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C A Netto

Publications and source records attributed to C A Netto.

At least 19 recordsLinked to original sources
PubMed1991

Posttraining presentation of a flashing light alters retrieval of a two-way active avoidance task in rats.

Rats were trained and tested in a two-way active avoidance task (30 trials, 0.4-mA footshock, 24-h training-test interval). Exposure to an open field with flashing light (60-W lamp, 30 Hz, for 7 min, OFL) 2 h after training caused a retrieval impairment for the avoidance task, a phenomenon called retroactive interference. Animals familiarized with the OFL 24 h before training showed no retrieval impairment when exposed to the OFL 2 h after training. Both adrenal medullectomy (performed 7 to 14 days before training) and dexamethasone treatment (2 mg/kg, injected IP 24 h and 12 h before training) prevented the OFL interfering effect. Time-course experiments revealed that OFL presented either 1 or 4 h after training caused no retrieval deficit, and that animals exposed to the OFL 2 h after training and receiving another OFL presentation 1 or 2 h, but not 4 h, prior to testing had normal retrieval performance. These results suggest: 1) that the retroactive interference caused by presentation of OFL 2 h after training is due to failure of retrieval of the avoidance task since it is counteracted by the pretest presentation to the OFL, 2) that the OFL-induced retrieval interfering effect partly depends on the novelty of the OFL situation, and on the functional integrity of pituitary ACTH and adrenomedullar-dependent mechanisms and 3) that there are different mechanisms involved in posttraining and pretest OFL effects since they present distinct time-courses.

Adrenal Medulla↗
PubMed1991

Reversal of retrieval impairment caused by retroactive interference on a two-way active avoidance task in rats.

Rats were exposed to an open field with flashing light (OFL; 60-W lamp, 30 Hz, for 7 min) 2 h after training and/or 2 h before testing in a two-way active avoidance task (30 trials, 0.5-mA footshock). Post-training OFL presentation caused retroactive interference, i.e., a retrieval impairment/amnesia for the avoidance task. Pretest OFL exposure reversed the post-training OFL-induced retrieval deficit. Diazepam (2.0 mg/kg), atropine (2.0 mg/kg), and methylatropine (0.1 mg/kg) administered before post-training OFL presentation blocked the OFL amnesic effect. However, these drugs did not counteract the pretest OFL-induced recovery of retrieval. Atropine and methylatropine administered 2 h before testing to rats receiving only post-training OFL presentation canceled the OFL-interfering effect. These results suggest: (1) that the amnesic effect of post-training OFL is due to failure of retrieval of the avoidance task, (2) that the reversal of this retrieval impairment by pretest OFL exposure may involve either priming or state-dependent mechanisms, and (3) that there are different modulatory mechanisms involved in post-training and pretest OFL effects.

Animals↗
PubMed1991

Retrieval effects of beta-endorphin and naloxone, and the novelty-induced antinociception in the developing rat.

Three experiments were conducted to assess the retrieval effects of a single dose of beta-endorphin and of naloxone, and of the novelty-induced antinociception response in the developing rat. Wistar rats 30, 45, 60, and 90 days old from our breeding stock were used. Animals were trained and tested, with a 24-h interval between sessions, in a two-way active avoidance task (using 20 presentations of a 5-s, 1-kHz tone and a 0.4-mA footshock) or in a step-down inhibitory avoidance task (using a 60-Hz, 0.2-mA footshock). Saline (1.0 ml/kg), beta-endorphin (2.0 microgram/Kg), or naloxone (0.8 mg/kg), was administered ip immediately after training, and saline or beta-endorphin was administered 6 min before testing. The retrieval enhancing effects of post-training naloxone and pretest beta-endorphin, and the retrieval impairing effect of post-training beta-endorphin, were consistently observed only in 60- and 90-day-old rats, on both tasks. In a third experiment, another group of naive rats was placed for 2 min in a novel environment (the shuttlebox) and nociception was assessed by the tail-flick method. Novelty-induced antinociception was observed only for 60- and 90-day-old rats, and this response was cancelled by naloxone given 6 min before exposure to novelty. These results suggest that both the retrieval effects of naloxone and beta-endorphin, in the doses used, and the novelty-induced antinociception response, which are possibly dependent on the activity of hypothalamic beta-endorphin system, become established between 45 and 60 days postnatal in the rat.

