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1.
Physiol Behav ; 74(4-5): 613-20, 2001.
Article in English | MEDLINE | ID: mdl-11790422

ABSTRACT

A two-choice, spatial delayed matching-to-sample (DMTS) water-escape task has proved to be a valuable of assay of trial-dependent memory. The task involves giving rats trials consisting of a forced-choice information run and a free-choice test run that are separated by a 5-m retention interval. Two experiments were conducted to determine the importance of making a complete response (R), partial response (P), or no response (NR; direct placement on escape platform) during the information "run" on acquisition and the subsequent performance of the task. Most of the naive, male, Sprague-Dawley rats were capable of attaining a 90% correct choice criterion when trained with P or NR information runs, but rats trained with R information runs required fewer trials to attain criterion and had shorter escape latencies during the criterion trials. Rats in all three groups showed significant retention at retention intervals as long as 1 h. Rats overtrained on the task with R information runs were subsequently able to perform the task at above chance level, regardless of the type information run given on the trial, but performed more accurately on trials where they made P or R information runs. Thus, rats use and perform better on place DMTS when allocentric environmental and egocentric response-associated cues are both available.


Subject(s)
Discrimination Learning , Escape Reaction , Maze Learning , Mental Recall , Orientation , Animals , Choice Behavior , Male , Problem Solving , Rats , Rats, Sprague-Dawley , Retention, Psychology
2.
Behav Neurosci ; 114(4): 707-12, 2000 Aug.
Article in English | MEDLINE | ID: mdl-10959529

ABSTRACT

Stimulation of the locus coeruleus (LC) and the subsequent release of norepinephrine contribute to memory consolidation processes. Excitatory input to the LC is derived primarily from neurons in the nucleus paragigantocellularis (PGi). The authors examined the effects of activating the pathway between PGi and the LC on memory. Rats received vehicle or the excitatory amino acid glutamate (25, 50, or 100 nmol/0.5 microl) into PGi after training in an inhibitory avoidance (IA) or delayed matching-to-sample (DMS) task. Rats given the 100-nmol dose had significantly longer retention latencies on a 48-hr IA retention test. Rats treated with the 50- or 100-nmol dose made significantly more correct responses than controls on an 18-hr DMS retention test. Results suggest that encoding and storage of memory for emotional and spatial events may be enhanced by activation of neuronal circuits afferent to the LC.


Subject(s)
Avoidance Learning/physiology , Glutamic Acid/physiology , Locus Coeruleus/physiology , Mental Recall/physiology , Orientation/physiology , Afferent Pathways/physiology , Animals , Arousal/physiology , Brain Mapping , Long-Term Potentiation/physiology , Male , Maze Learning/physiology , Nerve Net/physiology , Rats , Rats, Sprague-Dawley , Retention, Psychology/physiology
3.
Neurobiol Learn Mem ; 74(2): 135-45, 2000 Sep.
Article in English | MEDLINE | ID: mdl-10933899

ABSTRACT

These experiments examined the contribution of noradrenergic neurons in the nucleus of the solitary tract (NTS) in mediating the memory-facilitating effects of epinephrine. In Experiment 1, saline or 0.05 or 0.1 mg/kg of epinephrine was given intraperitoneally (ip) to rats after the second day of training in a light-dark Y-maze discrimination task. On a 20-trial retention test given 2 and 7 days later, the 0.1 mg/kg epinephrine group made significantly more correct responses than controls and required fewer trials to reach criterion. In Experiment 2, phosphate-buffered saline or the noradrenergic antagonist dl-propranolol (0.3 or 1.0 microg/0.5 microl) was infused into the NTS prior to an ip injection of saline or 0.1 mg/kg of epinephrine. The memory-enhancing effects of epinephrine were attenuated by the infusion of 0.3 microg/0.5 microl of dl-propranolol into the NTS. These findings indicate an involvement of NTS noradrenergic neurons in mediating the effects of peripheral epinephrine on memory storage processes.


