Ketamine alters behavior and decreases BDNF levels in the rat brain as a function of time after drug administration

Objective: To evaluate behavioral changes and brain-derived neurotrophic factor (BDNF) levels in rats subjected to ketamine administration (25 mg/kg) for 7 days. Method: Behavioral evaluation was undertaken at 1 and 6 hours after the last injection. Results: We observed hyperlocomotion 1 hour after the last injection and a decrease in locomotion after 6 hours. Immobility time was decreased and climbing time was increased 6 hours after the last injection. BDNF levels were decreased in the prefrontal cortex and amygdala when rats were killed 6 hours after the last injection, compared to the saline group and to rats killed 1 hour after the last injection. BDNF levels in the striatum were decreased in rats killed 6 hours after the last ketamine injection, and BDNF levels in the hippocampus were decreased in the groups that were killed 1 and 6 hours after the last injection. Conclusion: These results suggest that the effects of ketamine on behavior and BDNF levels are related to the time at which they were evaluated after administration of the drug. .

Enhancement of basolateral amygdaloid neuronal dendritic arborization following Bacopa monniera extract treatment in adult rats

OBJECTIVE: In the ancient Indian system of medicine, Ayurveda, Bacopa monniera is classified as Medhya rasayana, which includes medicinal plants that rejuvenate intellect and memory. Here, we investigated the effect of a standardized extract of Bacopa monniera on the dendritic morphology of neurons in the basolateral amygdala, a region that is concerned with learning and memory. METHODS: The present study was conducted on 2¹/2-month-old Wistar rats. The rats were divided into 2-, 4- and 6-week treatment groups. Rats in each of these groups were further divided into 20 mg/kg, 40 mg/kg and 80 mg/kg dose groups (n = 8 for each dose). After the treatment period, treated rats and age-matched control rats were subjected to spatial learning (T-maze) and passive avoidance tests. Subsequently, these rats were killed by decapitation, the brains were removed, and the amygdaloid neurons were impregnated with silver nitrate (Golgi staining). Basolateral amygdaloid neurons were traced using camera lucida, and dendritic branching points (a measure of dendritic arborization) and dendritic intersections (a measure of dendritic length) were quantified. These data were compared with the data from the age-matched control rats. RESULTS: The results showed an improvement in spatial learning performance and enhanced memory retention in rats treated with Bacopa monniera extract. Furthermore, a significant increase in dendritic length and the number of dendritic branching points was observed along the length of the dendrites of the basolateral amygdaloid neurons of rats treated with 40 mg/kg and 80 mg/kg of Bacopa monniera (BM) for longer periods of time (i.e., 4 and 6 weeks). CONCLUSION: We conclude that constituents present in Bacopa monniera extract have neuronal dendritic growth-stimulating properties.

Microinjection of NMDA receptor agents into the central nucleus of the amygdale alters water intake in rats

The central nucleus of the amygdala [CeA] is a forebrain structure which is important in regulation of ingestive behavior and there is direct and circumstantial evidence to indicate that some circuits involved with feeding behavior include glutamatergic elements. The present study examined whether administration of NMA [N-Methyl-DL-aspartic acid] or MK801 into the CeA altered water intake under deprivation. Animals were deprived for 24 hr before tested for water intake.NMDA [N-methyl-D-aspartate] glutamatergic receptor agonist, NMA and its antagonist, MK801 were infused bilaterally, and water intake measured for 1 hr thereafter. The intra-CeA injection of NMDA glutamatergic agonist, NMA [0.25, 0.5 and 0.75 microg/rat] increased water intake [P0.05]. However, administration of NMDA glutamatergic antagonist, MK801 [0.25, 0.5 and 1 micro g/rat] decreased water intake significantly [P0.05]. These data suggest that NMDA receptors in the CeA are responsible for the glutamatergic modulation of water intake in this nucleus

GABA in the central amygdaloid nucleus modulates the electrolyte excretion and hormonal responses to blood volume expansion in rats

