phase, where responding on another lever led to food delivery, i.e., a meal. Responding during the appetitive phase resulted in presentations of food-related stimuli only. Sibutramine increased the latency to the first meal of the session in females, and decreased consummatory behavior without affecting other appetitive behavior in males and females. In contrast, dexfenfluramine, increased the latency to the first meal of the session, and decreased both appetitive and consummatory behavior in males and females. The behavioral mechanism by which sibutramine decreases food intake is distinct from other anorectic drugs, including dexfenfluramine, that have been tested in this paradigm.     

Reinforcer-specificity of appetitive and consummatory behavior of rats after Pavlovian conditioning with food reinforcers

We examined the reinforcer-specificity of Pavlovian conditioning in the control of appetitive and consummatory behaviors in Pavlovian-to-instrumental transfer, cue-potentiated eating, and devaluation procedures. Rats received pairings of one conditioned stimulus with sucrose and another conditioned stimulus with maltodextrin. In Experiment 1, rats were also trained to earn sucrose for one instrumental response and maltodextrin for another. In a transfer test, the Pavlovian cues enhanced the rate of instrumental responding more when the food reinforcer predicted by the instrumental response and the Pavlovian cue were consistent than when they were inconsistent, but both cues enhanced both responses. In Experiment 2, sated rats' consumption of each food was potentiated in the presence of a cue for that food, but not in the presence of a cue for the other food. In Experiment 3, one food was devalued by pairing it with lithium chloride, prior to testing food consumption and food-cup directed behaviors. The food cues selectively controlled food-cup related behaviors, regardless of the presence of the devalued or nondevalued foods in the food cup. Together, these results are consistent with the view that conditioned cues modulate appetitive and consummatory behaviors with increasing levels of specificity. The closer an action comes to ingestion, the more it is controlled by sensory properties conveyed by learned cues. These data are discussed in the context of allostatic regulation of food foraging and intake.     

Evidence that appetitive responses for dehydration and food-deprivation are learned

Rats do not seek water when cellularly dehydrated until they are about 4 weeks of age. This lack of appetitive 'seeking' behavior in young rats differs from their precocious ingestive responses such as an increased intake of solutions infused into their mouths when they are dehydrated as young as 2 days of age. Using video analysis of appetitive behavior in a structured environment, we document this early absence of appetitive responding and the subsequent acquisition of dehydration-elicited appetitive behavior. Weaning age pups were separated into four conditions: (i) experienced, dehydrated; (ii) experienced, nondehydrated; (iii) inexperienced, dehydrated; and (iv) inexperienced, nondehydrated. 'Experienced' rats received a dehydration and drinking experience prior to the test, and 'dehydrated' rats were dehydrated (by injection of a salt load) at the time of test. At the test, all water and food was removed from the test cages, eliminating the confounding of appetitive and consummatory measures. Despite the fact that pups in all conditions had experience with water and had previously drunk, only the 'experienced' pups differentially sought water when dehydrated. Parallel experiments with food deprivation produced similar results. Pups did not exhibit food-seeking behavior when food-deprived unless they had previous experience with food deprivation and eating. The appetitive 'seeking' behavior for feeding also appears to be learned. Directed appetitive behavior in general may thus be acquired.     

The effects of NPY and 5-TG on responding to cues for fats and carbohydrates

Previous research has shown that glucoprivic and lipoprivic metabolic challenges selectively augment the performance of appetitive responses conditioned to carbohydrate- and fat-associated cues, respectively. The present experiment investigated whether intracerebroventricular (i.c.v.) infusion of neuropeptide Y (NPY) has a similar selective effect on appetitive behavior. We trained rats to associate two different conditioned stimuli (CSs) with two different macronutrient (peanut oil and sucrose pellets) unconditioned stimuli (USs). After training, the rats were food sated and responding to each CS was then tested in extinction. In one test session, the effects of NPY were compared to isotonic saline. A second test compared the effects of these two treatments with i.c.v. infusion of the glucose antimetabolite 5-thio-d-glucose (5-TG). Replicating our earlier result, 5-TG selectively promoted conditioned responding to the CS for sucrose pellets. In contrast, the capacity of NPY to promote appetitive behavior did not depend on the macronutrient that was signaled by the CS. These results suggest that NPY and 5-TG promote appetitive behavior via different mechanisms.     