Subject(s)
Appetitive Behavior/drug effects , Discrimination Learning/drug effects , Epinephrine/pharmacology , Light , Memory/drug effects , Norepinephrine/antagonists & inhibitors , Norepinephrine/metabolism , Receptors, Drug/antagonists & inhibitors , Receptors, Drug/metabolism , Solitary Nucleus/drug effects , Solitary Nucleus/metabolism , Animals , Behavior, Animal/drug effects , Male , Neurons/metabolism , Rats , Rats, Sprague-Dawley
4.
Behav Brain Res ; 112(1-2): 151-8, 2000 Jul.
Article in English | MEDLINE | ID: mdl-10862946

ABSTRACT

It is well documented that noradrenergic systems in the amygdala modulate memory formation, however, less research has examined how sources of limbic norepinephrine contribute to this process. The amygdala receives a dense supply of norepinephrine from neurons in the nucleus of the solitary tract (NTS). The present experiments examined whether adrenergic activation of these NTS neurons affects memory in learning tasks that are sensitive to amygdala norepinephrine release. Separate groups of male Sprague-Dawley rats were trained in either an emotionally arousing or spatial memory task. They then received vehicle or the adrenergic agonist epinephrine (50, 125, or 250 ng/0.5 microl) into the NTS. Rats given the 125 ng dose had significantly longer retention latencies on a 48 h inhibitory avoidance retention test and made a significantly higher percentage of correct responses on an 18 h delayed radial maze retention test. A third experiment using in vivo microdialysis and high performance liquid chromatography (HPLC) demonstrated that intra-NTS infusion of a memory-enhancing dose of epinephrine potentiated amygdala norepinephrine release. Collectively, these results suggest that stimulation of the NTS contributes to memory processing by influencing noradrenergic systems in the amygdala.


Subject(s)
Amygdala/metabolism , Avoidance Learning/physiology , Memory/physiology , Norepinephrine/metabolism , Solitary Nucleus/metabolism , Space Perception/physiology , Adrenergic Agonists/metabolism , Animals , Epinephrine/metabolism , Male , Maze Learning/physiology , Microinjections , Rats , Rats, Sprague-Dawley
5.
Neurobiol Learn Mem ; 73(2): 127-40, 2000 Mar.
Article in English | MEDLINE | ID: mdl-10704323

ABSTRACT

These experiments examined whether the nucleus paragigantocellularis (PGi) contributes to memory storage processing via its ascending excitatory influence on locus coeruleus (LC) neuronal activity. Activation of the LC leads to memory enhancement and also results in a widespread release of norepinephrine in target structures, such as the amygdala and hippocampus. Infusion of norepinephrine into either structure also improves memory for several types of learned responses. Thus, the capacity for norepinephrine to modulate memory within limbic structures may be contingent upon the functional connections between PGi and the LC. To examine this hypothesis, male Sprague-Dawley rats were implanted with cannula aimed above PGi (Experiments 1 and 2) or 1.5 mm dorsal or medial to PGi (Experiment 3). Immediately following inhibitory avoidance training (0.45 mA, 0. 5 s), phosphate-buffered saline, lidocaine (Experiment 1), or 12.5 or 25 nmol/0.5 microl of the GABA agonist muscimol (Experiment 2) was infused into PGi. On a retention test given 48 h later, the latency to reenter the footshock compartment was significantly shorter for subjects given either lidocaine or 12.5 or 25.0 nmol of muscimol compared to controls. In Experiment 3, infusion of lidocaine or muscimol into areas 1.5 mm dorsal or medial to PGi did not significantly alter retention, indicating that the memory impairment observed in Experiments 1 and 2 was site specific and not due to the spread of drug to cell groups surrounding PGi. These findings suggest that PGi may serve a vital function in relaying biologically relevant information to forebrain structures involved in memory via its excitatory influence on the LC.


