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PubMed1986

Unilateral fimbria/fornix lesions attenuate behavioral symptoms induced by subsequent dorsal hippocampal lesions in rats.

Adult rats were given a unilateral fimbria-fornix (5, 10, 15 micrograms colchicine or electrolytic) lesion 30 days before a restricted bilateral dorsal hippocampal lesion to assess the behavioral effects of temporally and structurally spaced lesions. The rats were tested 30 days after the second-stage surgery in the Hebb-Williams maze learning task. All rats with lesions were impaired in comparison with sham-operated control rats. However, those which sustained electrolytic or 5 micrograms colchicine fimbria-fornix lesions before hippocampal lesions were less impaired than rats which received hippocampal lesions alone or hippocampal lesions preceded by fimbria-fornix lesions with larger doses of colchicine.

Acetylcholinesterase↗

PubMed1975

Locomotor, avoidance and maze behavior in rats with the dorsal fornix transected.

Transection of the dorsal fornix bundle in rats resulted in impaired maze learning, while the behavior in open field, passive avoidance and spontaneous alternation test was unchanged. The results are discussed in terms of an association deficit. It is concluded that the dorsal fornix is probably not to be regarded as part of the hippocampal output system.

Animals↗

PubMed1975

Maze performance in rats with hippocampal perforant paths lesions: some aspects of functional recovery.

The performance of two experimental groups--one with lesions of the perforant paths projecting to the dorsal hippocampus (the D group) and one with lesions of the perforant paths to both the dorsal and ventral hippocampus (the DV group)--was compared with the performance of a lesioned control group and an intact control group during two test sessions in the Hebb-Williams maze. Both experimental groups displayed impaired maze learning in Session I. The DV group showed some recovery of function in Session II, and the D group was indistinguishable from controls. The results are discussed in terms of reduced sensory information to the hippocampal formation resulting from perforant paths lesions. It is suggested that the hippocampus is involved in relating new stimuli to previous experience.

Animals↗

PubMedDate not supplied

Puromycin's suppression of memory in mice as affected by caffeine.

It has previously been shown that expression of maze-learning in mice is blocked for long periods of time by puromycin injected intracerebrally one or more days after the training experience. Treatment with caffeine after training has now been found to reduce greatly the amnestic effects of puromycin. With a high dose of caffeine (200 mg/kg) this reduction is evident 6 days after treatment with puromycin. With a lower dose of caffeine (25 mg/kg) the effect becomes evident only after a more extended period of time. In view of control experiments, we suggest that caffeine modifies factors necessary for the expression of memory and that this alteration makes puromycin relatively ineffective in blocking memory.

Amnesia↗

PubMed1976

Effect of two inhibitors of dopamine beta-hydroxylase on maturation of memory in mice.

Bitemporal injections of puromycin that primarily affect the hippocampal-enthorhinal cortical areas suppress memory of maze-learning in mice for 3 days after training but are ineffective 6 or more days after training. At these later times, injections affecting widespread areas of the brain in addition to the hippocampal-entorhinal area are necessary for amnesia. These observations are interpreted to indicate that the locus of the memory trace has enlarged at 6 days to include other parts of the central nervous system in addition to the hippocampal-entorhinal area. To produce an imbalance of neurotransmitters and so to test their importance in enlargement of the memory trace's locus, we treated mice for 7 days after training with inhibitors of dopamine beta-hydroxylase. These mice, unlike untreated controls, developed amnesia after bitemporal injections of puromycin. In view of additional control experiments, we interpret these results to suggest that an imbalance of transmitters suppresses the normal enlargement of the locus of the memory trace.

Animals↗

PubMed1977

Induced PKU in rats: effects of age and melatonin treatment.

Newborn rats injected on Days 1-8 of life with L-phenylalanine (2 g/kg) and p-chlorophenylalanine (80 mg/kg) displayed biochemical symptoms analogous to human phenylketonuria (PKU) and maze learning impairments. The behavioral effects were less evident in rats treated on Days 9-16 or 7-24. None of the symptoms observed were alleviated by simultaneous administration of melatonin (10 mg/kg/day).

Aging↗

PubMed1979

Distribution, survival and biological effects in mice of a behaviorally active, enzymatically stable peptide: pharmacokinetics of cyclo(Leu-Gly) and puromycin-induced amnesia.

