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PubMedDate not supplied

Differential effects of pre- and/or post-natal d-amphetamine on avoidance response in genetically selected lines of rats.

Effects of pre- and post-natal d-amphetamine on avoidance response were investigated in genetically selected lines of rats. Pregnant animals of the Roman high- and low avoidance (RHA and RLA) lines were administered daily either 3 mg/kg d-amphetamine or physiological saline from day 7 to 20 of gestation. Either-way avoidance learning was studied in prenatally treated offspring over four days of training and subsequently under the effects of four dosages of d-amphetamine. Prenatal intervention with d-amphetamine contributed significantly to avoidance learning over four days of training. A significant genetic line X prenatal treatment X dose response interaction was found in one-way and two-way responses. Results were discussed in terms of inverted-U arousal function, and it is proposed that the prenatal amphetamine intervention may affect baseline levels of physiological arousal. This effect may enhance or impair learning depending upon the nature of the response and the genetic line.

Animals↗

PubMed1983

Facilitation of memory retrieval by centrally administered catecholamine stimulating agents.

Amnesia for inhibitory avoidance learning induced in mice by a post-training injection of the protein synthesis inhibitor anisomycin was alleviated in a dose-dependent fashion by introcerebroventricular injections of D-amphetamine (20 micrograms), dopamine (10, 25 and 50 micrograms) and the dopamine agonist lisuride (0.5 and 1.0 micrograms), given 5 min before the retention test. Animals which received avoidance training in a different apparatus did not show increased test latencies following drug treatment thus eliminating non-specific behavioral suppression as an explanation for the findings. Neither norepinephrine nor the norepinephrine agonist clonidine was able to reverse the amnesia. These findings indicate that central dopamine systems may play a role in the retrieval of inhibitory avoidance learning.

Animals↗

PubMed2000

Chronic corticosterone impairs inhibitory avoidance in rats: possible link with atrophy of hippocampal CA3 neurons.

The aim of our work was to evaluate the effect of a chronic (22 days) administration of corticosterone, which induces supraphysiological serum levels of the hormone, on an inhibitory avoidance learning in rats (one-trial step-through learning task, footshock: 0.5 mA, 2 s). We also studied hippocampal markers of neuroanatomical CA3 pyramidal neuron atrophy by using the Golgi staining method. Chronic exposure to high CORT serum levels induced a significant impairment of inhibitory avoidance learning. The CORT group also showed hippocampal glucocorticoid receptor (GR) downregulation and the decrease of hippocampal CA3 branch points and total dendritic length in the apical tree that would be causally related with the learning impairment.

Adrenal Glands↗

PubMed1982

In utero alcohol exposure and developmental delay of response inhibition.

Offspring of rats fed liquid alcohol diet during pregnancy exhibited age-related increased activity and deficits in passive avoidance learning and response perseveration which were not age-related. Alcohol-exposed offspring also elicited less maternal responsiveness from nontreated dams than did pair-fed controls. The results suggest that in utero alcohol exposure produces a developmental delay in ontogeny of response inhibition mechanisms underlying activity, but not passive avoidance learning or spontaneous alternation.

Alcohol Drinking↗

PubMed1980

Genetically heterogeneous and selected lines of rats: behavioral and reproductive comparison.

Avoidance learning, open-field, and reproductive behaviors of a genetically heterogeneous stock (derived from a four-way cross of selected lines) were compared with the corresponding behaviors of the parental lines. The heterogeneous stock showed heterosis on the body development, fertility rate, litter size at birth and at weaning, and directional dominance on the avoidance learning and open-field measures.

Animals↗

PubMed2000

Learning deficits induced by 4 belladonna alkaloids are preferentially attenuated by tacrine.