Subject(s)
Avoidance Learning/physiology , Locus Coeruleus/physiology , Memory/physiology , Nerve Net/physiology , Rhombencephalon/physiology , Anesthetics, Local/administration & dosage , Animals , Avoidance Learning/drug effects , GABA Agonists/administration & dosage , Inhibition, Psychological , Lidocaine/administration & dosage , Locus Coeruleus/drug effects , Male , Memory/drug effects , Microinjections , Muscimol/administration & dosage , Nerve Net/drug effects , Rats , Rats, Sprague-Dawley , Rhombencephalon/drug effects , Serotonin/biosynthesis
6.
Behav Neurosci ; 114(6): 1131-44, 2000 Dec.
Article in English | MEDLINE | ID: mdl-11142645

ABSTRACT

Although it is known that norepinephrine (NE) modulates memory by acting on limbic areas, few studies describe how structures supplying NE to the limbic system, such as the nucleus tractus solitarius (NTS) contribute to this process. The present study examined the effects on memory of activating the NE pathway between the NTS and the amygdala (AMYG). Rats received buffer or the beta-noradrenergic agonist clenbuterol (CLN; 10, 50, or 100 ng/0.5 microl) into the NTS after footshock training in a Y-maze discrimination task. Infusion of 100 ng CLN significantly improved memory when retention was tested in the absence or presence of cues associated with the footshock. Experiment 2 used in vivo microdialysis to determine whether the mnemonic effects of CLN are mediated by influencing NE output in the AMYG. Subjects were given an intra-NTS infusion of CLN or phosphate buffered saline, footshock (0.8 mA, 1 s), and injected with epinephrine (EPI; 0.3 mg/kg ip) or saline. CLN or EPI injection produced a significant increase in NE sampled from the AMYG. These findings indicate that activation of NTS neurons that project to and release NE in the AMYG modulates memory storage processing.


Subject(s)
Amygdala/physiology , Mental Recall/physiology , Norepinephrine/physiology , Solitary Nucleus/physiology , Animals , Association Learning/physiology , Brain Mapping , Conditioning, Classical/physiology , Discrimination Learning/physiology , Male , Maze Learning/physiology , Neural Pathways/physiology , Rats , Rats, Sprague-Dawley , Retention, Psychology/physiology
7.
Toxicon ; 37(7): 1025-39, 1999 Jul.
Article in English | MEDLINE | ID: mdl-10484738

ABSTRACT

Single injections of domoic acid, given either intraperitoneally to mice or directly into the hippocampal formation of rats, have been shown to impair learning on the place version of the Morris water maze task and the eight arm radial maze task. The present study was designed to test whether both single and repeated exposures of intraperitoneally administered domoic acid (1.0 or 2.0 mg/kg) impair spatial working memory in mice on a delayed matching-to-sample task. DBA strain mice were given a series of four injections over a 7-day period consisting of either saline or one of two doses of domoic acid. During the 18 days of testing, each subject was given one trial per day consisting of one information run, followed by three test runs. On non-alternation days (days in which the correct response was the same as the preceding day) the saline injected group significantly outperformed the single injection 2.0 mg/kg domoic acid group. This indicates that domoic acid-treated animals were incapable of forming a memory that persisted for 24 h and hence were less able to utilize the prior day's experience. However, the repeated exposure groups did not perform as poorly on non-alternation days than the single exposure groups, indicating that domoic acid may affect multiple mechanisms involved in memory consolidation.