Animals↗
PubMed1990

Bilateral injection of fasciculin into the amygdala of rats: effects on two avoidance tasks, acetylcholinesterase activity, and cholinergic muscarinic receptors.

These experiments examined the effects of the bilateral injection of fasciculin-2 (FAS), a natural acetylcholinesterase (AChE) inhibitory peptide, into the amygdala of rats on acquisition and retention of two avoidance behaviors. Intraamygdala injection of FAS (150 ng/amygdala) produced a pronounced and long-lasting inhibition of AChE activity: 85% and 74% on day 2 and day 5, respectively. After 48 hr, FAS-treated animals showed no changes in training or test session performance in a step-down inhibitory avoidance task (training-test interval was 24 hr). In a 2-way shuttle avoidance task, intraamygdala FAS slightly reduced retention test performance without modifying training session scores. Two and five days after FAS injections into the amygdala, the density of muscarinic receptor decreased about 50% as measured by the specific bindings of 3H-quinuclidinyl benzilate and 3H-oxotremorine. No alterations were observed in the apparent dissociation constants. On the other hand, the central-type benzodiazepine receptor population of the amygdala remained unchanged, suggesting that FAS microinjection did not produce damage to neuronal components of these nuclei. In conclusion, the results presented have indicated that a clear-cut and long-lasting inhibition of AChE activity in the amygdala is not accompanied by a facilitation of learning and memory of two different avoidance tasks. Compensation of the increased cholinergic activity by a down-regulation of muscarinic receptors could account for these findings.

Acetylcholinesterase↗
PubMed1990

Retrieval effects of both post- and presession beta-endorphin administration in a three-session paradigm.

Rats were submitted to three sessions, with a 24-hr interval between, of step-down inhibitory avoidance task using a 60-Hz, 0.3-mA footshock, or of two-way active avoidance task using 25 presentations of a 5-sec. 1-kHz tone and a 0.4-mA footshock. Animals received intraperitoneal injections of either saline or beta-endorphin (2.0 microgram/kg) after the first session, and before the second or the third sessions, in a 2 x 2 x 2 design. beta-Endorphin given before the second or the third sessions improved retention for both tasks, but when administered after the first session, it impaired retention for the second session. The administration of beta-endorphin after the first session prevented the retrieval enhancement by the opioid given before the third session. Rats receiving beta-endorphin both after the first and before the second sessions, whilst showing no retrieval impairment on the second session, also did not show the pre-third session beta-endorphin retrieval enhancing effect. These data suggest that the post-first session exaggeration of the endogenous opioid state by beta-endorphin administered after the first session causes a long-lasting change in retrievability for the active and inhibitory avoidance tasks, as shown by the lack of the retrieval enhancing effect of beta-endorphin given before the third session.

Animals↗
PubMed1990

Distinct mechanisms underlying memory modulation after the first and the second session of two avoidance tasks.

Rats were subjected to three consecutive sessions, one session per day, of either a step-down inhibitory avoidance task using a 60-Hz. 0.3-mA footshock, or a two-way active avoidance task using 20 presentations of a 5-s, 1-kHz tone and a 0.3-mA footshock. After either the first or the second training session animals received an intraperitoneal injection of ACTH (0.2 microgram/kg), epinephrine-HCl (5.0 micrograms/kg), or naloxone-HCl (0.8 mg/kg). All these treatments caused memory facilitation on both tasks when administered after the first training session. When administered after the second training session only ACTH and adrenaline were effective, on both tasks. As previous physiological and pharmacological reports point to the activation of the brain beta-endorphin system after the first, but not the second, session of a task, we propose that (a) memory facilitation by naloxone depends on the previous activation of the brain beta-endorphin system; and (b) memory facilitation due to ACTH or epinephrine does not depend on the opioid activity, so their effects are expressed after both the first and the second training sessions. It was also observed that the enhancement of performance in the second training session due to post-training facilitatory treatments carried over to the test session. These results suggest that some form of consolidation occurs both after the first and after the second training session.

Animals↗
PubMed1990

Dual action of post-training naloxone on memory.