The effects of agouti-related protein gene transfer in vivo by electroporation in mice

In the present study, the cDNA encoding agouti-related protein (AGRP) gene known as an orexigenic factor was transferred in vivo to test whether food intake and body weight gain is improved in mice. When the expression plasmid of AGRP gene driven by mouse β-actin, pActAGRP, was transferred into leg muscle by electroporation, body weight of gene-transferred mice was significantly increased at 14 days and afterwards compared with that of control counterparts (p < 0.05). Likewise, daily food intake was also significantly higher in the AGRP gene-transferred mice than in the control mice at 4 days and afterwards (p < 0.05). A significant increase in serum AGRP concentration of the AGRP gene-transferred group was detected compared with the control group at 1 week (p < 0.01), but the difference quickly disappeared at 3 weeks. However, the hypothalamic NPY mRNA abundance of AGRP gene-transferred mice was significantly higher than that of the control mice at 3 weeks (p < 0.05). These results suggested that instead of hormone administration per se, in vivo AGPR gene transfer into skeletal muscle was found to mimic hormonal effects. The present methodology of in vivo gene transfer by electroporation might be useful to promote growth and food intake in farm livestock as well as experimental animals.     

Conditioned changes in appetitive and consummatory responses to flavors paired with oral or nutrient reinforcement among adult rats

Recent studies of the behavioral organization of conditioned flavor preferences have suggested the involvement of at least two separate learning systems-an appetitive response system sensitive to the oral hedonic properties of the reinforcer, and a consummatory response system sensitive to its nutrient properties. However, these prior studies were conducted with weanling rats, that differ from adults in terms of their prior experience with food, their learning competencies, and the peculiar ontogenetic constraints on their behavior. It is, therefore, unknown whether flavor preference behaviors are similarly organized in adult rats. In this experiment, adult rats were trained to associate a specific CS flavor with either the sweet taste or the postingestive nutrient effects of sucrose. Conditioned appetitive orienting and consummatory oral responding to the CS flavors were then measured. Unlike weanling rats, adult rats exhibited both conditioned appetitive behavior and conditioned consummatory behavior in response a CS that was previously paired with either oral hedonic or nutrient reinforcement. These results suggest a set of important developmental changes in the neurobehavioral mechanisms of flavor preference learning in the postweaning period.     

Cannabinoid agonist, CP 55,940, facilitates intake of palatable foods when injected into the hindbrain

Cannabinoids have been shown to influence food intake, and until recently, the neural pathways mediating these effects have remained obscure. It has been previously shown that intracerebroventricular injection of delta-9-tetrahydrocannabinol (Δ⁹-THC) causes increased consumption of palatable foods in rats, and we postulated the involvement of the hindbrain in this cannabinoid-induced food intake. Cannulated rats (both female and male groups) trained to consume sweetened condensed milk received either lateral or fourth ventricle injections of CP 55,940 and were presented with sweetened condensed milk 15 min after injection. Rats were injected over a range of doses between 100 pg and 10 μg per rat. Milk intake was recorded for a total of 3 h. Lateral ventricle injection of CP 55,940 increased milk intake at doses in the microgram range. However, CP 55,940 was effective in increasing food intake at nanogram doses when injected into the fourth ventricle. Finally, male rats appeared to be more sensitive to CP 55,940 than female rats inasmuch as milk consumption was increased at the 1 ng dose in male rats, whereas only the 10 ng dose was effective in females. These results indicate that CP 55,940 may act in the hindbrain to influence feeding behavior in rats.     

Effect of lithium chloride-induced aversion on appetitive and consummatory behavior

The effect of lithium chloride-induced conditioned taste aversions on appetitive and consummatory behavior was determined. Rats were given access to a 0.1% saccharin solution for 15 min either in bottles or by infusion through an intraoral cannula. Bottle-fed rats given postprandial injections of lithium chloride showed greater aversion to saccharin than cannula-fed rats. During extinction, cannula-fed rats gradually recovered to control levels of intake, whereas bottle-fed rats continued to avoid the saccharin. These results suggest that lithium chloride affects appetitive behavior to a greater extent than it affects consummatory behavior.     

The hypothalamus and the control of energy homeostasis: different circuits, different purposes.