We investigated the involvement of GABAergic mechanisms of the central amygdaloid nucleus (CeA) in unanesthetized rats subjected to acute isotonic or hypertonic blood volume expansion (BVE). Male Wistar rats bearing cannulas unilaterally implanted in the CeA were treated with vehicle, muscimol (0.2 nmol/0.2 µL) or bicuculline (1.6 nmol/0.2 µL) in the CeA, followed by isotonic or hypertonic BVE (0.15 or 0.3 M NaCl, 2 mL/100 g body weight over 1 min). The vehicle-treated group showed an increase in sodium excretion, urinary volume, plasma oxytocin (OT), and atrial natriuretic peptide (ANP) levels compared to control rats. Muscimol reduced the effects of BVE on sodium excretion (isotonic: 2.4 ± 0.3 vs vehicle: 4.8 ± 0.2 and hypertonic: 4.0 ± 0.7 vs vehicle: 8.7 ± 0.6 µEq·100 g-1·40 min-1); urinary volume after hypertonic BVE (83.8 ± 10 vs vehicle: 255.6 ± 16.5 µL·100 g-1·40 min-1); plasma OT levels (isotonic: 15.3 ± 0.6 vs vehicle: 19.3 ± 1 and hypertonic: 26.5 ± 2.6 vs vehicle: 48 ± 3 pg/mL), and ANP levels (isotonic: 97 ± 12.8 vs vehicle: 258.3 ± 28.1 and hypertonic: 160 ± 14.6 vs vehicle: 318 ± 16.3 pg/mL). Bicuculline reduced the effects of isotonic or hypertonic BVE on urinary volume and ANP levels compared to vehicle-treated rats. However, bicuculline enhanced the effects of hypertonic BVE on plasma OT levels. These data suggest that CeA GABAergic mechanisms are involved in the control of ANP and OT secretion, as well as in sodium and water excretion in response to isotonic or hypertonic blood volume expansion.

[Influence of basolateral amygdala lesion on the inhibitory effects of propranolol on voluntary exercise- induced enhancement of learning and memory

The beneficial effects of physical activity and exercise on brain functions such as improvement in learning and memory are well documented. In a recent study, we have found that blockade of beta-adrenergic receptors by propranolol attenuates an improvement of learning and memory by exercise. However, the anatomical sites of propranolol actions are not known. The aim of this study was to determine the role of Basolateral amygdala [BLA] in the inhibitory effects of propranolol on the beneficial effects of exercise on learning and memory. In order to block the beta-adrenergic receptors, male mice were received the beta-antagonist propranolol [10 mg/kg], before each night of five consecutive nights of exercise. The BLA lesion was made by electrolytic lesion [2mA, 2 s]. Learning and memory were tested on the Morris water maze task using a two-trials-per-day for five consecutive days. A probe trial was performed two days after the last training day. Our results showed that propranolol reversed the exercise-induced improvement in learning and memory in rat. This effect was not blocked by the BLA lesion. However, lesion of the BLA alone blocked exercise-induced enhancement of learning and memory. These findings indicate beta-adrenergic receptors located outside the BLA may mediate the effects of exercise on learning and memory. Also, the BLA play an important role in the mediating the effects of physical activity on learning and memory

[Mechanism of the interaction of cannabinoid system in central amygdale with opioid system]

