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Biomedical subjects

J F Flood

Publications and source records attributed to J F Flood.

At least 109 records · Page 6Linked to original sources
PubMed1977

Protein synthesis inhibition and memory for pole jump active avoidance and extinction.

This study utilizes a pole jump active avoidance task to investigate the effects of protein synthesis on memory formation. An extinction training procedure for this task is also described. Amnesia for extinction is produced by inhibition of protein synthesis and is also demonstrated by active responding, so it is clear that there is no general impairment sufficient to disrupt motor skill, motivation, or retrieval of stored memories. It was found that while inhibition of protein synthesis in brain for 2 hr did not produce amnesia, inhibition for 6 to 8 hr did. These results demonstrate that for both shock-motivated learning and non-shock motivated extinction learning, the duration of inhibition of protein synthesis is important in determining whether amnesia occurs. We conclude that inhibition of cerebral protein synthesis can best account for amnesia induced by anisomycin, cycloheximide, and acetoxycycloheximide.

Animals↗
PubMed1976

Effects of ACTH peptide fragments on memory formation.

The effects of peptides derived from ACTH on the formation of long-term memory have been investigated in male mice. Post-training administration of ACTH 4-10-L-Phe-7 (ACTH-L) improved retention for both passive and active avoidance tasks. Administration of ACTH 4-10-D-Phe-7 (ACTH-D) impaired retention for both tasks. The optimum dose for ACTH-L was about 0.3 mg/kg; the optimum dose for ACTH-D was in the range of 1.0-3.0 mg/kg. Using the passive avoidance task, it was shown that either drug had to be administered within 60 min of training to be highly effective. Amnesia produced by anisomycin (Ani), an inhibitor of protein synthesis, was lessened by ACTH-L and increased by ACTH-D, ACTH-D opposed the memory facilitating effects of ACTH-L. Using intact mice, ACTH-L or ACTH-D did not significantly change the incorporation of valine into protein, nor did these peptides influence the inhibition of protein synthesis caused by anisomycin. The results show that ACTH may play a major role in memory processing, perhaps by facilitating essential protein synthesis at sites specific for the memory being established.

Adrenocorticotropic Hormone↗
PubMed1975

Effects of protein synthesis inhibition on memory for active avoidance training.

Inhibition of brain protein synthesis by anisomycin and acetoxycycloheximide was studied in mice for its biochemical and behavioral effects. By employing both drugs in low doses in a series of injections, we were able to maintain inhibition of protein synthesis of 80% or greater for up to 14 hr without causing detectable permanent physiological impairment. The drugs were employed as amnestic agents in mice trained to avoid footshock in a T-maze. As the duration of inhibition increased, the percentage of mice classed as amnesic increased. This amnesia could be reduced by increasing (a) the rate of acquisition, or (b) the number of training trials. Anisomycin was shown to cause a significant degree of amnesia for the escape component as well as the avoidance component of the learning. A single injection of anisomycin given 15 min prior to training did not cause significant changes in the acquisition or retention of avoidance conditioning, when comparison was made with saline-injected controls. Only additional injections given after training to prolong inhibition caused amnesia. Thus, those injections critical in obtaining amnesia were given at a time at which interference with acquisition could not have occurred, so the results bear clearly on memory processes.

Animals↗
PubMed1975

Relation of memory formation to controlled amounts of brain protein synthesis.

Anisomycin, an inhibitor of brain protein synthesis, was used to control the time and duration of protein synthesis occurring in mice after they were trained on a one-trial passive avoidance task. It was found that if synthesis was strongly inhibited for 6 to 8 hr, a high percentage of the animals was amnesic. However, if small amounts of protein synthesis were allowed to occur by permitting intervals of partial recovery of protein synthesis during the period of inhibition, then fewer mice were amnesic. The longer the duration of this interval of controlled synthesis and the closer it occurred to training, the greater the percentage of subjects remembering the training.

Amnesia↗
PubMedDate not supplied

Effects of systemic pancreastatin on memory retention.

