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C A Netto

Publications and source records attributed to C A Netto.

51 records · Page 3Linked to original sources
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↗
PubMed1986

Distribution of proline endopeptidase activity in sub-synaptosomal fractions of rat hypothalamus.

1. Proline endopeptidase (E.C.3.4.21.26) is an enzyme which cleaves several peptides at the carboxyl side of proline residues. Because brain contains relatively large amounts of this enzyme and because of its specificity it has been suggested that it plays a role in the metabolism of neuropeptides, acting both on their processing and their degradation. 2. Since the final steps of neuropeptide processing occur in the synaptic vesicles and the degradation of most of these peptides is believed to occur in the synaptic cleft, we studied the distribution of proline endopeptidase activity in sub-fractions of rat hypothalamus. 3. Proline endopeptidase activity is present in synaptosomal fractions and is released by hypo-osmotic shock. Its specific activity is higher in the synaptoplasma than in synaptic membranes or vesicles (7.98 vs 0.18 and 0.24 nmol min-1 mg protein-1 carbobenzoxy-glycyl-prolyl-sulfamethoxazole hydrolysis). 4. Inhibitory avoidance training, a situation which releases hypothalamic vasopressin and beta-endorphin, both in vitro substrates, did not affect the specific or total activity of proline endopeptidase in synaptosomal plasma membranes.

Animals↗
PubMed1985

Posterior hypothalamic deafferentation abolishes the amnestic effect of electroconvulsive shock in rats.

The amnestic effect of immediate post-training transcorneal electroconvulsive shock ECS (15.0 mA, 60 Hz, 2 sec) on step-down inhibitory avoidance learning (0.5 mA, 60 Hz training footshock) was studied in intact rats and in rats submitted to bilateral surgical transection of the dorsal fornix, to anterior or posterior hypothalamic deafferentation, and in sham-operated animals. Animals were tested for retention 24 hr after training. The amnestic effect of ECS was observed in all groups except in the one with the posterior hypothalamic lesion. Fornix-lesioned animals showed a moderate retention deficit which was considerably worsened by the ECS treatment. The results indicate that the amnestic effect of ECS requires integrity of posterior hypothalamic pathways. One possibility is that the amnestic effect of ECS may be mediated by posterior afferent fibers to the hypothalamus acting on hypothalamic opioid systems such as have been previously proposed to play a role in ECS-induced amnesia.

Afferent Pathways↗
PubMed1985

The brain beta-endorphin system and behavior: the modulation of consecutively and simultaneously processed memories.

This article shows how new memories may be acquired, or old ones retrieved, in animals who have recently released brain beta-endorphin and why some memories may be insensitive to beta-endorphin modulation even if they are processed in parallel to others that are sensitive to that system. In addition, one example is given of an interaction between tasks that is possibly independent from the brain beta-endorphin system. The data examined here represent a new approach to memory modulation in that they apply findings previously obtained in isolated tasks to the analysis of interactions between training and test sessions of the same or different tasks. This may be viewed as a step toward understanding the organization of memory mechanisms in everyday behavior, which consists of consecutive and simultaneous, rather than isolated, behavioral training and test paradigms. The present approach, however, still relies on the individual analysis of separate behaviors, and is therefore no substitute for studies on complex behaviors per se. Indeed, both approaches may be complementary for a full understanding of the organization of memory processes, along with further investigations studying isolated tasks.

Acoustic Stimulation↗
PubMed1985

Interaction between consecutive learnings: inhibitory avoidance and habituation.

Rats were submitted to step-down inhibitory avoidance training and to habituation of a rearing response to a tone with a 2-h interval between the two tasks, and were tested for retention of both tasks on the next day. When animals were trained first in inhibitory avoidance and then in habituation, retention of the avoidance behavior was impaired. When the animals were trained first in the habituation task and then in the avoidance task, retention of the two tasks was normal. The same results were obtained regardless of the order in which the two tasks were presented on the day of testing. This asymmetrical influence of habituation training on inhibitory avoidance retention could be due either to cognitive or, more likely, to task-specific neurochemical interactions.

Animals↗
PubMed1985

Response of the rat brain beta-endorphin system to novelty: importance of the fornix connection.