Cyclo(Leu-Gly), the enzymatically resistant diketopiperazine formally derived from the C-terminal dipeptide sequence of oxytocin, exhibits activity in several behavioral systems. The distribution of cyclo(Leu-14C(U)Gly) in brain, and the time course of the disappearance of this labeled peptide from brain and plasma after subcutaneous injection into mice have been studied. The intact peptide was distributed equally in the five cerebral areas studied, for up to 96 hours after injection. Two exponential components were determined for peptide disappearance rates in plasma and brain; peptide half-lives in plasma up to 10 hr and from 24--96 hr after injection were, respectively, 0.8 and 33 hr; in brain, 1.0 and 42 hr. The peptide was found to accumulate in brain intracellular space to some degree. The time course of distribution of labeled cyclo(Leu-Gly) in subcellular fractions of mouse brain was also examined, and the concentration of peptide in the synaptosomal fraction was significantly correlated with the degree of protection against puromycin-induced amnesia of a maze-learning test. The results obtained not only confirm that cyclo(Leu-Gly) penetrates brain tissue intact and remains intact after peripheral administration in order to exert its behavioral effects, but, moreover, suggest an intriguing dynamic relationship between peptide concentration in the synaptosomal fraction and behavioral activity.

Amnesia↗

PubMed1981

Ethanol-Metrecal diets: II. Failure to obtain impaired performance on a series of appetitively and aversively motivated tasks.

Rats were chronically maintained on ethanol-Metrecal diets where either 37%, 41%, 49% or 57% of the total kilocalories were derived from ethanol. In three experiments animals were tested on a series of problems (passive avoidance, shuttle avoidance, simultaneous and successive discrimination, and complex spatial maze learning) 6 to 8 weeks after the diet had been withdrawn. There was no evidence that chronic ethanol regimes impaired either learning or memory processes.

Alcohol Drinking↗

PubMed1983

Studies on memory: the cerebral spread of an engram in mice as affected by inhibitors of dopamine beta-hydroxylase.

Bitemporal injections of puromycin that primarily affect the hippocampal-entorhinal areas consistently cause amnesia of maze-learning in mice for 3 days after training but become consistently ineffective if given 6 or more days after training. At these later times, additional puromycin injection sites covering widespread areas of the forebrain are necessary to induce amnesia. These observations are interpreted to indicate that the locus of the engram has become more widespread within the 6-day period. Treatment with inhibitors of dopamine beta-hydroxylase for 3 days following training, retarded the spread of memory from a matter of days to a period of weeks. Repeated treatment with the inhibitors restricted engram spread for about 3 months; again spread was evident about a month after the last treatment. These observations imply that the mechanisms responsible for engram spread are capable of surviving for extraordinarily long periods of time.

Animals↗

PubMed1989

Long-term suppression of the cerebral spread of a memory: effects of idazoxan and clonidine.

Bitemporal injections of puromycin consistently induce amnesia of aversive maze-learning in mice when administered within 3 days of training. These bitemporal puromycin injections lose their amnestic effectiveness if the latency between training and injection is extended beyond 6 days. Consistent with other evidence, we believe that memory (in our task) "spreads" during the 6 days following training. Since previous experiments have indicated that the central noradrenergic system is involved in this process of "memory spread," we have examined the effect of stimulation or blockade of the alpha 2-receptor. To this end, we administered a single dose of the alpha 2-adrenoceptor antagonist, idazoxan, or the alpha 2-agonist, clonidine. Idazoxan (1 mg/kg, SC) had no effect on engram spread. Clonidine (25 micrograms-125 ng/kg, SC), by contrast, suppressed engram spread for at least 30 days after treatment. When mice were tested at 60 and 90 days after treatment, spontaneous recovery (i.e., engram spread) was evident in only about 50% of the clonidine treated mice. Coadministration of idazoxan with clonidine blocked the effects of clonidine on "memory spread."

Animals↗

PubMed1990

T-maze performance in rats following chronic neuroleptic treatment.

The effects of chronic haloperidol treatment (0.5 mg/kg/day for 21 days) on maze learning in the rat were studied. There were no differences between haloperidol- and saline-treated groups in percentage of correct responses, but the latency to respond was longer and extinction was faster in the haloperidol-treated group. We speculated that differences between both groups were due to a decrease of appetitive motivation in haloperidol-treated animals, probably caused by a decrease of dopaminergic neurotransmission.

Animals↗

PubMed1991

Long-term suppression in mice of the development of complementary memory storage sites: effect of a muscarinic antagonist.

Amnesia↗

PubMed1992

Long-term suppression of the development of complementary memory storage sites in mice: functional interdependence of acetylcholine and dopamine.

Bitemporal injections of puromycin consistently induce amnesia of aversive maze learning in mice when given within 3 days after training. These injections consistently fail to induce amnesia when given 6 or more days after training. Consistent with the evidence from other laboratories, we interpret these results to indicate that the initial, temporal memory storage sites are supplemented 6 days after training by the development of complementary storage sites in other cerebral areas. Previous experiments have shown that this process is suppressed for 30-60 days by a single SC injection of scopolamine, a muscarinic antagonist. We now find that this suppressive action of scopolamine can be completely nullified by haloperidol, a dopaminergic antagonist. This finding supports the view that there may be a therapeutic role for dopamine antagonists in the treatment of cognitive dysfunction associated with cholinergic loss.

