Involvement of β3-adrenergic receptors in the control of food intake in rats

This study examined the food intake changes evoked by intracerebroventricular (icv) injection of a selective agonist (BRL37344, 2 and 20 nmol) or antagonist (SR59230A, 10 and 50 nmol) of β3-adrenergic receptors in 24-h fasted rats (adult male Wistar rats, 200-350 g, N = 6/treatment). The animals were also pretreated with saline icv (SAL) or SR59230A (50 nmol) followed by BRL37344 (20 nmol) or SAL in order to determine the selectivity of the effects evoked by BRL37344 on food intake or the selectivity of the effects evoked by SR59230A on risk assessment (RA) behavior. The highest dose of BRL37344 (N = 7) decreased food intake 1 h after the treatment (6.4 ± 0.5 g in SAL-treated vs 4.2 ± 0.8 g in drug-treated rats). While both doses of SR59230A failed to affect food intake (5.1 ± 1.1 g for 10 nmol and 6.0 ± 1.8 g for 50 nmol), this treatment reduced the RA frequency (number/30 min) (4 ± 2 for SAL-treated vs 1 ± 1 for 10 nmol and 0.5 ± 1 for 50 nmol SR59230A-treated rats), an ethological parameter related to anxiety. While pretreatment with SR59230A (7.0 ± 0.5 g) abolished the hypophagia induced by BRL37344 (3.6 ± 0.9 g), BRL37344 suppressed the reduction in RA frequency caused by SR59230A. These results show that the hypophagia caused by BRL37344 is selectively mediated by β3-adrenergic receptors within the central nervous system. Moreover, they suggest the involvement of these receptors in the control of anxiety.

Involvement of ß3-adrenergic receptors in the control of food intake in rats.

This study examined the food intake changes evoked by intracerebroventricular (icv) injection of a selective agonist (BRL37344, 2 and 20 nmol) or antagonist (SR59230A, 10 and 50 nmol) of ß3-adrenergic receptors in 24-h fasted rats (adult male Wistar rats, 200-350 g, N = 6/treatment). The animals were also pretreated with saline icv (SAL) or SR59230A (50 nmol) followed by BRL37344 (20 nmol) or SAL in order to determine the selectivity of the effects evoked by BRL37344 on food intake or the selectivity of the effects evoked by SR59230A on risk assessment (RA) behavior. The highest dose of BRL37344 (N = 7) decreased food intake 1 h after the treatment (6.4 ± 0.5 g in SAL-treated vs 4.2 ± 0.8 g in drug-treated rats). While both doses of SR59230A failed to affect food intake (5.1 ± 1.1 g for 10 nmol and 6.0 ± 1.8 g for 50 nmol), this treatment reduced the RA frequency (number/30 min) (4 ± 2 for SAL-treated vs 1 ± 1 for 10 nmol and 0.5 ± 1 for 50 nmol SR59230A-treated rats), an ethological parameter related to anxiety. While pretreatment with SR59230A (7.0 ± 0.5 g) abolished the hypophagia induced by BRL37344 (3.6 ± 0.9 g), BRL37344 suppressed the reduction in RA frequency caused by SR59230A. These results show that the hypophagia caused by BRL37344 is selectively mediated by ß3-adrenergic receptors within the central nervous system. Moreover, they suggest the involvement of these receptors in the control of anxiety.

The role of nitric oxide in the emotional learning of rats in the plus-maze.

The present study evaluated the role of nitric oxide (NO) in the transfer latency (TL) paradigm in the elevated plus-maze. Male Wistar rats received i.p. injections of either 0.9% Saline, N(omega) Nitro-L-arginine-methyl-ester (L-NAME, an inhibitor of NO synthesis), d-NAME (inert isomer), scopolamine (SCO, antagonist of muscarinic receptors), or MK-801 (antagonist of NMDA receptors) and, after 30 min, were submitted to TL procedure. In an independent experiment, the ability of the same L-NAME treatments in changing the arterial pressure and blood glucose level (BGL) was evaluated in conscious rats. The treatment with SCO (1 mg kg(-1)), MK-801 (0.15 mg kg(-1)) and L-NAME (10 and 50 mg kg(-1)), but not with D-NAME, impaired the TL learning. The L-NAME-induced TL deficit was counteracted by L-ARG (100 and 200 mg kg(-1)), while the co-administration of sub-effective doses of L-NAME and MK-801 failed to impair the TL learning. The L-NAME (50 mg kg(-1)) treatment failed to alter the BGL. All treatments with L-NAME induced hypertension, but the rats treated with L-NAME (5 mg kg(-1)) were still able to learn the TL task. The data indicate that the TL deficit induced by L-NAME (10 and 50 mg kg(-1)) is not due to either hypertension or changes in the BGL. It is also possible to establish that NO production is important for emotional learning underlying the TL procedure in rats.