Cannabinoids which are active compounds of marijuana show some pharmacological effects similar to the opioids. There are also functional interactions between both cannabinoid and opioid systems. In this study we investigated the role of cannabinoid receptors in central amygdala and its interaction with opioid system. In the present study, we investigated the effects of intraperitoneal injection of opioid drugs on response-induced by intra-amygdala [intra-Amyg] microinjection of cannabinoid agents in rats, using elevated plus-maze test of anxiety. Intraperitoneal injection of morphine [3, 6 and 9 mg/kg] increased%OAT and%OAE, but not locomotor activity, showing an anxiolytic response. However, some doses of the opioid receptor antagonist, naloxone reduced%OAT and locomotor activity as well. Intra-Amyg administration of CB1 cannabinoid receptor agonist, ACPA [at the dose of 1.25 and 5 ng/rat] increased%OAT and%OAE but not locomotor activity, thus showing an anxiolytic response, which was increased by morphine [6 mg/kg, i.p.] without any interaction. Naloxone also reduced ACPA effects. Intra-Amyg administration of CB1 cannabinoid receptor antagonist, AM251 [2.5, 25 and 100 ng/rat] did not alter%OAT and%OAE but higher doses of drug [25 and 100 ng/rat] reduced locomotor activity. However, the drug in combination of morphine anxiolytic response and with naloxone decreased anxiety. The results may indicate an anxiolytic for CB1 cannabinoid. Our results also showed that opioid system may have interaction with cannabinoid receptor in the amygdale

The effect of 5-HT2a/2c receptor agonist microinjected into central amygdaloid nucleus and median preoptic area on maternal aggressive behavior in rats

OBJETIVO: Resultados de muitos estudos sustentam a hipótese de que a serotonina (5-HT) está relacionada com a inibição do comportamento agressivo. Foram examinados os efeitos potenciais pró e anti-agressivos do agonista de receptores 5-HT2A/2C em regiões específicas do cérebro. MÉTODO: Ratas fêmeas Wistar no sétimo dia pós-parto receberam microinjeções do agonista seletivo de receptores 5-HT2A/2C, a-methyl-5-hydroxytryptamine maleate (0,2 a 1,0 µg/0,2 µl), no núcleo central da amígdala e núcleo pré-óptico medial. Para cada área estudada, as freqüências dos comportamentos: locomoção, investigação social, postura de ameaça, ataques (frontal e lateral) e ato de morder um intruso, foram comparadas entre os diferentes tratamentos por uma análise da variância, seguida quando apropriado do teste de Tukey. RESULTADOS: Os resultados mostraram que a microinjeção do agonista seletivo a-methyl-5-hydroxytryptamine maleate no núcleo central da amígdala aumentou a agressividade materna, mas não foram encontrados efeitos estatisticamente significativos no comportamento agressivo após a microinjeção do agonista seletivo de receptores 5-HT2A/2C no núcleo pré-óptico medial nas diferentes diluições estudadas. CONCLUSÕES: Os dados atuais e prévios sobre os efeitos pró e anti-agressivos do agonista dos receptores 5-HT2a/2c quando microinjetado no núcleo pré-óptico medial, em comparação com a microinjeção no núcleo central da amígdala, no septo medial (MS) e substância cinzenta periaqueductal em ratas apontam para populações funcionalmente independentes de receptores na amígdala-septo-hipotálamo e substância cinzenta periaqueductal, que são responsáveis pelo controle do comportamento agressivo. É possível que os receptores 5-HT2a/2c da amígdala possam aumentar o comportamento agressivo das fêmeas lactantes, como resultado de mudanças decorrentes do estado emocional de medo.

The inactivation of the basolateral nucleus of the rat amygdala has an anxiolytic effect in the elevated T-maze and light/dark transition tests

Pharmacological evidence indicates that the basolateral nucleus of the amygdala (BLA) is involved in the mediation of inhibitory avoidance but not of escape behavior in the elevated T-maze test. These defensive responses have been associated with generalized anxiety disorder (GAD) and panic disorder, respectively. In the present study, we determined whether the BLA plays a differential role in the control of inhibitory avoidance and escape responses in the elevated T-maze. Male Wistar rats (250-280 g, N = 9-10 in each treatment group) were pre-exposed to one of the open arms of the maze for 30 min and 24 h later tested in the model after inactivation of the BLA by a local injection of the GABA A receptor agonist muscimol (8 nmol in 0.2 æL). It has been shown that a prior forced exposure to one of the open arms of the maze, by shortening latencies to withdrawal from the open arm during the test, improves the escape task as a behavioral index of panic. The effects of muscimol in the elevated T-maze were compared to those caused by this GABA agonist in the avoidance reaction generated in the light/dark transition test. This defensive behavior has also been associated with GAD. In the elevated T-maze, intra-BLA injection of muscimol impaired inhibitory avoidance (control: 187.70 ± 14.90 s, muscimol: 37.10 ± 2.63 s), indicating an anxiolytic effect, without interfering with escape performance. The drug also showed an anxiolytic effect in the light/dark transition test as indicated by the increase in the time spent in the lighted compartment (control: 23.50 ± 2.45 s, muscimol: 47.30 ± 4.48 s). The present findings point to involvement of the BLA in the modulation of defensive responses that have been associated with GAD.