AIM: To examine the antagonism of tacrine on the amnesic effects of scopolamine (Sco), anisodine (AT3), atropine (Atr), and anisodamine (Ani). METHODS: Cognitive functions and locomotor activities were determined using two sessions of step-through and open-field tests, respectively. Mice were injected with one of the belladonna alkaloids (0.05-50 mumol.kg-1, i.p.) and tacrine (50 mumol.kg-1, s.c.) 30 min before the first session. RESULTS: Tacrine completely blocked the avoidance-learning deficit caused by Sco 0.5 mumol.kg-1, AT3 and Atr 5 mumol.kg-1, or Ani 50 mumol.kg-1. But tacrine partly antagonized the learning deficit induced by Sco 5-50 mumol.kg-1 or Atr and AT3 50 mumol.kg-1. The avoidance-memory deficit caused by Sco 0.05-5 mumol.kg-1 or Atr 5 mumol.kg-1 was completely or partly attenuated by tacrine, which did not antagonize the memory deficit elicited by Sco and Atr 50 mumol.kg-1, AT3 5 and 50 mumol.kg-1, and Ani 50 mumol.kg-1. During the acquisition, the locomotor activity of the mice was inhibited by tacrine. This reduction was completely antagonized by Sco 0.5-50 mumol.kg-1, AT3 5-50 mumol.kg-1, Atr 5-50 mumol.kg-1, and only partly antagonized by AT3 and Atr 0.5 mumol.kg-1 or Ani 50 mumol.kg-1. CONCLUSION: Compared with the avoidance-memory deficit, the avoidance-learning deficit caused by belladonna alkaloids is more preferentially attenuated by tacrine.

Animals↗

PubMed2005

Differential role of dopamine in drug- and lithium-conditioned saccharin avoidance.

Rats learn to avoid palatable saccharin solutions that predict the systemic administration of reinforcing drugs as well as malaise-inducing lithium chloride (conditioned saccharin avoidance, CSA). In the present study the involvement of dopamine (DA) transmission in the acquisition of morphine, nicotine and lithium-conditioned CSA was investigated in a two-bottle choice paradigm. Nicotine tartrate (0.2 and 0.4 mg/kg s.c.) administered 15 min after saccharin presentation induced CSA, with a maximum effect at 0.4 mg/kg. The DA D1 receptor antagonist, SCH 39166 (0.1 mg/kg s.c.) and the DA D2 receptor antagonist raclopride (0.3 mg/kg s.c.), administered immediately after saccharin, prevented CSA induced by the lower but not by the higher dose of nicotine. However, combined administration of the two antagonists prevented CSA induced by the higher dose of nicotine. SCH 39166 prevented CSA induced by all morphine doses while raclopride prevented only CSA induced by the lowest dose of morphine (1.75 mg/kg). CSA induced by different doses of lithium given by the same schedule of drug-CSA (i.e. two pairings, 15 min after saccharin) was not affected by SCH 39166. However SCH 39166 impaired the acquisition of lithium-CSA when lithium was given 60 min after saccharin. In contrast, raclopride failed to affect lithium-CSA independently from the delay between saccharin and lithium. These results suggest that DA can play different roles in drug- and in lithium-CSA and are consistent with a different mechanism of drug- as compared to lithium-CSA.

Analysis of Variance↗

PubMedDate not supplied

Reflections on ethics, technology, and learning disabilities: avoiding the consequences of ill-considered action.

Over the last several years, the field of learning disabilities has directed considerable attention toward the area of technology. However, there have been few discussions regarding the larger ethical implications that surround the use of technology with persons with learning disabilities. This article employs the fundamental ethical principles of beneficence, justice, and autonomy as a framework from which to reflect upon the use of technology with persons with learning disabilities to help ensure that the greatest possible rewards will be gained, while simultaneously minimizing any potential negative consequences. These principles are applied to a number of topics, including instructional/remedial, assistive, and diagnostic technology; technology and special abilities; social/psychological impact of technology; health-related concerns; technological access; and medical technologies.

Education, Special↗

PubMed2001

Effects of prenatal rubratoxin-B exposure on behaviors of mouse offspring.

The effects of prenatal rubratoxin-B (RB) exposure on 8 behavioral parameters in JCL:ICR mice were assessed. Pregnant mice were injected intraperitoneally with 0.1 or 0.2 mg/kg/day of RB dissolved in propylene glycol water solution on days 7-9 (Group A) or 10-12 (Group B) of gestation. Controls received the vehicle similarly on days 7-12 of gestation. Before weaning, the offspring of both sexes were examined to test their the surface righting reflex (5 days of age), cliff avoidance response (6 days), negative geotaxis response (7 days), and swimming development (8, 10, and 12 days). After weaning, male animals were examined using the rotarod test (6 weeks of age), the open-field test (7 weeks), the shuttle-box-avoidance-learning test (9 weeks), and the water E-maze test (10 weeks). The preweanling offspring in the 0.2 mg/kg-B group showed significantly lower success rates and longer response times than controls in the cliff-avoidance response. In swimming development, the offspring in the 0.2 mg/kg B group had significantly lower scores than controls for swimming angle at 10 and 12 days of age. The avoidance learning of the mice in all RB-exposed A and B groups was significantly poorer than that of controls. These results indicate that prenatal exposure to RB produced a delay of early response development and impaired learning ability in the offspring of mice exposed to RB during middle pregnancy.