Muscarinic cholinergic receptor blockade impairs free fatty acid mobilization during fasting in pigeons (Columba livia).

The effects of intracerebroventricular pretreatment with muscarinic (scopolamine or methylscopolamine; 2.7 nmol or 5.4 nmol) or nicotinic (mecamylamine, 2.7 nmol or 5.4 nmol) cholinergic receptor antagonists on plasma free fatty acid increases induced by intracerebroventricular injections of carbachol in conscious resting pigeons (Columba livia) were examined. Plasma glucose levels were also measured throughout the experiments. Pretreatment with methylscopolamine suppressed the lipolytic effect of carbachol injections, while mecamylamine left this response unchanged. Neither carbachol treatment alone, nor the pretreatments with cholinergic agents affected glucose levels. Subsequently, the effects of intracerebroventricular injections of methylscopolamine were investigated in 24-h food-deprived pigeons. The increase in free fatty acid levels after fasting was of a magnitude similar to that observed after carbachol treatment; intracerebroventricular injections of methylscopolamine (5.4 nmol) transiently but powerfully decreased plasma free fatty acids in 24-h food-deprived pigeons to levels comparable to those of free-feeding animals. The fasting-induced decrease in glucose levels was not affected by this treatment. These data indicate that the lipolytic response induced by carbachol may be mediated by central muscarinic cholinergic receptors and that this central cholinergic mechanism partially contributes to plasma free fatty acid increases observed during fasting. Furthermore, the absence of effects on glucose levels suggests that these cholinergic mechanisms participate selectively in the lipolytic component of the metabolic response to fasting.

Atypical angiotensin receptors may mediate water intake induced by central injections of angiotensin II and of serotonin in pigeons.

Intracerebroventricular (i.c.v.) injection of serotonin (5-HT) in pigeons dose-dependently evokes a prompt and intense drinking behavior, which resembles that evoked by i.c.v. injections of angiotensin II (ANGII) in the same species. In the present study, we have examined the possible participation of central ANGII receptors in both ANGII- and 5-HT-evoked drinking behavior. The effects of i.c.v. injections of 5-HT (155 nmol), avian ANGII ([Asp(1),Val(5)]-ANGII, 0.1 nmol) or vehicle were studied in pigeons pretreated 20 min before with i.c.v. injections of the nonspecific ANGII receptor antagonist [Sar(1),Ile(8)]-ANGII (SAR; 1, 0.1 or 0.01 nmol), the AT(1) receptor antagonist losartan (2 or 4 nmol), the AT(2) receptor antagonist PD 123,319 (2 or 4 nmol) or vehicle (NaCl 0.15 M, 1 microl, n = 8/group). Immediately after treatment, they were given free access to water and drinking behavior was recorded during the next 60 min. At the doses presently used both 5-HT and ANGII treatments evoked comparable water intake amounts with similar behavioral profiles. While pretreatment with SAR dose-dependently reduced the water intake evoked by both 5-HT and ANGII, neither losartan nor PD 123,319 pretreatment affected the drinking induced by these treatments. The present results indicate that ANGII- and 5-HT-induced drinking in pigeons may be mediated by AT receptors possibly different from mammalian AT(1) and AT(2) receptors and suggest that activation of ANGII central circuits is a necessary step for the intense drinking induced by i.c.v. injections of 5-HT in this species.

Central injections of noradrenaline and adrenaline differentially affect plasma free fatty acid and glucose in conscious pigeons (Columba livia).