Acetylcholine↗

PubMed1988

Experience during suckling increases weight and volume of rat hippocampus.

Changes in brain anatomy resulting from early suckling experience were explored by measuring wet weight of whole brain, cortex, hippocampus and cerebellum in juvenile rats. Rats provided with ample opportunity to nipple-shift, a behavior associated with enhanced maze learning, had much larger hippocampal mass than rats whose nipple-shifting experience had been restricted. No differences were observed in the other areas measured. This effect of experience was confirmed by histological measurement of hippocampus volume following differential rearing.

Animals↗

PubMed1982

Analysis of behavioural responses to an ACTH analog in CXB/By recombinant inbred mice.

Male mice of the C57BL/6By and BALB/cBy inbred strains, their reciprocal F1 hybrids, and 7 recombinant inbred strains, were tested for open-field activity, a shock-motivated successive reversal position discrimination problem in a T-maze, and a toggle box exploration task. The test battery was repeated one month later. Finally, mice were tested for the acquisition and extinction of a taste aversion conditioned by ethanol injection. Mice of each strain were tested after injection with saline or one of 3 doses of an ACTH analogue. Highly significant genotypic differences were found for all measures, an expected result. The strain distribution pattern seen in the toggle box suggested single gene mediation of exploratory activity after habituation. One aspect of avoidance responding and extinction of conditioned taste aversion also yielded strain distribution pattern consistent with single gene control. Peptide treatment reduced internal field crossings in the open field. This effect was not strain dependent. Peptide treatment had no effect on T-maze learning, conditioned taste aversion, or toggle-box exploration.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

MIF-1 can accelerate neuromotor, EEG and behavioral development in mice.

Newborn mice were injected SC daily with 1 mg/kg of MIF-1 or saline during the first 19 days of life. The progress of each pup was monitored for physical (body weight, eye and ear opening), neurobehavioral (reflexes) and neurophysiological (EEG) development until the weaning stage. In early adulthood (40 days of age) mice were tested on a maze learning task. Results indicate that MIF-1 can accelerate neurologic (days 3-9), somatic (days 10-14) and electroencephalographic (days 16-19) parameters, and that the effects of treatment last into the early adult stage with increased learning abilities in an appetitive task.

Amino Acid Sequence↗

PubMed1990

Teratological, neurochemical, and postnatal neurobehavioral assessment of METASYSTOX-R, an organophosphate pesticide in the rat.

The purpose of this study was to assess the embryotoxic, fetotoxic, and teratogenic potential of METASYSTOX-R (MSR) in the rat. Furthermore, the study was designed to determine if maternally toxic doses of MSR altered fetal brain acetylcholinesterase (AChE), compromised neonatal survival, growth, and development, or affected neurobehavioral development. Inseminated female rats (45/dose group) received single daily oral doses of 0, 0.5, 1.5, or 4.5 mg/kg of MSR from Days 6 to 15. Dose groups were subdivided into three termination phases: Phase I, 5 females terminated on Day 16 of gestation; Phase II, 28 females terminated on Day 20 of gestation; Phase III, 12 females terminated on Day 21 postpartum. MSR produced a dose-related reduction in maternal plasma (30-72%), red blood cell (18-56%), and brain (21-68%) cholinesterase (ChE) activity, when measured on Day 16 of gestation. The high dose of MSR significantly (p less than or equal to 0.05) reduced food consumption, suppressed body weight gain, and produced tremors in 98% of the dams. MSR administered at maternally toxic doses as high as 4.5 mg/kg was devoid of embryotoxic, fetotoxic, and teratogenic effects. Fetal brain AChE was not substantially different from control for any dose level in Day 20 fetuses. Furthermore, neonatal survival, growth, and development were unaffected and an extensive neurobehavioral testing scheme demonstrated no alteration of sensory or reflex functions, maze learning ability, or open field activity for neonates.

Abnormalities, Drug-Induced↗

PubMed1994

Reproductive and neurobehavioral effects of Allura Red AC administered to mice in the diet.

The color additive, Allura Red AC, was given in the diet to provide levels of 0.42, 0.84, and 1.68% (control, 0%), from 5 weeks of age of the F0 generation to 9 weeks of age of the F1 generation in mice, and selected reproductive and neurobehavioral parameters were measured. There were few adverse effects of Allura Red AC on either litter size or weight, and ratio of male to female was significantly reduced in the lowest dosed group. Average body weight of offspring during the lactation period was significantly increased in the lower dosed groups of each sex. As regards the neurobehavioral parameters, no adverse effect was observed in the behavioral development during lactation period. There were few adverse effects of Allura Red AC on either movement activity or maze learning in F1 generation mice, compared with controls in each sex. The dose levels of Allura Red AC in the present study (approximately 86-1430 times greater than human ADI) produced few adverse effects in reproductive and neurobehavioral parameters in mice.

Animals↗