Naloxone administered at a dose of 0.2 mg/kg post-training antagonizes the deleterious effect of post-training beta-endorphin administration and prevents the enhancing effect of pretest beta-endorphin administration, on retention of a step-down inhibitory avoidance task in rats. Given at a higher dose (0.4 mg/kg), naloxone caused, in addition to these effects, a pronounced retrograde facilitation which was additive with that caused by post-training ACTH or epinephrine administration. These findings show that post-training naloxone has two different effects or sets of effects, each with a different dose threshold: An interference with beta-endorphin induced state dependency and a true modulatory effect.

Adrenocorticotropic Hormone↗
PubMed1990

Beta-endorphin enhancement of retrieval in a three-session paradigm.

Rats were submitted to three consecutive sessions, one session per day, of step-down inhibitory avoidance task (60-Hz, 0.3-mA footshock) or of two-way active avoidance task (25 trials of a 5-s, 1-kHz tone and a 0.4-mA footshock). Animals received intraperitoneal (ip) injections of saline or beta-endorphin (2.0 micrograms/kg) before or after the second session and before the third session. beta-Endorphin given before either the second or the third session improved retention of both tasks, while its administration after the second session had no effect upon performance on both tasks. In Experiment 2, it was shown that rats receiving naloxone (0.2 mg/kg) ip after the first session did not exhibit the enhancement of retrieval by beta-endorphin administration before the second session, so a non-state-dependent improvement of retrieval by the opioid seems to be unlikely. In view of these results we can propose that the presession retrieval enhancing effect of beta-endorphin is due to an endogenous state dependency on the opioid that can be expressed either in the second or in the third session of aversive tasks.

Animals↗
PubMed1990

Effect of atropine and propranolol on retrieval enhancement by a novel experience or by injection of beta-endorphin prior to testing in rats.

Wistar rats were trained in step-down inhibitory avoidance and tested 24 h later. One h prior to testing they were exposed to an open field or to an open field with flashing light (OFL) for 2 min. The OFL-exposed group showed retrieval enhancement for the avoidance task. This effect was mimicked by an injection of beta-endorphin (2.0 micrograms/kg) 1 h prior to testing, and both effects were blocked by the concomitant administration of naloxone (0.8 mg/kg, ip). Propranolol (2.0 mg/kg, ip) and atropine (0.5 mg/kg, ip) injected 6 min before the test completely blocked the retrieval-enhancing effect of both beta-endorphin and OFL. These results suggest that: 1) in rats, novel experiences may induce retrieval enhancement provided they are alerting; 2) the retrieval-enhancing effect of pre-testing exposure to OFL is probably due to activation of the brain beta-endorphin system which triggers late beta-noradrenergic and cholinergic mechanisms acting at the moment of retrieval.

Analysis of Variance↗
PubMed1990

Effects of ACTH, epinephrine and Met-enkephalin on brain beta-endorphin-like immunoreactivity, and of ACTH, epinephrine, Met-enkephalin and naloxone on retention, in normal and in protein-malnourished rats.

Rats raised and maintained on a normal-protein diet (25% protein) responded to the ip administration of ACTH-(1-24), epinephrine or Met-enkephalin with a decrease in hypothalamic beta-endorphin-like immunoreactivity, which is attributable to a release of this substance. This effect was not seen in rats raised and maintained on a low-protein diet (8% protein). In the normal animals, the pre-test administration of ACTH, epinephrine or Met-enkephalin and the post-training administration of naloxone enhanced retention-test performance of a step-down inhibitory avoidance task. These behavioral effects were absent in the protein-malnourished rats. Previous studies have shown that the behavioral effect of post-training naloxone is secondary to the release of brain beta-endorphin during training, and that the pre-test effect of the hormones is due to a release of brain beta-endorphin induced by the substances themselves. Since it is not likely that the differences were caused by hyperreactivity to the aversive stimuli employed, the suggested interpretation is that protein-malnourished rats present a dysfunction in the brain beta-endorphin system which renders it unresponsive not only to novel training experiences, but also to the pre-test retrieval enhancing effects of ACTH, epinephrine and Met-enkephalin.