In control rats, a step-down inhibitory avoidance training trial using a 0.8 mA footshock, or simple exposure to the training apparatus without footshock, was followed by a decrease of beta-endorphin-like immunoreactivity measured in the hypothalamus and ventral thalamus. The effect of inhibitory avoidance training was also measured in rats submitted to a brain sham operation, to bilateral transection of the dorsal fornix, to anterior or to posterior hypothalamic deafferentation, to adrenal medullectomy, to an adrenal sham operation, to 16 daily ip injections of 0.2 mg/kg dexamethasone, or to 16 daily ip injections of 1 ml/kg saline. The diencephalic beta-endorphin-like immunoreactivity response to training was abolished by fornix transection and was unaffected by all other treatments. This suggests that the response is not mediated by anterior or posterior neural afferents to the hypothalamus, or by a hypersecretion of epinephrine by the adrenal medullae, or of ACTH by the pituitary gland. The response, instead, appears to require the integrity of the pathway that sends projections from the septo-hippocampal system to the hypothalamus. Previous evidence had suggested that the diencephalic beta-endorphin-like immunoreactivity response to training is a result of novelty, and the septo-hippocampal system has been postulated to play a role in the registration of novelty.

Adrenal Medulla↗
PubMed1985

Factors that influence test session performance measured 0, 3, or 6 h after inhibitory avoidance training.

UNLABELLED: Rats were trained in a step-down inhibitory avoidance task using a 0.3-mA, 60-Hz footshock, and were tested at 0, 3, and 6 h from training. Retrieval scores (test session minus training session step-down latencies) were higher in control groups at 0 than at 3 or 6 h. Test session performance at 0 h was unaffected by the pretraining ip injection of ACTH1-24 (0.2 microgram/kg), epinephrine-HCl (5.0 micrograms/kg), human beta-endorphin (1.0 microgram/kg), or naloxone-HCl (0.4 mg/kg); or by a pretreatment with dexamethasone phosphate (2.0 mg/kg in divided doses 24 and 12 h before training); or by anterior or posterior hypothalamic deafferentation. Test session performance at 0 h was depressed by prior bilateral transection of the fornix, which suggests it depends on hippocampal function. The effect of the fornix lesion on test session performance at 0 h was not counteracted by ACTH, epinephrine, or beta-endorphin administration. When animals were tested 3 h after training, the post-training administration of ACTH and epinephrine caused an enhancement of test session performance; neither post-training beta-endorphin or naloxone, nor pretest ACTH, epinephrine, or beta-endorphin administration, had any effect in these animals. At 6 h from training, the post-training facilitatory action of ACTH and epinephrine was still present and the post-training depressant effect of beta-endorphin and the post-training facilitatory effect of naloxone became manifest, and so did the naloxone-reversible pretest facilitation induced by ACTH, epinephrine, or beta-endorphin. The influence of post-training naloxone or pretest beta-endorphin on retrieval scores at 6 h was not observed in the fornix-lesioned animals. IN CONCLUSION: Test session performance of this task at 0 h from training is regulated by different mechanisms than those which regulate test session performance at 3 or 6 h; in particular, it is less susceptible to modulation by the drugs used in the present study and it depends on the fornix; At least two major classes of modulatory factors influence retrieval scores at later times: consolidation-enhancing effects of ACTH and epinephrine, which become manifest at 3 h, and mechanisms related to beta-endorphin, which involve a form of state dependency and only become manifest at 6 h from training.

Adrenocorticotropic Hormone↗
PubMed1985

On how passive is inhibitory avoidance.

Rats were trained in a step-down inhibitory avoidance task using a 25 X 25-cm platform and either a 0.3- or a 0.8-mA training footshock. Immediately after training retrieval was good in all animals; but at 24 h there was a decline in the group trained with 0.3-mA footshock. This decline was not observed in animals submitted to an immediate retrieval test and then tested again at 24 h. Thus, the immediate retrieval test apparently served the purpose of a rehearsal. A considerable degree of activity (rearing, ambulation, sticking the head out of the platform) was observed in test sessions. Activity scores were lower in the animals trained with the 0.8-mA footshock. The amount of activity, however, was unrelated to retrieval performance (i.e., to test session step-down latency).