Infusions of AP5 into the basolateral amygdala impair the formation, but not the expression, of step-down inhibitory avoidance

We evaluated the effects of infusions of the NMDA receptor antagonist D,L-2-amino-5-phosphonopentanoic acid (AP5) into the basolateral nucleus of the amygdala (BLA) on the formation and expression of memory for inhibitory avoidance. Adult male Wistar rats (215-300 g) were implanted under thionembutal anesthesia (30 mg/kg, ip) with 9.0-mm guide cannulae aimed 1.0 mm above the BLA. Bilateral infusions of AP5 (5.0 µg) were given 10 min prior to training, immediately after training, or 10 min prior to testing in a step-down inhibitory avoidance task (0.3 mA footshock, 24-h interval between training and the retention test session). Both pre- and post-training infusions of AP5 blocked retention test performance. When given prior to the test, AP5 did not affect retention. AP5 did not affect training performance, and a control experiment showed that the impairing effects were not due to alterations in footshock sensitivity. The results suggest that NMDA receptor activation in the BLA is involved in the formation, but not the expression, of memory for inhibitory avoidance in rats. However, the results do not necessarily imply that the role of NMDA receptors in the BLA is to mediate long-term storage of fear-motivated memory within the amygdala.

Increased training prevents the impairing effect of intra-amygdala infusion of the non-NMDA receptor antagonist CNQX on inhibitory avoidance expression

Intra-amygdala infusion of the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) prior to testing impairs inhibitory avoidance retention test performance. Increased training attenuates the impairing effects of amygdala lesions and intra-amygdala infusions of CNQX. The objective of the present study was to determine the effects of additional training on the impairing effects of intra-amygdala CNQX on expression of the inhibitory avoidance task. Adult female Wistar rats bilaterally implanted with cannulae into the border between the central and the basolateral nuclei of the amygdala were submitted to a single session or to three training sessions (0.2 mA, 24-h interval between sessions) in a step-down inhibitory avoidance task. A retention test session was held 48 h after the last training. Ten minutes prior to the retention test session, the animals received a 0.5-µl infusion of CNQX (0.5 µg) or its vehicle (25 percent dimethylsulfoxide in saline). The CNQX infusion impaired, but did not block, retention test performance in animals submitted to a single training session. Additional training prevented the impairing effect of CNQX. The results suggest that amygdaloid non-NMDA receptors may not be critical for memory expression in animals given increased training

Activación del sistema de los opiodes endógenos por dosis subconvulsivamantes de metrazol / Activation of the endogenous opioid system with metrazol subconvulsivant dosis

Se investigaron las alteraciones en el sistema de los opioides endógenos en el cerebro de la rata, inducidas por la administración de una dósis subconvulsivante de metrazol (PTZ) (30 mg/kg i.p.). Por medio de experimentos de microdiálisis, encontramos durante los primeros 60 min después del tratamiento, una liberación importante de opiodes endógenos en el hipocampo y la amígdala cerebral. Posteriormente, los valores regresaron a los niveles basales. Por autorradiografía se observó un decremento en los niveles de los receptores mu en varias estructuras cerebrales. Mediante el análisis de la unión a receptores las membranas cerebrales, se confirmó un decremento en el número de estos receptores, sin cambios en su afinidad. En la aplicación de la prueba de Randall-Sellito, se encontró un aumento en el umbral de respuesta a estímulos dolorosos, durante los primeros 30 min. después del PTZ. Finalmente, experimentos de hibridación in situ revelaron un incremento en los niveles de la proencefalina a las 24 hrs después del tratamiento. Nuestros resultados indican que la administración de dosis subconvulsivante de PTZ activan de manera importante al sistema de los opiodes endógenos. Estos cambios resultan relevantes para entender el proceso del epileptogénesis y los mecanismos involucrados en el mismo