Animals↗

PubMed1991

Memory modulation by brain benzodiazepines.

1. Recent evidence indicates that post-training memory processes are down-regulated by benzodiazepine/GABA-A systems in the amygdala, septum and hippocampus. Habituation and avoidance learning are accompanied by a decrease of benzodiazepine-like immunoreactivity in the three structures, explainable by a release of benzodiazepines. Immediate post-training microinjection of the benzodiazepine antagonist flumazenil into the hippocampus enhances retention of habituation. The post-training administration of flumazenil into any of the three structures enhances retention of avoidance learning. 2. The mode of operation of these systems was studied in detail in the amygdala using avoidance paradigms. The release of endogenous benzodiazepines during and particularly after training enhances sensitivity of local GABA-A receptors to muscimol, activation of the GABA-A receptors opens chloride channels that can be selectively blocked by picrotoxin and by Ro5-4864. Training enhances, and flumazenil reduces, sensitivity of the amygdala to the amnestic effect of locally injected muscimol by a factor of 100. Post-training intra-amygdala administration of picrotoxin or Ro5-4864 enhances retention. 3. These findings suggest that the endogenous benzodiazepine/GABA-A mechanisms that down-regulate memory in the amygdala, septum and hippocampus are activated in response to the anxiety and/or stress associated with each task. Memory lability which occurs in the post-training period and characterizes consolidation would thus be a consequence of the brain's response to anxiety or stress.

Animals↗

PubMed1978

Open field activity and avoidance behavior following serotonin depletion: a comparison of the effects of parachlorophenylalanine and electrolytic midbrain raphe lesions.

Three experiments were performed in order to compare the behavioral effects of electrolytic destruction of the dorsal and median mesencephalic raphe nuclei (MR lesion) and parachlorophenylalanine (pCPA; 300 mg/kg, IP) administration. Forebrain 5-hydroxytryptamine (5-HT) was measured in all animals following completion of behavioral testing. In the first experiment open field behavior (one 50 min session) and two-way (shuttle) conditioned avoidance acquisition (50 massed trials) were examined 68-72 hr after vehicle or pCPA administration in rats which had received control operations or MR lesions two weeks earlier. Only the MR lesion and the MR lesion + pCPA groups evidenced increased open field activity and facilitated two-way avoidance learning. Although the reduction in forebrain 5-HT of the pCPA group (85%) was greater than in the MR lesion group (55%), the pCPA treated animals did not differ from the control group. In the second experiment animals were tested in the open field 24, 48 or 72 hr after pCPA treatment to determine its effects on activity level as a function of the time after injections. No differences between the vehicle and pCPA groups, however, were found. In the third experiment, the effects of pCPA (72 hr postinjection) on the acquisition of an unsignalled one-way avoidance response was examined. MR lesion rats tested in the same apparatus and with the same procedure repeatedly have been shown to be impaired in this task. The pCPA and vehicle animals, however, did not differ. Reduction in 5-HT following electrolytic MR lesions and pCPA administration, thus, produce different behavioral effects. MR lesions, but not pCPA treatment, result in (1) increased activity in a novel environment, (2) facilitated two-way conditioned avoidance learning, and (3) impaired acquisition of an unsignalled one-way avoidance response. These data support earlier studies suggesting that the behavioral effects of electrolytic MR lesions are not due primarily to their disruption of ascending 5-HT pathways. The role of 5-HT in avoidance conditioning and the regulation of activity level, furthermore, remains to be elucidated.

Animals↗

PubMed1976

The effect of pyrithioxine and pyridoxine on individual behavior, social interactions, and learning in rats malnourished in early postnatal life.

