The mesencephalic GCt-ICo complex and tonic immobility in pigeons (Columba livia): a c-Fos study.

Tonic immobility (TI) is a response to a predator attack, or other inescapable danger, characterized by immobility, analgesia and unresponsiveness to external stimuli. In mammals, the periaqueductal gray (PAG) and deep tectal regions control the expression of TI as well as other defensive behaviors. In birds, little is known about the mesencephalic circuitry involved in the control of TI. Here, adult pigeons (both sex, n = 4/group), randomly assigned to non-handled, handled or TI groups, were killed 90 min after manipulations and the brains processed for detection of c-Fos immunoreactive cells (c-Fos-ir, marker for neural activity) in the mesencephalic central gray (GCt) and the adjacent nucleus intercollicularis (ICo). The NADPH-diaphorase staining delineated the boundaries of the sub nuclei in the ICo-GCt complex. Compared to non-handled, TI (but not handling) induced c-Fos-ir in NADPH-diaphorase-rich and -poor regions. After TI, the number of c-Fos-ir increased in the caudal and intermediate areas of the ICo (but not in the GCt), throughout the rostrocaudal axis of the dorsal stratum griseum periventriculare (SGPd) of the optic tectum and in the n. mesencephalicus lateralis pars dorsalis (MLd), which is part of the ascending auditory pathway. These data suggest that inescapable threatening stimuli such as TI may recruit neurons in discrete areas of ICo-GCt complex, deep tectal layer and in ascending auditory circuits that may control the expression of defensive behaviors in pigeons. Additionally, data indicate that the contiguous deep tectal SCPd (but not GCt) in birds may be functionally comparable to the mammalian dorsal PAG.

Defensive behaviors and prosencephalic neurogenesis in pigeons (Columba livia) are affected by environmental enrichment in adulthood.

Neurogenesis in the adult brain appears to be phylogenetically conserved across the animal kingdom. In pigeons and other adult non-oscine birds, immature neurons are observed in several prosencephalic areas, suggesting that neurogenesis may participate in the control of different behaviors. The mechanisms controlling neurogenesis and its relevance to defensive behaviors in non-oscine birds remain elusive. Herein, the contribution of the environment to behavior and neurogenesis of pigeons was investigated. Adult pigeons (Columba livia, n = 6/group), housed in standard (SE) or enriched environment (EE) for 42 days, were exposed to an unfamiliar environment (UE) followed by presentation to a novel object (NO). Video recordings of UE+NO tests were analyzed and scored for latency, duration and frequency of angular head movements, peeping, grooming, immobility and locomotion. Twenty-four hours later, pigeons were submitted to the tonic immobility test (TI) and number of trials for TI and TI duration were scored, followed by euthanasia 2 h later. Brains were immunohistochemically processed to reveal doublecortin (DCX), a marker for newborn neurons. Compared to those housed in SE, the pigeons housed in EE responded to a NO with more immobility. In addition, the pigeons housed in EE presented longer TI, more DCX-immunoreactive (DCX-ir) cells in the hippocampus and fewer DCX-ir cells in the lateral striatum than those housed in SE. There was no correlation between the number of DCX-ir cells and the scores of immobility in behavioral tests. Together, these data suggest that enrichment favored behavioral inhibition and neurogenesis in the adult pigeons through different, parallel mechanisms.

Distribution and characterization of doublecortin-expressing cells and fibers in the brain of the adult pigeon (Columba livia).

Doublecortin (DCX) is a microtubule-associated protein essential for the migration of immature neurons in the developing and adult vertebrate brain. Herein, the distribution of DCX-immunoreactive (DCX-ir) cells in the prosencephalon of the adult pigeon (Columba livia) is described, in order to collect the evidence of their immature neural phenotype and to investigate their putative place of origin. Bipolar and multipolar DCX-ir cells were observed to be widespread throughout the parenchyma of the adult pigeon forebrain. Small, bipolar and fusiform DCX-ir cells were especially concentrated at the tips of the lateral walls of the lateral ventricles (VZ) and sparsely distributed in the remaining ependyma. Multipolar DCX-ir cells populated the pallial regions. None of these DCX-ir cells seemed to co-express NeuN or GFAP, suggesting that they were immature neurons. Two different migratory-like routes of DCX-ir cells from the VZ toward different targets in the parenchyma were putatively identified: (i) rostral migratory-like bundle; and (ii) lateral migratory-like bundle. In addition, pial surface bundles and intra-ependymal fascicles were also observed. Pigeons treated with 5-bromo-desoxyuridine (BrdU, 3 intraperitoneal injections of 100mg/kg 2h apart, sacrificed 2h after last injection) displayed BrdU-immunoreactive cells (BrdU-ir) in VZ and ependyma whereas the parenchyma was free of such cells. Despite the regional overlapping, there was no evidence of double-labeling between BrdU and DCX. Therefore, the VZ in the brain of adult pigeons seems to have rapidly dividing cells as putative progenitors of newborn neurons populating the forebrain. The distribution of the newborn neurons in the avian prosencephalon and their migration pathways appear to be larger than in mammals, suggesting that the morphological turnover of forebrain circuits is an important mechanism for brain plasticity in avian species during adulthood.

Repeated rat-forced swim test: reducing the number of animals to evaluate gradual effects of antidepressants.