Antinociception induced by stimulating amygdaloid nuclei in rats: changes produced by systemically administered antagonists

The antinociceptive effects of stimulating the medial (ME) and central (CE) nuclei of the amygdala in rats were evaluated by the changes in the latency for the tail withdrawal reflex to noxious heating of the skin. A 30-s period of sine-wave stimulation of the ME or CE produced a significant and short increase in the duration of tail flick latency. A 15-s period of stimulation was ineffective. Repeated stimulation of these nuclei at 48-h intervals produced progressively smaller effects. The antinociception evoked from the ME was significantly reduced by the previous systemic administration of naloxone, methysergide, atropine, phenoxybenzamine, and propranolol, but not by mecamylamine, all given at the dose of 1.0 mg/kg. Previous systemic administration of naloxone, atropine, and propranolol, but not methysergide, phenoxy-benzamine, or mecamylamine, was effective against the effects of stimulating the CE. We conclude that the antinociceptive effects of stimulating the ME involve at least opioid, serotonergic, adrenergic, and muscarinic cholinergic descending mechanisms. The effects of stimulating the CE involve at least opioid, beta-adrenergic, and muscarinic cholinergic descending mechanisms.

Agents that affect cAMP levels or protein kinase A activity modulate memory consolidation when injected into rat hippocampus but not amygdala

Male Wistar rats were trained in one-trial step-down inhibitory avoidance using a 0.4-mA footshock. At various times after training (0, 1.5, 3,6 and 9 h for the animals implanted into the CA1 region of the hippocampus; 0 and 3 h for those implanted into the amygdala), these animals received microinfusions of SKF38393 (7.5 mug/side), SCH23390 (0.5 mug/side), norepinephrine (0.3 mug/side), timolol (0.3 mug/side), 8-OH-DPAT (2.5 mug/side), NAN-190 (2.5 mug/side), forskolin (0.5 mug/side), KT5720 (0.5 mug/side) or 8-Br-cAMP (1.25 mug/side). Rats were tested for retention 24 h after training. When given into the hippocampus 0 h post-training, norepinephrine enhanced memory whereas KT5720 was amnestic. When given 1.5 h after training, all treatments were ineffective. When given 3 or 6 h post-training, 8-Br-cAMP, forskolin, SKF38393, norepinephrine and NAN-190 caused memory facilitation, while KT5720, SCH23390, timolol and 8-OH-DPAT caused retrograde amnesia. Again, at 9 h after training, all treatments were inffective. When given into the amygdala, norepinephrine caused retrograde facilitation at 0 h after training. The other drugs infused into the amygdala did not cause any significant effect. These data suggest that in the hippocampus, but not in the amygdala, a cAMP/protein kinase A pathway is involved in memory cosolidation at 3 and 6 h after training, which is regulated by D1, Beta, and 5HT1A receptors. This correlates with data on increased post-training cAMP levels and a dual peak of protein kinase A activity and CREB-P levels (at 0 and 3-6 h) in rat hippocampus after training in this task. These results suggest that the hippocampus, but not the amygdala, is involved in long-term storage of step-down inhibitory avoidance in the rat.