The hypothalamus regulates many aspects of energy homeostasis, adjusting both the drive to eat and the expenditure of energy in response to a wide range of nutritional and other signals. It is becoming clear that various neural circuits operate to different degrees and probably serve specific functions under particular conditions of altered feeding behaviour. This review will discuss this functional diversity by illustrating hypothalamic neurones that express neuropeptide Y (NPY), the melanocortin-4 receptor (MC4-R) and the orexins. NPY neurones in the arcuate nucleus (ARC) release NPY, a powerful inducer of feeding and obesity, in the paraventricular nucleus (PVN) and the lateral hypothalamic area (LHA). ARC-NPY neurones are inhibited by leptin and insulin and become overactive when levels of these hormones fall during undernutrition. They may function physiologically to protect against starvation. With disruption of the inhibitory leptin signals due to gene mutations, the NPY neurones are overactive, which contributes to hyperphagia and obesity in the ob/ob and db/db mice and fa/fa Zucker rat. The MC4-R is activated by alpha-melanocyte-stimulating hormone [alpha-MSH; a cleavage product of pro-opiomelanocortin (POMC), which is expressed in the other ARC neurones] and inhibits feeding. This effect is antagonised by agouti gene-related peptide (AGRP), which is coexpressed by the ARC-NPY neurones only. Activation of MC4-R, possibly mediated by blockade of AGRP release, appears to restrain overeating of a palatable diet. This response may be programmed by a transient rise in leptin soon after presentation of palatable food, and rats that fail to do this will overeat and become obese. Orexin-A and -B (corresponding to hypocretins 1 and 2) are expressed in specific LHA neurones. These have extensive reciprocal connections with many areas involved in appetite control, including the nucleus of the solitary tracts (NTS), which relays vagal afferent satiety signals from the viscera. Orexin neurones also have close anatomical connections with LHA glucose-sensitive neurones. Orexin-A induces acute feeding but does not cause obesity. Orexin neurones are stimulated by hypoglycaemia partly via the NTS and inhibited by food ingestion. These neurones may therefore be involved in the severe hyperphagia of hypoglycaemia and short-term control of feeding.     

Nicotinamide induces male-specific body weight loss in the postnatal period through molecular regulation of the hypothalamus and liver

Molecular mechanisms of body weight control have been discovered recently and much research focuses on the hypothalamic regulation of food intake and the hepatic regulation of glucose utility. We previously reported that postnatal nicotinamide treatment reduced brain dopamine and body weight. To further investigate the differential effects of nicotinamide-mediated body weight loss, nicotinamide (i.p. 100 mg/kg) was injected into postnatal and adult mice twice a week for 4 weeks. Interestingly, following nicotinamide treatment, male postnatal mice displayed reduced body weight and spontaneous motor activity. No significant changes were observed in adult and postnatal female mice or adult male mice following nicotinamide treatment. In male postnatal mice, hypothalamic agouti-related peptide (AGRP) and proopiomelanocortin (POMC) levels were increased in the arcuate nucleus following nicotinamide treatment. Neuropeptide Y (NPY) levels were unchanged in both male and female mice. Additionally, nicotinamide-injected male postnatal mice had increased glucose 6-phosphatase (G6Pase) and decreased phosphoenolpyruvate carboxykinase (PEPCK) expression in liver. These results indicate that hypothalamic POMC and hepatic PEPCK are important molecules that mediate nicotinamide-induced weight loss in postnatal male mice.     

Dopamine: helping males copulate for at least 200 million years: theoretical comment on Kleitz-Nelson et al. (2010)

Brain dopamine (DA) systems are implicated in a variety of behavioral responses and clinical syndromes, including sex, drug addiction, feeding, satiety, sleep, wakefulness, arousal, attention, reward, decision-making, depression, anxiety, psychosis, and movement disorders. The paper in this issue by Kleitz-Nelson, Dominguez, and Ball (2010) shows how DA release in the medial preoptic area of male quail are activated in an androgen-dependent manner during appetitive and consummatory phases of sexual behavior, similar to that reported previously in male rats. Those data suggest that the steroid-dependent role of hypothalamic DA in male sexual behavior has been conserved through evolutionary time.     