Subject(s)
Brain/drug effects , Kainic Acid/analogs & derivatives , Maze Learning/drug effects , Memory Disorders/chemically induced , Animals , Behavior, Animal/drug effects , Drug Administration Schedule , In Vitro Techniques , Injections, Intraperitoneal , Kainic Acid/administration & dosage , Kainic Acid/toxicity , Male , Mice , Random Allocation , Time Factors
8.
Behav Neurosci ; 112(6): 1414-22, 1998 Dec.
Article in English | MEDLINE | ID: mdl-9926823

ABSTRACT

Several findings based largely on lesions and drug manipulations within the amygdala suggest that norepinephrine (NE) systems in the amygdala contribute to enhancement of memory processes by epinephrine (EPI). However, no studies to date have directly measured changes in the release of NE in the amygdala after EPI injection. In Experiment 1, in vivo microdialysis was used to assess amygdala NE release after systemic injection of saline, EPI (0.1 or 0.3 mg/kg), and administration of an escapable footshock (0.8 mA, 1 s). Both doses of EPI produced a significant elevation in NE release that persisted for up to 60 min. In Experiment 2, the local anesthetic lidocaine (2%) was infused (0.5 microl) into the nucleus of the solitary tract (NTS) immediately before injection of 0.3 mg/kg EPI. The EPI-induced elevation in amygdala NE release observed in Experiment I was attenuated by inactivation of the NTS. These findings indicate that systemic injection of EPI increases release of NE in the amygdala and suggest that the effects are mediated in part by activation of brainstem neurons in the NTS that project to the amygdala.


Subject(s)
Amygdala/drug effects , Arousal/drug effects , Avoidance Learning/drug effects , Fear/drug effects , Norepinephrine/metabolism , Solitary Nucleus/drug effects , Amygdala/physiology , Animals , Arousal/physiology , Avoidance Learning/physiology , Brain Mapping , Dose-Response Relationship, Drug , Fear/physiology , Injections , Lidocaine/pharmacology , Male , Neural Pathways/drug effects , Neural Pathways/physiology , Rats , Rats, Sprague-Dawley , Solitary Nucleus/physiology
9.
Fundam Appl Toxicol ; 40(1): 63-7, 1997 Nov.
Article in English | MEDLINE | ID: mdl-9398488

ABSTRACT

Domoic acid (DA) is an environmental neurotoxin to humans. This work examines whether repeated exposure to subsymptomatic or symptomatic nonlethal doses of domoic acid leads to enhanced symptomatic toxicity in ICR outbred and DBA inbred strains of laboratory mice. A multiple independent exposure paradigm was designed in which doses were administered intraperitoneally every other day for 7 days to achieve four separate exposures to domoic acid. We first examined the effect of repeated exposure on serum clearance of domoic acid. Serum domoic acid levels did not differ following a single or repeated exposure. We next examined the effect of repeated exposure on symptomatic toxicity. The mean toxicity scores did not show a significant difference between single and repeated exposures of either subsymptomatic (0.5 mg/kg) or symptomatic sublethal (2.0 mg/kg) doses of domoic acid. We then examined the effects of repeated domoic acid exposure on a second strain of mouse. DBA mice were chosen based upon their sensitivity to kainic acid-induced seizures; however, the ICR mice were more sensitive to low-dose domoic acid toxicity, particularly in terms of onset and duration of stereotypic scratching behavior. Our results indicate that both strains of mice have comparable concentration-dependent toxic responses to domoic acid; however, differences exist in the magnitude of the response and in specific symptoms. The mean toxicity scores did not show a significant difference when a single exposure (1.0 and 2.0 mg/kg domoic acid) and repeated exposure of the same dose were compared in the DBA mice. This study provides no evidence that short-term repeated exposure to domoic acid in laboratory mice alters domoic acid clearance from the serum, or leads to a more sensitive or a greater neurotoxic response.


Subject(s)
Kainic Acid/analogs & derivatives , Neurotoxins/toxicity , Seizures/physiopathology , Animals , Behavior, Animal/drug effects , Excitatory Amino Acid Agonists , Female , Kainic Acid/administration & dosage , Kainic Acid/pharmacokinetics , Kainic Acid/toxicity , Mice , Mice, Inbred DBA , Mice, Inbred ICR , Nervous System Diseases/chemically induced , Nervous System Diseases/physiopathology , Neurotoxins/administration & dosage , Neurotoxins/pharmacokinetics , Seizures/chemically induced , Seizures/genetics , Species Specificity
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