The possible involvement of central noradrenergic and/or adrenergic circuits in central mechanisms controlling free fatty acids and glucose levels was investigated in conscious pigeons. The effects of intracerebroventricular injections of noradrenaline (80 nmol) or adrenaline (80 nmol) on plasma free fatty acids and glucose concentrations were examined. The possible role of the autonomic nervous system, of sympathetic terminals and of pituitary hormone release in the metabolic responses induced by intracerebroventricular injections of adrenaline and noradrenaline was investigated by systemic pretreatment with a ganglionic blocker (hexamethonium, 1 mg/100 g), guanethidine (5 mg/100 g), and somatostatin (15 microg/100 g), respectively, 15 min before intracerebroventricular administration of adrenaline, noradrenaline or vehicle. Intracerebroventricular noradrenaline injections strongly increased plasma free fatty acid concentration but evoked no change in blood glucose levels, while adrenaline treatment increased glycemia without affecting free fatty acid levels. Hexamethonium did not block the increase in plasma free fatty acids induced by noradrenaline, while somatostatin pretreatment abolished noradrenaline-induced lipolysis during the experimental period. Adrenaline-induced hyperglycemia was blocked by systemic injections of somatostatin, hexamethonium and guanethidine. The present results suggest that: (1) adrenergic and noradrenergic mechanisms may participate in central control of blood glucose and free fatty acids, respectively, as observed in mammals. (2) noradrenaline-induced lipolysis may be mediated by pituitary mechanisms, and (3) postganglionic sympathetic fibers, possibly innervating the endocrine pancreas, may be involved in adrenaline-induced hyperglycemia.

Glutamatergic control of food intake in pigeons: effects of central injections of glutamate, NMDA, and AMPA receptor agonists and antagonists.

The possible involvement of glutamatergic mechanisms in the control of food intake was studied in free-feeding and in 24-h food-deprived (FD24) pigeons for 1 h after intracerebroventricular (i.c.v.) treatment with glutamate (Glu, 0, 50, 150, 300, and 600 nmol). Glu injections dose dependently induced decreases (30-65%) in food intake (FI) and feeding duration (FD), and increases in latency to start feeding (LSF) in FD24 animals, but not in free-feeding ones. None of these treatments affected noningestive behaviors (locomotion, sleep, and preening). In FD24 pigeons, i.c.v. treatments with N-methyl-D-aspartic acid (NMDA, 0.1, 1, 4, 8, or 16 nmol) or D,L-alpha-amino-3-hydroxy-isoxazole proprionic acid (AMPA, 0.1, 1, 4, or 8 nmol) decreased FI and FD, but left LSF unchanged compared to vehicle-treated FD24 controls. Kainic acid (0.1, 0.5, and 1 nmol), or [trans-(1S,3R)-ACPD-(5NH4OH)] (ACPD, 0.1, 1, 4, 8, and 16 nmol) left unchanged the ingestive profile of FD24 pigeons. Pretreatment with the NMDA receptor antagonist MK-801 (15 nmol) and the AMPA-kainate receptor antagonist CNQX (390 nmol), 20 min before an i.c.v. injection of Glu (300 nmol) induced a partial blockade of the Glu-induced decreases in FI and FD and completely inhibited the Glu-induced increase in LSF in FD24 pigeons. I.c.v. injections of MK-801 (30 nmol) and of CNQX (780 nmol) increased FI and FD and reduced LSF in free-feeding pigeons. A lower dose of MK-801 (15 nmol) increased FI and FD, but not LSF. Conversely, a lower dose of CNQX (390 nmol) reduced LSF without changing FI or FD. These findings indicate the involvement of Glu as a chemical mediator in the regulation of food intake in the pigeon, possibly acting on multiple central mechanisms in this species through NMDA- and AMPA-sensitive Glu receptors.

Food intake after adrenaline and noradrenaline injections into the hypothalamic paraventricular nucleus in pigeons.

The effects of local injections of adrenaline (Adr, 6 nmol) or noradrenaline (Nor, 16 nmol) into the paraventricular nucleus (PVN) and into other anterior hypothalamic districts on feeding behavior were examined in satiated pigeons bearing a chronically implanted cannula. When infused into the PVN, both Adr and Nor reliably elicited feeding responses during the first hour after the injection. Feeding responses to Adr injections were significantly higher than those evoked by Nor. Other behavioral measurements (sleep, exploratory, and preening) were not affected by these treatments. Local pretreatment with phentolamine (20 nmol) but not with propranolol (20 nmol) abolished the feeding response induced by both Adr and Nor into the PVN. Lateral hypothalamic sites were also shown to respond to catecholamine injections with an increase in feeding, followed also by an increased sleep-like behavior duration. Together with other evidence, the present results indicate that adrenergically mediated circuits into the avian PVN play an important role in the mechanisms of food intake control, equivalent to that observed in mammalian species.

Hypophagic and dipsogenic effects of central 5-HT injections in pigeons.