Adrenocorticotropic Hormone↗
PubMed1989

Beta-endorphin and electroconvulsive shock alter the retrieval of two avoidance tasks when given after the first, but not the second, training session.

1. Rats were submitted to three consecutive sessions, one session per day, of two-way active avoidance or of step-down inhibitory avoidance, and received 1 microgram/kg beta-endorphin intraperitoneally or an electroconvulsive shock immediately after the first or after the second training session. 2. Administration of either treatment after the first session caused a reduction of performance in the second session in both tasks. There was no impairment of performance in the third session. 3. Administration of either treatment after the second session did not affect performance during the third session. 4. Therefore the effect of beta-endorphin and of electroconvulsive shock on active and inhibitory avoidance performance was expressed only when treatments were administered after the first, i.e., novel, training experience. We suggest this effect is on mechanisms acting on retrieval, since the retention performances of all groups for the third session were identical.

Animals↗
PubMed1989

Undernutrition during suckling does not change the specific or total activity of hypothalamic proline endopeptidase in adult rats.

Undernutrition during suckling causes a decrease in hypothalamic beta-endorphin-like immunoreactivity in rats. Since proline endopeptidase (E.C. 3.4.21.26) has been proposed to play a role in the processing of beta-endorphin, we examined the effects of undernutrition during suckling on the enzyme activity. Rats were undernourished by feeding their dams an 8% casein diet from the day of birth until weaning (21 days). Dams of well-nourished rats were fed a 25% casein diet during the same period. After weaning, all rats received a 20% protein diet until 90 to 120 days of age when they were killed for the enzyme assay. The specific and total activity of hypothalamic proline endopeptidase was not altered by undernutrition followed by nutritional rehabilitation (2.37 +/- 0.24 nmol sulphamethoxazole min-1 mg-1 for well-nourished rats vs 2.68 +/- 0.24 nmol sulphamethoxazole min-1 mg-1 for undernourished rats). This lack of correlation suggests that proline endopeptidase is probably not responsible for the low levels of hypothalamic beta-endorphin found in adult rats submitted to undernutrition during suckling.

Animals↗
PubMed1988

Construction and reconstruction of memories.

1. Recent evidence suggests that treatments given after training may influence memory in two ways: by becoming themselves incorporated to the experience, or by altering post-training mechanisms involved in the storage of the experience. The two processes may be called consolidation. 2. Some endogenous substances that are normally released during or after training (brain beta-endorphin; the peripheral stress hormones, ACTH, epinephrine and vasopressin) appear to be of particular importance. Their effect may become incorporated to the experiences as a conditioned stimulus (CS), generating state dependency. The effect of beta-endorphin appears to be physiological, since the substance is released by novel experiences. 3. Post-event information provided by other training experiences, in rats, or by comments or leading words, in humans, may also incorporate to the experiences, altering their content qualitatively or quantitatively. 4. A variety of substances including the stress hormones at low doses and analeptic drugs may facilitate retention when given after training. In this case, the effect is best explained by an enhancement of the post-training strengthening of memory traces. 5. The reiteration of part of the experiences at the time of testing facilitates retrieval. This may be viewed as a reconstruction of consolidation at the time of retrieval, and may be obtained using cognitive material ("priming"), or neurohumoral stimuli (a beta-endorphin injection, or a presumable release of brain beta-endorphin by an interpolated novel experience). The effect can be seen in animals rendered amnestic by electroconvulsive shock, and in humans with amnesia of organic and non-organic nature. 6. The human amnesic syndrome seems, thus, largely explainable by a deficit of retrieval. It is possible that the stimulation of retrieval by priming, or by drugs, through the "reconstruction" of consolidation, may be useful for the relief or treatment of the human amnesic syndrome.

Amnesia, Retrograde↗
PubMed1987

Analgesia induced by exposure to a novel environment in rats: effect of concurrent and post-training stressful stimulation.

Exposure of rats for 2 min to a new environment (a 50 X 25 X 25-cm box) induced a mild analgesia measured by the tail-flick method. Additional stressful stimuli (0.5 mA, 1.5-s footshocks, light flashes, or tones) presented during the 2-min exposure did not alter the analgesia. However, the postexposure presentation of light flashes or tones, for either 10 s or 2 min, while the animals were alone in a waiting cage, prevented the analgesic response. Similarly, placing the subjects with their conspecifics in the home cage for 2 min after the exposure prevented the analgesic response. The data suggest that the analgesia may represent a physiological correlate of novelty and that the response can be impaired by post-training treatments.