Forebrain sites of NPY action on estrous behavior in Syrian hamsters

Food deprivation and similar metabolic challenges inhibit estrous behavior in female Syrian hamsters. The relevant metabolic cues appear to be detected in the hindbrain, and this information is then relayed synaptically to the forebrain circuits controlling estrous behavior. Neuropeptide Y (NPY) may be one of the neuropeptides/neurotransmitters serving this function. Infusion of NPY or the Y2/Y5 agonist, peptide YY3-36 (PYY3-36), into the lateral ventricles rapidly inhibits estrous behavior in ovariectomized, steroid-primed hamsters. This experiment sought to determine the neural loci where NPY acts to inhibit estrous behavior. Steroid-primed animals received infusions of artificial cerebrospinal fluid (aCSF) vehicle, 0.024 nmol PYY3-36 and 0.24 nmol PYY3-36 in separate tests 30 min prior to testing for sexual receptivity. Infusion of 0.24 nmol, but not 0.024 nmol, of PYY3-36 reduced lordosis duration when infused into the paraventricular nucleus of the hypothalamus (PVN), the caudal part of the medial preoptic area (MPO), the anterior hypothalamus (AH) or the lateral ventricles. Placements in the ventromedial hypothalamus (VMH), the arcuate nucleus (ARC) and the fourth ventricle were generally without effect. These data suggest that increased endogenous release of NPY into the caudal MPO-AH-PVN continuum during food deprivation could contribute to the observed inhibition of sexual receptivity. The possible contributions of other neuropeptides and neural estrogen receptors to this action of NPY are discussed.     

Increased hypothalamic neuropeptide Y expression in deprived preweanling rats is reversed by intragastric infusion of milk

Lean, preweanling Zucker rat pups increase neuropeptide Y (NPY) expression in the hypothalamic arcuate nucleus in response to a 24-h deprivation of food, water, and maternal interaction as early as postnatal day 2 (P2). In this study, we examined if replacing nutritive or tactile aspects of maternal behavior to deprived rat pups could block the increased expression of hypothalamic NPY measured by in situ hybridization. On P2, P12, or P15, littermates were assigned to one of four treatment groups: (1) left with the dam for 24 h, (2) deprived of the dam for 24 h and given tactile stimulation in the form of periodic anogenital stroking to elicit urination and defecation, (3) deprived of the dam and given periodic anogenital stroking plus continuous gastric infusion of milk for 24 h, or (4) deprived of the dam and given periodic anogenital stroking plus continuous infusion of water for 24 h. We found that gastric infusions of milk normalized NPY expression at all three ages, gastric infusions of water did not on P2 and P15, and anogenital stroking alone had no effect. We suggest that the lack of milk is the major cause of increased hypothalamic NPY expression during maternal deprivation in lean Zucker pups.     

AGRP neurons are sufficient to orchestrate feeding behavior rapidly and without training

Two intermingled hypothalamic neuron populations specified by expression of agouti-related peptide (AGRP) or pro-opiomelanocortin (POMC) positively and negatively influence feeding behavior, respectively, possibly by reciprocally regulating downstream melanocortin receptors. However, the sufficiency of these neurons to control behavior and the relationship of their activity to the magnitude and dynamics of feeding are unknown. To measure this, we used channelrhodopsin-2 for cell type-specific photostimulation. Activation of only 800 AGRP neurons in mice evoked voracious feeding within minutes. The behavioral response increased with photoexcitable neuron number, photostimulation frequency and stimulus duration. Conversely, POMC neuron stimulation reduced food intake and body weight, which required melanocortin receptor signaling. However, AGRP neuron-mediated feeding was not dependent on suppressing this melanocortin pathway, indicating that AGRP neurons directly engage feeding circuits. Furthermore, feeding was evoked selectively over drinking without training or prior photostimulus exposure, which suggests that AGRP neurons serve a dedicated role coordinating this complex behavior.     

Plasma catecholamines associated with hypothalamically-elicited defense behavior

Sympatho-adrenal (SA) activation was determined by measuring levels of norepinephrine (NE) and epinephrine (E) in bilateral adrenal venous and peripheral venous plasma of 20 anesthetized cats following stimulation of medial hypothalamic sites. Hypothalamic sites were selected that elicited affective defense behavior in the freely moving cat. Fifty-eight percent of these hypothalamic sites elicited a bilateral increase greater than or equal to 10 ng/min in the output of both adrenal catecholamines (CAs); these increases were greater from the gland ipsilateral to the side of stimulation. Other SA responses included both preferential increases or decreases in either NE or E. Under baseline conditions, an average of 67% of the NE in the peripheral venous plasma was contributed by the sympathetic noradrenergic nerves; hypothalamic stimulation at "defense" sites increased the contribution to 75%. The data suggest that hypothalamic regions that elicit defense behaviour may overlap with regions that activate the adrenal medullary and sympathetic nervous systems.     