Pancreastatin, a peptide isolated from the pancreas, was shown to enhance memory retention after peripheral administration in mice when administration following T-maze footshock avoidance training. The effect of pancreastatin on memory retention, one week after training, was time dependent showing enhancement of retention when pancreastatin was administered 0 and 30 min but not 60 min after training. Pancreastatin reversed the amnesia produced by scopolamine. The pancreastatin fragment (33-49) also enhanced memory. Pancreastatin did not increase glucose in vivo. We conclude that peripherally administered pancreastatin modulates memory processing.

Amnesia↗
PubMedDate not supplied

Effect of gastrointestinal peptides on ingestion in old and young mice.

Early satiety may play a role in the anorexia of aging. The effects of the peripheral satiety agents cholecystokinin (CCK), bombesin, glucagon, and calcitonin were studied in 8 and 25 month old mice. During normal feeding behavior, the older mice consumed more than their younger counterparts, however, when food deprived, the younger consumed more. All peptides inhibited food intake over the first hour after administration in young and old mice. CCK, bombesin, and calcitonin suppressed feeding in 25 month old mice to a greater extent than in 8 month old mice. However, CCK demonstrated the greatest age-related suppression of food intake. CCK has a potential role to play in the pathogenesis of the anorexia of aging.

Aging↗
PubMedDate not supplied

Cholecystokinin receptors mediate enhanced memory retention produced by feeding and gastrointestinal peptides.

Ingestion of food in mice following training on T-maze footshock avoidance enhanced memory retention when tested 7 days later. This eating-induced improvement of retention was blocked by a specific cholecystokinin antagonist, L-364,718. The cholecystokinin antagonist prevented enhancement of memory retention resulting from posttraining administration of the gastrointestinal hormones, cholecystokinin, bombesin or gastrin releasing peptide. L-364,718 neither impaired or improved retention when given alone. Specificity of the effect of L-364,718 was demonstrated by the failure of L-364,718 to block improved memory retention resulting from administration of arecoline and D-amphetamine. The studies provide evidence that activation of cholecystokinin receptors plays a physiological role in the mediation of meal-induced enhancement of memory retention.

Animals↗
PubMedDate not supplied

Dissociation of the effects of neuropeptide Y on feeding and memory: evidence for pre- and postsynaptic mediation.

In mice not deprived of food, centrally administered neuropeptide Y (NPY) increases feeding and improves retention. In this study, we examined the effect of C-terminal NPY fragments on feeding and on memory retention. Mice were trained to avoid footshock in a T-maze. After training NPY, NPY fragments (20-36 and 26-36) or saline were administered intracerebroventricularly. Food consumption was measured during the first hour after training and memory retention was measured one week after training. NPY elicited a 544% increase in feeding compared to the saline control. Neither NPY fragment significantly increased feeding. Both NPY and NPY(20-36) improved retention compared to the saline-treated group. NPY(26-36) did not improve retention. NPY administered to well-trained mice results in amnesia. As a further test of the differential effect of NPY on memory processing and eating, we determined in well-trained mice whether administration of NPY and NPY(20-36) resulted in amnesia. Both NPY and NPY(20-36) resulted in amnesia, but only NPY stimulated feeding. These results are compatible with NPY effects on feeding being mediated through postsynaptic (Y1)NPY receptors and effects on memory retention being mediated through presynaptic (Y2)NPY receptors.

Animals↗
PubMedDate not supplied

Vasoactive intestinal peptide (VIP): an amnestic neuropeptide.