The present work describes a series of experiments designed to examine the possible role of central 5-HT circuits in the control of feeding and drinking in pigeons. Acute effects (within 1 h) of intracerebroventricular (ICV) injections of 5-HT (0, 9.7, 19.4, 38.7, 77.5, 155, and 310 nmol) in 24-h food-deprived (24FD) pigeons included strong hypophagic and dipsogenic responses at the three higher doses. Total food intake and the duration of feeding behavior were reduced, and latency for the start of eating increased. Total 1-h water intake in 5-HT-treated pigeons usually increases to reach a volume equivalent to 10% of their body weight. Similarly, potent dipsogenic effects of ICV 5-HT, but no food intake decreases, were observed in food-satiated animals. Feeding behavior induced by ICV injection of adrenaline (30 nmol) in satiated pigeons was abolished by previous (20 min before) ICV 5-HT (155 nmol) injections. Catecholamine treatment did not affected the dipsogenic effect of 5-HT injections. Decreases in food intake were similarly observed after ICV or subcutaneous injections of equimolar 5-HT doses (155 nmol) in 24FD pigeons, but systemic 5-HT injections evoked no drinking behavior. Central injections of the 5-HT(2a/2c) agonist DOI (56 nmol) induced similar decreases in duration and amount of food intake in 24FD animals. No dipsogenic effect was observed with either DOI doses. In 24FD pigeons, the 5-HT1a agonist 8-OH-DPAT (30.5 nmol) induced strong dipsogenic effects, as well as increase in food intake duration. These data may indicate an involvement of 5-HT circuits in food intake as well as in water intake control systems in the pigeon, and that serotoninergic effects in these functional domains are mediated by independent mechanisms.

Central beta-adrenoceptor involvement in neural control of blood glucose in pigeons.

The effects of ICV injections of adrenaline (30 nmol in 1 microL of saline) on blood glucose levels were investigated in conscious adult pigeons. This procedure increased blood glucose levels at 15-45 min after treatment. Previous ICV injection of propranolol (50 nmol) suppressed the increase observed at 15 min. The higher propranolol dose (100 nmol) was more effective than the lower dose (50 nmol) at blocking adrenaline-induced hyperglycemia. On the other hand, the ICV pretreatment with an alpha-adrenergic antagonist, phentolamine, slightly potentiated the hyperglycemia caused by ICV injection of adrenaline. The IP administration of propranolol (100 nmol) or phentolamine (100 nmol) before adrenaline ICV failed to induce change in the hyperglycemic response induced by this catecholamine. Both IP and ICV injections of these adrenergic blockers, before ICV injections of saline, evoked no changes in baseline glycemic levels. Therefore, elevation of blood glucose concentration by ICV adrenaline and blockade of the response by propranolol suggest the involvement of a central beta-adrenergic mechanism in the neural control of glycemia in pigeons.

Participation of the autonomic nervous system in lipolysis induced by intraventricular injection of carbachol in the pigeon.

The possible involvement of central cholinergic neurotransmission in lipomobilization in avian species was investigated by injecting carbachol into the brain lateral ventricle (i.c.v.) of conscious pigeons (N = 9 per experimental group). I.c.v. injections of carbachol (27 nmol in 1 microliter) induced an intense increase (nearly 91% above baseline levels) in the concentration of plasma free fatty acids (FFA). Previous intraperitoneal administration of hexamethonium (10 mg/kg) completely blocked the lipomobilizing effect of i.c.v. injections of carbachol. These results suggest that cholinergic neurons may be involved in central mechanisms controlling FFA mobilization in pigeons, and that this response is mainly mediated by activation of autonomic nervous system.

Electrographic patterns of postprandial sleep after food deprivation or intraventricular adrenaline injections in pigeons.

Intense postprandial sleep-like behavior was previously reported to occur, in a similar fashion, either after feeding evoked by intracerebroventricular adrenaline injections or after interruption of prolonged (96 h) fasting in conscious pigeons. These behavioral similarities were taken as indication of a physiological role for central adrenergic circuits in avian food intake regulation. In the present study we compared sleep-related electrographic signs (EEG, EMG, and EOG) that develop following both food intake-inducing situations to further examine these correspondences and their corollaries. Our data indicate that postprandial behaviors in the pigeon include dramatic increases in the incidence of slow-wave (SWS) and rapid eye movement sleep (REMS). The temporal distribution, total amount, and mean bout duration of these sleep states, as well as the latency for the first SWS episode, were statistically similar in both feeding behavior-inducing situations. Besides confirming early behavioral data, indicative of an engagement of adrenergic central components in food intake control, our results suggest that postprandial SWS could represent an important element of the feeding-related metabolic changes in pigeons, in a similar fashion to the observed in mammalian forms.