Alpha 2-adrenoceptor blockade attenuates feeding behavior induced by neuropeptide Y and epinephrine

Neuropeptide Y (NPY, 0.47 nmol) and epinephrine (28.9 nmol) evoked robust, and quantitatively similar, increments in food intake and local eating rate following administration into the third cerebral ventricle (IIIV). Whereas IIIV pretreatment with phentolamine (71 nmol), a nonselective alpha-adrenoceptor antagonist, or prazosin (9.5 nmol), a selective alpha 1-adrenoceptor antagonist, was without effect on NPY-induced feeding behavior, pretreatment with the alpha 2-adrenoceptor antagonist yohimbine (15 nmol) dramatically attenuated the stimulatory effects of NPY or epinephrine on both food intake (by over 50%) and local eating rate. Additionally, yohimbine administered alone was associated with a stimulatory effect on food intake for the periods of 80-110, and 110-140 minutes posttreatment. These data demonstrate that feeding behavior induced by IIIV administration of NPY or epinephrine is attenuated by prior blockade of alpha 2-adrenoceptors and suggest that, as in other systems innervated by neurons displaying NPY and adrenergic transmitter colocalization, the effects of NPY on feeding behavior may, at least in part, be mediated via alpha 2-adrenoceptors.     

Performance of appetitive or consummatory components of male sexual behavior is mediated by different brain areas: a 2-deoxyglucose autoradiographic study

The in vivo autoradiographic deoxyglucose method was used to identify the functional brain circuits that are involved in the performance of appetitive and consummatory components of male sexual behavior in Japanese quail (Coturnix japonica). Two groups of castrated, testosterone-treated male quail were trained during 12 sessions to associate the view of a female behind a window with the opportunity to interact freely and to copulate with her. They developed, as a consequence, a social proximity response (staying close and looking through the window providing a view of the female) that has been used in previous experiments to measure appetitive sexual behavior. A third control group (also castrated and treated with testosterone) was allowed to view the female but not to copulate with her and therefore did not develop this proximity response. 2-14C-deoxyglucose was then injected i.p. to these birds and they were allowed to either copulate freely with a female (consummatory sexual behavior group) or express the social proximity response (appetitive sexual behavior group). The control group was provided a view of the female but these birds, although they were exposed to the same stimuli as birds in the appetitive group, did not express the social proximity response because they had never learned the association with the opportunity to copulate. Birds were killed 45 min after the deoxyglucose injection and their brains were processed for autoradiography. Densitometric analyses of the autoradiograms revealed that the expression of appetitive or consummatory aspects of male sexual behavior was associated with significant increases by comparison with the control group in the deoxyglucose incorporation in the nucleus mesencephalicus lateralis, pars dorsalis and in the nucleus leminsci lateralis. In addition, an increase in the deoxyglucose incorporation was specifically observed in the paleostriatum primitivum, rostral preoptic area, nucleus intercollicularis, nucleus interpeduncularis and third nerve but a decrease was observed in the dorsomedial part of the hippocampus and in the nucleus nervi oculomotori in birds of the consummatory sexual behavior group by comparison with controls. By contrast, in the appetitive sexual behavior group, significant increases in deoxyglucose incorporation were observed in two telencephalic areas, the intermediate hyperstriatum ventrale and neostriatum caudolaterale by comparison with the controls, but decreases were detected in the stratum griseum et fibrosum superficiale of optic tectum by comparison with the consummatory behavior group. These studies demonstrate that the performance of appetitive or consummatory components of male sexual behavior affects in a specific manner the deoxyglucose uptake and accumulation in specific regions of the quail brain. Changes in metabolic activity were observed in steroid-sensitive areas, in auditory, visual and vocal brain regions, and in brain nuclei related to motor behavior but also in association telencephalic and limbic structures. These changes in oxidative metabolism overlap to some extent with metabolic changes as revealed by immunocytochemistry for the immediate early gene products Fos and Zenk, but many specific reactions are also detected indicating that these techniques are not necessarily redundant and, together, they can provide a more complete picture of the brain circuits that are implicated in the control and performance of complex behaviors.