Vasoactive intestinal peptide (VIP) is a neuropeptide present in high concentrations in the hippocampus. The studies reported here demonstrate that VIP administered into the third ventricle of the brain caused amnesia in mice trained on a left-right footshock avoidance task in a T-maze. VIP resulted in amnesia when administered directly into the rostral portion of the hippocampus at a 10-fold lower dose than was needed to produce amnesia when VIP was administered intracerebroventricularly. When VIP was administered 24 hr after training, it failed to impair retention measured a week later. VIP receptor antagonist ([4-Cl-D-Phe6,Leu17]VIP) enhanced retention when administered into the rostral portion of the hippocampus, suggesting that VIP plays a physiological role in memory modulation. VIP receptor antagonist administered 24 hr after training did not facilitate retention. To gain some insight as to how VIP may be affecting memory processing, we determined if some memory-improving compounds showed a selective ability to block amnesia induced by VIP. The amnestic effect of VIP was blocked by peripheral administration of the memory-enhancing agents, arecoline, naloxone and ST 587 (a noradrenergic receptor agonist) but not by cholecystokinin octapeptide. Central administration of arecoline, but not neuropeptide Y, blocked the amnestic effect of VIP. It is concluded that VIP is a potent amnestic peptide.

Amnesia↗
PubMedDate not supplied

Do peptide-induced changes in feeding occur because of changes in motivation to eat?

The usual paradigm in which peptides are tested for their effect on food intake involves measuring intake of readily available food. In the lever press apparatus, the subjects must "work" to get food. Such work has traditionally been used as a means of measuring motivation. Mice were trained to press a lever for milk reinforcement. After achieving a stable level of performance, we tested the effects of gastrin-related peptide (GRP), bombesin (BBS) and cholecystokinin octapeptide (CCK-8) on lever pressing. All three peptides suppressed lever pressing for milk reinforcement. Prefeeding mice with milk increased the suppression of lever pressing to a greater extent in peptide-treated mice than in saline-treated mice. As the duration of prefeeding increased, lever pressing decreased. When mice were required to make more lever presses to obtain milk, both saline- and CCK-8-treated mice increased their lever pressing. However, saline-treated mice pressed at a higher rate than CCK-8-treated mice. Unlike the results obtained with saline and CCK-8, administration of a known gustatory adversant, lithium chloride, suppressed lever pressing to the same degree in mice fed or not fed prior to training. The results are consistent with the hypothesis that these peptides act as satiety agents.

Analysis of Variance↗
PubMedDate not supplied

Amylin decreases food intake in mice.

The isolation of amylin from pancreatic islets has stimulated interest in its potential role in the pathogenesis of type II diabetes mellitus and in its possible physiological roles. Amylin administered intraperitoneally decreased food intake in non-food-deprived and food-deprived diabetic and nondiabetic mice. Amylin also decreased feeding induced by insulin administration without significantly affecting blood glucose levels. Amylin also decreased food intake following intracerebroventricular administration. It is possible that amylin plays a physiological role in appetite regulation and may play a pathophysiological role in the altered appetites seen in some persons with type II diabetes mellitus.

Amyloid↗
PubMedDate not supplied

Increased food intake by neuropeptide Y is due to an increased motivation to eat.

Neuropeptide Y (NPY), administered intracerebroventricularly, is a potent orexigenic agent. To determine if NPY-induced eating represented an increase in motivation to eat (e.g., hunger) rather than pathological or stimulus-bound eating, we determined its effect on eating in three paradigms, including lever press, appetitive passive avoidance and quinine-adulterated milk. NPY-injected mice consumed more milk when required to work for it in a lever press apparatus and tolerated shock to the tongue for drinking milk. Increasing the dose of NPY also allowed mice to overcome a taste aversion for quinine-adulterated milk. Overall, these studies support the hypothesis that NPY causes a specific increase in the motivation to eat, rather than nonspecific or stimulus-bound behavior.

Animals↗
PubMedDate not supplied

Effects of thermal peptides on retention of footshock avoidance training in mice.

Some hydrophobic polypeptides known as thermal proteins have been found to have neurotrophic effects. Thermal proteins were synthesized from aspartic acid, glutamic acid, proline, and tryptophan. Two hydrophobic and one nonhydrophobic polymers were injected intracerebroventricularly into brains of mice after partial training on footshock avoidance run in a T-maze. When retention was tested 1 week later, the hydrophobic polymers enhanced retention while the nonhydrophobic polymer did not. Thermal proteins exhibiting hydrophobicity and having neurotrophic effects may aid in altering synaptic connections by facilitating cell recognition.

Animals↗