Food deprivation- vs. intraventricular adrenaline-induced feeding and postprandial behaviors in the pigeon (Columba livia).

The present study was designed to investigate possible similarities between the feeding and postprandial behavioral profile observed after different periods of food deprivation and after intracerebroventricular (ICV) injections of adrenaline (A) (30 nmol/microliter) in satiated pigeons (Columba livia). The results indicate that the postprandial sleep-like behavior increases observed after A treatment are similar only to those observed after prolonged periods of fasting. These parallel behavioral effects are discussed as representing the product of similar levels of satiety signals, obtained after equivalent signaling of challenges to energy homeostasis, in both 96-h deprived and A-treated animals. Our data may also suggest that ICV A injections evoke a central state comparable to that of prolonged fasting, and that this neurotransmitter may participate as a chemical mediator in the regulation of food intake in the pigeon.

Modulation of food and water intake by catecholamines injected into the lateral ventricle of the pigeon brain.

The effects of noradrenaline, adrenaline and dopamine on food and water intake were investigated in satiated (food ad libitum) adult pigeons weighing 320-360 g (N = 10 per group). Catecholamines (80 nmol in 1 microliter of saline) were injected into the right lateral ventricle. A significant increase in food consumption during the first hour was induced only by noradrenaline (8.1 +/- 1.8 g) and adrenaline (8.0 +/- 2.7 g) vs 1.9 +/- 0.6 g for the saline control. Noradrenaline also caused a significant drop during the second hour (1.7 +/- 0.6 g vs 3.5 +/- 0.7 g for the saline control). Dopamine decreased food intake at 2 h (1.4 +/- 0.3 g vs 3.5 +/- 0.7 g for the saline control) and 3 h (1.4 +/- 0.4 g vs 3.2 +/- 0.7 g for the saline control) post-injection, with a subsequent elevation in the feeding response during the 4th h (4.9 +/- 0.9 g vs 2.6 +/- 0.7 g for the saline control). The total food ingestion for the 6-h period was similar for the control and experimental groups. Water consumption was not significantly affected by any catecholamine during any specific period but total ingestion was increased by noradrenaline (44.7 +/- 3.0 ml vs 29.6 +/- 5.1 ml for the saline control). These results suggest that catecholamines are involved in the neural control of food, but not water, intake in pigeons.

Modulation of food and water intake by catecholamines injected into the lateral ventricle of the pigeon brain

The effects of noradrenaline, adrenaline and dopamine on food and water intake were investigated in satiated (food ad libitum) adult pigeons weighing 320-360 g (N+10 per group). Catecholamines (80 nmol in 1 ul of saline) were injected into the right lateral ventricle. A significant increase in food consumption during the first hour was induced only by noradrenaline (8.1 ñ 1.8 g) and adrenaline (8.0 ñ 2.7 g) vs 1.9 ñ 0.6 g for the saline control. Noradrenaline also caused a significant drop during the secondar hour (1.7 ñ 0.6 g for the saline control). Dopamine decreased food intake at 2 h (1.4 ñ 0.3 g vs 3.5 ñ 0.7 g for the saline control) and 3 h (1.4 ñ 0.4 g vs 3.2 ñ 0.7 g for the saline control) post-injection, with a subsequent elevation in the feeding response during the 4th h (4.9 ñ 0.9 g vs 2.6 ñ 0.7 gf for the saline control). The total food ingestion for the 6-h period was similar for the control and experimental groups. Water consumption was not significantly affected by any catecholamine during any specific period but total ingestion was increased by noradrenaline (44.7 ñ 3.0 ml vs 29.6 ñ 5.1 ml for the saline control). These results suggest that catecholamines are involved in the neural control of food, but not water, intake in pigeons

Participation de alpha receptors in the neural control of food intake in pegeons

The effects of noradrenaline (NA) on food intake were investigated in 69 satiated (food ad libitum) adult pigeons (320-360 g). NA (30 nmol, N = 10, and 80 nmol, N = 12, in 1 µl NaCl) was injected into the right lateral ventricle. Both doses caused a significant increase in food consumption; the higher dose caused a more prolonged effect. The 30-nmol NA injection induced significant increases in the 1st (from 1.6 to 4.5 g) and 6th (19.4 to 25.9g) hours. The 80-nmol dose caused significant increases from the 1st to the 5th hour (1.6 to 6.8,4.4 to 8.7,7.1 to 10.8,10.1 to 14.1 and 14.9 to 21.0g). Previous intracerebroventricular administration of phentolamine (50 nmol, N = 12), but not of propranolol (100 nmol, N= 13) suppressed food ingestion increased by NA administration, with identical results to those of the control group (N = 22). These results indicate that central adrenergic synapses are likely to be involved in the mediation of food intake regulation

Participation of alpha receptors in the neural control of food intake in pigeons.