Low protein (LP) or low calorie (LC) dietary regimens were applied in early postnatal life(1st-40th day of life) in male rats. After nutritional rehabilitation, open-field behavior in larger more illuminated boxes (HI, high intensity stimulus), and smaller, less illuminated boxes (HI, high intensity stimulus), and smaller, less illuminated boxes (HI, high intensity stimulus), and smaller, less illuminated boxes (HI, high intensity stimulus), dyadic interactions, and learning ability were investigated in these animals as adults (between the 200th to 300th day of life). LP malnutrition induced an increase of open-field activity with features of sterotypy both in LI and HI situations, an increase number of intersignal reactions during learning procedures without changes in other registered criteria of learning ability (latency, number of correct responses), and an increase of aggressive behavior in pair interaction. LC rats revealed only significant inhibition in LI--open-field activity and a slightly increased number in intersignal reactions during avoidance learning. With the aim of preventing previously described long-term deviations in early malnourished rats, some groups of animals with the above-mentioned early calorie or protein deficits were treated with pyrithioxine (Encephabol Merck) or pyridoxine in 10 doses of 40 mg/kg i.p. administered in the period when nutritional rehabilitation was carried out (between the 40th--50th day of life). The treatment with pyrithioxine reduced significantly behavioral disturbances in adult LP rats except the increase of intersignal reactions which was even potentiated. Pyridoxine was less effective but normalized the increase number of intersignal reactions both in LP and LC rats. The effect of pyridoxine of adult LC rats was interesting. There was significant improvement in all registered parameters of avoidance learning and a significant increase of sexual acts was recorded.

Aggression↗

PubMed1994

Phencyclidine prevents spatial navigation and passive avoidance deficits in ibotenate lesioned rats.

The potential neuroprotective effects of phencyclidine (5 mg/kg i.p.) were assessed in rats which had been treated with the excitotoxin, ibotenic acid (IBO) (0.015 M) to lesion the nucleus basalis magnocellularis. IBO treated rats showed a significant impairment in 13 of the 25 test trials in the spatial navigation Morris water maze task and deficits in passive avoidance learning. Phencyclidine was found to prevent the IBO-induced impairment in 4 of the 13 test trials in which the IBO Morris maze deficit was observed and also successfully prevented the passive avoidance learning deficits. Neurochemically, IBO was shown to reduce the levels of gamma amino-n-butyric acid (GABA) in the cortex. This effect of IBO on the inhibitory GABAergic system may contribute to the direct toxic effects of IBO which is mediated through excitatory amino acid receptors. Phencyclidine had no effect on the changes in GABA produced by IBO. The effect of phencyclidine treatment on IBO behavioural toxicity observed in this study demonstrates that antagonism of the phencyclidine receptor site on the N-methyl-D-aspartate receptor complex may be partially protective against the excitotoxic damage induced by IBO.

Animals↗

PubMed2005

Toluene exposure during the brain growth spurt reduces behavioral responses to noncompetitive N-methyl-D-aspartate receptor antagonists in adult rats.

RATIONALE: Toluene exposure during brain growth spurt has been shown to elevate the seizure susceptibility induced by N-methyl-D: -aspartate (NMDA). In the present study, behavioral responses to NMDA antagonists were studied to determine whether neonatal toluene exposure produces residual deficits in the NMDA glutamatergic system controlling behaviors. We also investigated if the effect of toluene exposure depends strongly on the developmental stage. OBJECTIVES: The long-term effects of neonatal and adolescent toluene exposure on MK-801 and/or ketamine-induced hyperlocomotor activity, motor coordination, hypnotic response, and cognitive deficits in early adulthood were compared. METHODS: Sprague-Dawley male rats were treated with toluene (500 mg/kg i.p.) daily over postnatal day (PN) 4-9 or 25-30. Locomotor activity was analyzed in a computerized open-field system, motor coordination was measured by rotarod, hypnotic response was tested by loss of righting reflex, and long-term memory was assessed with the inhibitory avoidance learning task during PN 56-60. RESULTS: Toluene exposure during brain growth spurt reduced behavioral responses including locomotor activity, motor incoordination, and hypnosis to MK-801 and/or ketamine, while leaving cognitive deficits in inhibitory avoidance learning tasks unaffected. No significant change in behavioral responses to NMDA antagonists was observed following adolescent toluene exposure. CONCLUSION: These results indicate that neonatal but not adolescent toluene exposure produces long-term effects on selective behaviors induced by NMDA antagonists. Theses findings further support the hypothesis that functional changes in NMDA receptors may be related to the neurobehavioral dysfunction associated with fetal solvent syndrome.

Age Factors↗

PubMed1993

Long-term effects of postnatal hypoxia and flunarizine on the dopaminergic system.