Involviment of the hippocampus, amygdala, entorhinal cortex and posterior parietal cortex in memory consolidation

A total of 182 young adult male Wistar rats were bilaterally implanted with cannulae into the CA1 region of the dorsal hippocampus and into the amygdaloid nucleus, the entorhinal cortex, and the posterior parietal cortex. After recovery, the animals were trained in a stepdown inhibitory avoidance task. At various times after training (0, 30, 60 or 90 min) the animals received a 0.5-mul microinfusion of vehicle (saline) or O.5 mug of muscimol dissolved in the vehicle. A retention test was carried out 24 h after training. Retention test performance was hindered by muscimol administered into both the hippocampus and amygdala at 0 but not at 30 min posttraining. The drug was amnestic when given into the entorhinal cortex 30, 60 or 90 min after training, or into the parietal cortex 60 or 90 min after training, but not before. These findings suggest a sequential entry in operation, during the posttraining period, of the hippocampus and amygdala, the entorhinal cortex, and the posterior parietal cortex in memory processing.

D-Fenfluramine selectively releases 5-HT from dorsal raphe terminals

The aim of this study was to investigate whether D-fenfluramine (FEN) releases 5-hydroxytryptamine (5-HT) selectively from dorsal raphe (DR) terminais. Male Wistar rats, 180-200 g, were implanted with microdialysis probes in the amygdala (Am; N = 5) and dorsal hippocampus (DH; N = 6) and 5-HT levels were measured by electrochemical detection. Under basal conditions, 5-HT levels were approximately 50 and 230 fmol per 30 min sample, in the Am and DH, respectively. FEN (1O mg/kg, ip) produced a 3-4-fold increase in 5HT relesse in the Am, but not in the DH. Since the Am is mainly innervated by DR fibers while the DH receives 5-HT input chiefly from the median raphe (MR), the present results support the view that FEN selectively releases 5-HT from DR terminals.

Effect of adrenergic stimulation of the amygdalois complex on water intake

O efeito da noradrenalina, isoproterenol, fentolamina e propanolol, injetados no núcleo basolateral da amigdala, sobre a ingestäo de água, foi investigado em ratos Holtzman. A injeçäo de noradrenalina (40nmol) no complexo amigdalóide (CA) de ratos saciados näo produziu nenhuma mudança na ingestäo de água em ratos saciados (1,93 ñ 0,23 ml/lh). A noradrenalina injetada no CA produziu uma diminuiçäo na ingestäo de água de ratos privados (0,40 ñ 0,19 ml/lh). A injeçäo de isoproterenol no CA de ratos privados näo produziu nenhuma mudança na ingestäo de água em comparaçäo aos controles (11,65 ñ 1,02 e 10,92 ñ 0,88 ml/lh, respectivamente). Quando comparado com valores controles, a fentolamina injetada prévia à noradrenalina bloqueou o efeito inibitório da noradrenalina sobre a ingestäo de água em ratos privados 10,40 ñ 1,31 ml/lh). O propanolol bloqueou o efeito do isorpoterenol em ratos saciados (0,85 ñ 0,49 ml/lh) e também bloqueou a ingestäo água induzida por privaçäo (0,53 ñ 0,38 ml/lh). Tanto em animais saciados quanto em privados, a injeçäo de fentolamina, antes da administraçäo de hexametônio, bloqueou o efeito inibitório do hexametônio na ingestäo de água. Em animais saciados, quando o hexametônio foi injetado sozinho, a ingestäo de água foi de 0,39 ñ 0,25 ml/lh; quando acompanhado de fentolamina, a ingestäo de água foi de 1,04 ñ 0,3 ml/lh. Em ratos privados, o hexametônio sozinho bloqueou a ingestäo de água (0,40 ñ 0,17 ml/lh) e quando injetado com fentolamina produziu uma ingestäo de 9,7 ñ 1,8 ml/lh. Este resultados demonstram claramente a participaçäo de receptores catecolaminérgicos do CA na regulaçäo da ingestäo de água.