The forced swim test (FST) is a pre-clinical test to short and long term treatment with antidepressant drugs (ADT), which requires between-subject designs. Herein a modified protocol of the FST using within-subject design (repeated rat-FST) was evaluated. Male Wistar rats were submitted to 15 min of swimming (Day 1: pretest) followed by three subsequent 5 min-swimming tests one week apart (Day 2: test, Day 7: retest 1, Day 14: retest 2). To determine the temporal and factorial characteristics of the variables scored in the repeated rat-FST, the protocol was carried out in untreated animals (E1). To validate the method, daily injections of Fluoxetine (FLX, 2.5mg/kg, i.p.) or saline were given over a 2-week period (E2). Tests and retests have been videotaped for further register of the latency, frequency and duration of behaviors. Over retesting the latency to immobility decreased whereas duration of immobility tended to increase. Factorial analysis revealed that the test, the retest 1 as well as the retest 2 have variables suitable to detection of antidepressant-like effects of ADT. Compared to saline, FLX chronically administrated reduced duration of immobility whereas increased duration of swimming in retest 2. The data suggest that repeated rat-FST detected the gradual increase in the efficacy of low doses of FLX over time. Therefore, repeated rat-FST seemed suitable to detect short and long term effects of selective serotonin reuptake inhibitors, or other ADT, thus reducing the number of animals used in the screenings of this type of compounds.

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.

Phenylethanolamine N-methyltransferase-immunoreactive neurons in the medulla oblongata of the pigeon (Columba livia) projecting to the hypothalamic paraventricular nucleus.

The distribution and ascending projections to the hypothalamic paraventricular nucleus of phenylethanolamine N-methyltransferase (PNMT)-immunoreactive perikaria were studied in adult pigeons using a combination of retrograde transport of Fluorogold injected into the paraventricular nucleus, and double immunohistochemical procedures for PNMT, tyrosine hydroxylase and neuropeptide Y. PNMT-immunoreactive cell bodies were found in the subtrigeminal reticular nucleus of the ventrolateral medulla and in the nucleus of the solitary tract, mainly in the subnuclei: medialis superficialis, pars posterior, and medialis ventralis, pars posterior. PNMT-immunoreactive perikaria were also tyrosine hydroxylase immunoreactive, and are located within the rostral tyrosine hydroxylase immunoreactive cell groups of these areas. No perikaria double-labeled for neuropeptide Y and PNMT were found. Retrograde labeled cell bodies were observed in the subtrigeminal reticular nucleus and in the nucleus of the solitary tract. PNMT-immunoreactive retrogradely labeled cells were mainly observed in the subtrigeminal reticular nucleus. These data suggest the presence in the pigeon of medullary adrenergic cell groups partially comparable to mammalian C1 and C2 groups. Comparison of these results with data previously obtained in amphibians and reptiles suggests that the presence of a hypothalamically-projecting C1-like group might be a plesiomorphic medullary attribute in amniotes, whereas the variable presence of C2 and C3-like groups, as well as the content of NPY in the putative adrenergic perikaria, seem to be species-specific.

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.

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.

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.

Behavior effects of adrenaline and noradrenaline injected into the lateral ventricles of the pigeon (Columba Livia)

The behavioral effects of intravrnticular 1-micronl injections of adrenaline and noradrenaline (both in a concentration of 30 nmol/micronl) were wxamined in pigeons bearing cannule chronically implanted into the lateral ventricles. Injections of either catcholoamine evoked immediate and intense bouts of feeding behavior, followed by long-lasting incrases 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 durngi 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

A stereotaxic atlas for the telencephalon of the Siamese fighting fish (Betta splendens).

1. A stereotaxic technique for electrode positioning in the telencephalic nuclei of the Siamese Fighting fish (Betta splendens) is described. 2. The forebrain atlas was based on paraffin-embedded, in situ-sectioned, Nissl-stained material. Brain measurements were corrected for tissue shrinkage due to histological procedures. The atlas and methods have already been tested and have shown good accuracy and reproducibility.

A stereotaxic atlas for the telencephalon of the siamese fighting fish (Betta splendens)

1. A stereotaxic technique for electrode positioning in the telencephalic nuclei of the Siamese Fighting fish (Beta splendens) is described. 2. The forebrain atlas was based on paraffin-embedded, in situ-sectioned, Nissl-stained material. Brain measurements were corrected for tissue shrinkage due to histological procedures. The atlas and methods have aledy been tested and have shown good accuracy and reproducibility

Discrete telencephalic lesions accelerate the habituation rate of behavioral arousal responses in Siamese fighting fish (Betta splendens).

Stereotaxic electrolytic lesions were made in the dorsomedial telencephalic area, laterally to the dorsal commissure, in male Siamese Fighting Fish (Betta splendens). The startle and orienting responses to regularly delivered taps on the side of the aquarium were recorded for lesioned, sham-operated and unoperated groups. Lesioned fish showed increased reactivity to environmental modifications, including tonic immobility and changes in body color. Although no changes in the arousal responses were detected, the lesioned fish showed an increased frequency of startle responses and habituated to the orienting responses faster than sham-operated and unoperated animals. The long-term inter-session retention of habituation was also decreased. The effects observed are the opposite of those obtained after complete or unilateral telencephalic ablation in teleosts and suggest the existence of antagonic telencephalic systems playing a modulatory role in arousal control.