The effects of noradrenaline (NA) on food intake were investigated in 69 satiated (food ad libitum) adult pigeons (320-360 g). NA (30 nmol, N = 10, and 80 nmol, N = 12, in 1 microliter NaCl) was injected into the right lateral ventricle. Both doses caused a significant increase in food consumption; the higher dose caused a more prolonged effect. The 30-nmol NA injection induced significant increases in the 1st (from 1.6 to 4.5 g) and 6th (19.4 to 25.9 g) hours. The 80-nmol dose caused significant increases from the 1st to the 5th hour (1.6 to 6.8, 4.4 to 8.7, 7.1 to 10.8, 10.1 to 14.1 and 14.9 to 21.0 g). Previous intracerebroventricular administration of phentolamine (50 nmol, N = 12), but not of propranolol (100 nmol, N = 13) suppressed food ingestion increased by NA administration, with identical results to those of the control group (N = 22). These results indicate that central adrenergic synapses are likely to be involved in the mediation of food intake regulation.

Participation of the CNS in the control of FFA mobilization during fasting in rabbits.

The presence of FFA-mobilizing areas in the rabbit central nervous system was investigated by injecting minute amounts of 2-deoxyglucose, glucose or insulin directly into the cerebrospinal fluid of conscious, unrestrained rabbits. Intracerebroventricular administration of minute amounts (10 mg) of deoxyglucose to fed rabbits produced a rapid increase in the concentration of plasma free fatty acids (FFA) and a slower increase in plasma glucose. Conversely, small amounts of insulin (50 microU) or glucose (2.5 mg) intraventricularly reduced the elevated plasma FFA of normal fasted rabbits without affecting plasma levels of glucose or insulin. The elevated levels of plasma FFA of diabetic rabbits were not affected by glucose administration, but clearly decreased after intraventricular insulin. Adrenodemedullation suppressed the hyperglycemia but not the plasma FFA increase induced by intraventricular 2-deoxyglucose. The data suggest that insulin-sensitive centers in the rabbit central nervous system participate in the control of FFA mobilization during fasting by modulating the lipolytic sympathetic tonus of adipose tissue, and that the activity of these centers is regulated by their rate of glucose utilization.

Central glucoregulation in the pigeon Columba livia. Effects of intraventricular injections of carbachol and catecholamines on blood glucose concentration.

The effect of chemical stimulation of the central nervous system on glucoregulation was studied in pigeons (Columba livia). Adrenaline (30 nmol), noradrenaline (30 or 80 nmol) and carbachol (27 nmol) were injected in 1 microliter NaCl directly into the lateral ventricle and changes in blood glucose concentration were measured. The intraventricular injection of adrenaline resulted in rapid hyperglycemia, whereas the injection of either carbachol or noradrenaline into the lateral ventricle did not cause any significant changes in blood glucose concentration. These results suggest that adrenaline-containing neurons may be involved in central mechanisms controlling blood glucose concentration in the pigeon.

Behavioral effects of adrenaline and noradrenaline injected into the lateral ventricles of the pigeon (Columba livia).

The behavioral effects of intraventricular 1-microliter injections of adrenaline and noradrenaline (both in a concentration of 30 nmol/microliters) were examined in pigeons bearing cannulae chronically implanted into the lateral ventricles. Injections of either catecholamine evoked immediate and intense bouts of feeding behavior, followed by long-lasting increases in sleep duration (50-90% higher than vehicle-treated subjects) in pigeons given free access to food during the observation period. Pigeons treated with adrenaline or vehicle only, and placed in a cage without the feeder set (food-deprived during the observation period), exhibited late increases in exploratory and preening behaviors, and less sleep than controls (vehicle-treated pigeons with free access to food). These data suggest that post-prandial sleep in this situation may represent a by-product of feeding-related processes evoked by both catecholamines.