Long-term changes of learning behavior and of the striatal dopaminergic system were observed in a rat model of early postnatal hypoxia. Striatal dopamine (DA) concentration, K(+)-stimulated DA release from slices, and DA uptake into crude synaptosomal preparations (S1 fractions) were used as markers of the striatal DAergic system. Active avoidance learning was tested as behavioral criterion. Cyclodextrin and flunarizine were found to produce long-term effects on the DAergic system in control animals. While cyclodextrin normalized hypoxia-induced effects in DA release, flunarizine prevented those in DA uptake and improved avoidance learning.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1983

Comparative effects of ACTH-related peptides on acquisition of shuttle-box avoidance behavior of hypophysectomized rats.

Hypophysectomy resulted in a marked impaired acquisition of shuttle-box avoidance learning, when lower shock intensity (0.05 mA) was used as the unconditioned stimulus, but not when shock intensity was increased to 0.12 mA. Daily subcutaneous treatment with ACTH4-10 (6 micrograms/day), ACTH4-7 (6 micrograms/day), [Met(O2)4]ACTH4-7 (2 micrograms/day), ACTH4-9 analog (Org 2766) (60 ng/day), and an ACTH4-16 analog (HP 953 A) (60 ng/day) for 7 days normalized avoidance acquisition of hypophysectomized rats during the treatment period. The beneficial effect of the peptides was of a short-term nature, since it disappeared after discontinuation of the treatment. Microgram amounts of Org 2766 did not influence acquisition of hypophysectomized rats. [D-Phe7]ACTH4-10 (60 micrograms/day) further reduced the already deficient acquisition of avoidance behavior of hypophysectomized rats. This latter effect may be due to an antagonistic effect towards brain-borne ACTH-related peptides. ACTH1-16 -NH2 antiserum administered intracerebroventricularly 30 min prior to a massed-trial shuttle-box acquisition session reduced avoidance acquisition in hypophysectomized rats. This suggests that in addition to ACTH and related peptides from the pituitary, brain-borne ACTH-like peptides are involved in avoidance learning.

Adrenocorticotropic Hormone↗

PubMed2006

Choline supplementation facilitates short-term memory consolidation into intermediate long-term memory of young Sprague-Dawley rats.

Choline is important for the synthesis of acetylcholine, an integral neurotransmitter involved in memory formation. In order to investigate the effect of choline supplementation on memory consolidation, the study utilized a T-maze to facilitate passive avoidance learning and memory in young female Sprague-Dawley rats. Rats were placed in two groups; choline-supplemented that received choline chloride daily for two weeks, and control that received vehicle daily for two weeks. Rats were evaluated to determine their ability to avoid an aversive electric foot-shock (0.1 mA at 60V) when they characteristically entered the preferred dark area (DA) of the T-maze. Both groups of rats showed preference, without significant difference, for entry into DA of the T-maze. However, fifteen minutes after passive avoidance both choline supplemented and control rats avoided entry into DA. This display of DA avoidance 15 minutes after training, suggests that both groups of rats had acquired short-term memory of the aversive stimulus. However, when the test was repeated 24 hours after training, the control group did not avoid entry into DA, whereas the choline-supplemented group either avoided entry or entered after a significantly longer latency period (p < 0.01). These results suggest that supplementation with choline facilitated the consolidation of short-term memory of the avoidance learning into intermediate long-term memory in young rats.

Age Factors↗

PubMed1991

Milacemide enhances memory storage and alleviates spontaneous forgetting in mice.

The objective of this study was to evaluate the effectiveness of milacemide as a memory-enhancing drug in mice. Experiment 1 showed that forgetting of active avoidance learning produced by a 14-day training to test delay could be alleviated by milacemide (10 mg/kg) administered before the retention test. Experiment 2 demonstrated that the same dose of milacemide could also attenuate spontaneous forgetting of passive avoidance learning, thereby ruling out nonspecific effects as an explanation for the enhancement of performance following pretesting drug administration. A third experiment showed that the facilitation of retrieval induced by milacemide could be blocked by the NMDA receptor antagonist AP-7, suggesting that the effects of milacemide on memory may be mediated by NMDA receptor activation. A final experiment demonstrated that retention was improved when milacemide was administered immediately following active avoidance training, indicating that the drug can also facilitate remembering by its actions on consolidation and storage processes.

2-Amino-5-phosphonovalerate↗