Synaptic messenger substances in memory processes

Nitric oxide (NO), carbon monoxide (CO), the platelet-activating factor (PAF) and arachidonic acid are released by stimulated neurons, enhance glutamate release at nerve terminals and have been proposed as synaptic messengers involved in plastic phenomena, such as the long-term potentiation of glutamatergic synapses. Long-term potentiation has been suggested to be a basic mechanism of memory processes. The microinjection of inhibitors of the synthesis of NO and CO or of antagonists of the receptors to PAF into brain structures known to be involved in memory (hippocampus, amygdala, entorhinal cortex), during its early phases, causes amnesia. This indicates that NO, CO and PAF modulate the early phases of memory, perhaps by modulating long-term potentiation. In addition, microinjections of a NO releaser or of a soluble form of PAF into the hippocampus produce memory enhancement.

Experiments suggesting a role for the platelet-activating factor in hippocampal and amygdala synapses in memory in rats

Platelet-activating factor (1-O-alky1-2-acetyl-sn-glycero-3-phosphocholine, PAF) is present in brain, is released from neurons in culture and, in hippocampal slices, enhances glutamate release and long-term potentiation (LTP) through an action on membrane receptors sensitive to the antagonist, BN 52021. This led to the proposal that PAF may be a retrograde messenger in the genesis of LTP. LTP has been, in turn, proposed as a mechanism of memory. Male Wistar rats were implanted bilaterally with cannulae aimed at the amygdala and the dorsal hippocampus. After recovery from surgery, the animals were trained in step-down inhibitory avoidance using a 0.5 mA footshock, and tested for retention 24 h later. BN 52021 (0.5 mug) was amnestic when given into the hippocampus or the amygdala either before or immediately after training but not 30 min later. The findings support the idea that memory of this task depends on the generation of LTP at the time of training in hippocampus and amygdala, and further suggest that PAF is involved in the development of this LTP.

Effect of nicotinic stimulation of the amygdaloid complex on water and sodium chloride intake

No presente trabalho foi estudado o efeito da estimulaçäo e nicotínica do complexo amigdalóide (CA) sobre a ingestäo de sódio e água em ratos saciados e privados de água. A nicotina näo produziu nenhuma alteraçäo no apetite ao sódio e água em ratos saciados. Em ratos privados, a nicotina injetada no núcleo basolateral somente bloqueou a ingestäo de cloreto de sódio. Nós demonstramos previamente que o carbacol, injetado no CA, inibiu a ingestäo de água e cloreto de sódio em ratos saciados e privados de água. A injeçäo de hexametônio no CA bloqueou totalmente a ingestäo de água em ratos saciados e privados de água. A administraçäo de hexametônio no CA, antes da injeçäo de nicotina,näo produziu alteraçäo na ingestäo de sódio. Assim, estes resultados sugerem que a populaçäo de neurônios colinoceptivos específicos do CA medeiam a ingestäo de água e cloreto de sódio

Behavioral effects of intra-amygdala injections of GABA and 5-HT acting drugs in the elevated plus-maze

The effect of drugs bilaterally injected into the basolateral/medial nuclei of the amygdala on the behavior of male Wistar rats (300-330 g) in the elevated plus-maze was measured. The benzodiazepine agonist midazolam (MDZ, 20 and 40 nmol, 0.2 µl; N = 8-14) significantly increased open-arm exploration (percent open-arm entries; control = 20.27 + or - 3.71; 40 nmol MDZ = 42.63 + or - 7.16), having thus an anxiolytic effect. On the contrary, the non-selective 5-HT2 antagonist ketanserin (KET, 1 and 10 nmol, 0.2 µl; N = 8-11) had an anxiogenic effect (percent open-arm entries: control = 35.61 + or - 6.41; 10 nmol KET = 18.65 + or - 3.89). The 5-HT1A full agonist 8-OH-DPAT (2, 4 and 8 nmol, 0.2 µl; N = 9.12) did not significantly achange rat behavior in the plus-maze. While the present anxiolytic effect of midazolam agrees with results reported by others using punished behavior, the effect of the serotonergic drugs does not. Therefore, the effect of 5-HT acting drugs injected into the amygdala may be determined by the type of experimental model of anxiety used