Animals↗
PubMed1987

Exposure to novelty induces naltrexone-reversible analgesia in rats.

The exposure of rats for 2 min to an open field, to a small box, or to inhibitory avoidance training in the small box was followed by a mild analgesia measured by the tail-flick method. The analgesia was observed as soon as 10 s after the exposure and lasted between 10 and 30 min. It was not observed in animals previously made familiar with the test situation, and it was reversed by the administration of naltrexone (0.1 mg/kg). The data suggest that novelty per se is a sufficient stimulus to activate an opioid-mediated analgesic stimulus.

Animals↗
PubMed1986

Differential effect of posttraining naloxone, beta-endorphin, leu-enkephalin and electroconvulsive shock administration upon memory of an open-field habituation and of a water-finding task.

Rats were trained and tested in an open field for habituation of rearing responses, for a water-finding task, or for both tasks simultaneously. Training-test interval was 24 hr. The water-finding task consisted of locating a metal tube in one of the walls of the box, which was attached to a water bottle on the outside; animals were water deprived between training and testing. Retention was estimated by measuring the latency to lick from the tube on the test session. Rats learned this task either with or without water deprivation, also prior to training. Habituation learning (reduction of the number of rearings between the training and test session) occurred either simultaneously with the water-finding task or in animals trained without the water tube, so that they could not learn the water-finding task. As happens with many other tasks, training in the open field was followed by a large decrease of hypothalamic beta-endorphin immunoreactivity, attributable to a release of this substance. Posttraining IP naloxone (1.6 mg/kg) administration facilitated, and posttraining beta-endorphin (2.0 micrograms/kg), leu-enkephalin (5.0 micrograms/kg), or electroconvulsive shock (15 mA, 60 Hz, 2 sec) depressed the retention of habituation; this occurred regardless of whether the animals were trained and/or tested with or without water deprivation, and whether the task was acquired alone or simultaneously with the water-finding task. By contrast, none of these treatments had any effect on retention of the water finding task, acquired either with or without prior water deprivation. Thus, habituation was, and water-finding was not, sensitive to posttraining treatments known to affect endogenous opioids: the opioids themselves, their antagonist, naloxone, and electroconvulsive shock which releases brain opioids and causes naloxone-reversible retrograde amnesia. Learning of the water-finding task was merely incidental to exploration of the open field; it took place even when the animals were trained without the water tube. This suggests that the posttraining treatments that affect endogenous opioid function affect memory only of the task(s) that actually cause the release of brain beta-endorphin (in this case, probably habituation), and not of others that may occur simultaneously but are merely incidental (water-finding). A feature apparently common to the former is that they must directly involve either the recognition of novelty, or the initiation of an interaction with a new environment, or perhaps the habituation of such interaction.

Animals↗
PubMed1986

Hypothalamic proline endopeptidase activity is not changed by various behavioral procedures.

Proline endopeptidase (E.C.3.4.21.26) is an enzyme which cleaves several neuropeptides at the carboxyl-side of proline residues. Some peptide substrates of this enzyme may be found in the rat hypothalamus (thyrotropin releasing hormone, neurotensin, substance P, oxytocin, vasopressin, beta-endorphin). Recent research has shown that the hypothalamic levels of some of these substances (e.g., vasopressin, beta-endorphin) change by a variety of training procedures. We studied the effect of various forms of training on the activity of proline endopeptidase of rat hypothalamus. The present results show that the activity of this enzyme is not altered by electroconvulsive shock or inhibitory avoidance training when measured, 0, 1, or 3 hr after these procedures. Other behavioral procedures (habituation to an open field, two-way active avoidance conditioning, or 1 min of inescapable footshock) also had no effect on hypothalamic proline endopeptidase activity measured immediately after training or test sessions. We conclude that proline endopeptidase probably does not play a regulatory role in the effect of synaptically released hypothalamic neuropeptides on behavior.

Animals↗