Animals↗
PubMed1985

The course of the decrease of hypothalamic beta-endorphin induced by training, and the development of the effect of beta-endorphin on the retrieval of inhibitory avoidance in rats.

Step-down inhibitory avoidance training or the simple exposure of rats to the training apparatus is followed by a decrease of hypothalamic beta-endorphin immunoreactivity at 0.1, 1.0 or 2.0 h after training. Immunoreactivity returns to normal at 6.0 h. The ip administration of 1.0 microgram/kg of human beta-endorphin 6 min prior to training produces an inhibition of the retrieval of the step-down task at 6.0 h, but not at 0, 1.0 or 2.0 h after training. This effect is reversed by a second injection of the substance immediately before testing. The possible physiological significance of this parallel development of the effect of beta-endorphin on retrieval and the depletion of the substance caused by training is discussed. The data indicate that retrieval is insensitive to the peptide when its hypothalamic stores are depleted.

Animals↗
PubMed1984

Effect of various behavioral training and testing procedures on brain beta-endorphin-like immunoreactivity and the possible role of beta-endorphin in behavioral regulation.

Beta-Endorphin-like immunoreactivity is reduced in the rat diencephalon after the animals are exposed for the first time to any of the following behavioral situations: 50 tones (habituation), 50 tone-footshock shuttle avoidance trials, one step-down inhibitory avoidance trial, simple exposure to the avoidance apparatus with no footshocks, or inescapable shock. The effect is not observed when animals are exposed to any of these situations for a second time. The reduction of brain beta-endorphin-like immunoreactivity is attributable to release and subsequent metabolism of the substance, and correlates with the novelty inherent in the diverse training or test situations. The role of beta-endorphin in behavior is discussed in the light of these and previous results which showed that it causes both retrograde amnesia and a facilitation of retrieval. The substance would appear to serve an adaptive function when animals are exposed to a new experience, by inducing a temporary forgetting of the experience together with (or leading to) a state of alertness or preparedness for what may happen next.

Acoustic Stimulation↗
PubMed1984

Amnesia as a major side effect of electroconvulsive shock: the possible involvement of hypothalamic opioid systems.

Electroconvulsive shock (ECS) is used in the treatment of depression and causes antero- and retrograde amnesia as a side effect. One of the many neurochemical effects of ECS is depletion of brain beta-endorphin and Met-enkephalin. These two opioid peptides cause antero- and retrograde amnesia also. Naloxone antagonizes the amnestic effect of ECS and of the opioid peptides. Thus, it is possible that the amnestic effect of ECS is mediated by an endogenous release of the peptides. Surgical posterior hypothalamic deafferentation, but not anterior deafferentation or fornix transection, abolishes the amnestic effect of ECS. This suggests that the hyperactivation of endogenous opioid systems by ECS that leads to amnesia is mediated by posterior ascending fibers to the hypothalamus. The relevance of these considerations to the treatment of depression merits investigation.

Amnesia↗
PubMedDate not supplied

Pre-test administration of beta-endorphin, or of electroconvulsive shock reverses the memory disruptive effect of posttraining electroconvulsive shock.

Memory disruption by posttraining electroconvulsive shock was studied in adult Wistar rats using three different tasks: step-down inhibitory avoidance, two-way active avoidance, and habituation of rearing to an open field. The animals were given training and test sessions 24 hours apart in each of these tasks. Immediate posttraining transcorneal, 15 mA, 60 Hz, 2 sec electroconvulsive shock disrupted memory of the three tasks. The effect was completely reversed by the IP administration of beta-endorphin (2.0 micrograms/kg), 6 min prior to testing, or of another electroconvulsive shock, 30 min prior to testing. These findings indicate that the posttraining electroconvulsive shock did not affect memory storage. In view of the fact that electroconvulsive shock has been previously shown to cause a pronounced decrease of brain beta-endorphin immunoreactivity, attributable to a release of the peptide, the present findings can be interpreted as showing that memory disruption by posttraining electroconvulsive shock results from the induction of state dependency on beta-endorphin.

Animals↗