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At least 631 records · Page 35Linked to original sources
PubMed2001

The potential for toxic effects of chronic, low-dose exposure to organophosphates.

Organophosphorus esters have the potential to produce several forms of toxicity. Most produce acute intoxication as a result of inhibition of acetylcholinesterase and, if severe, this can have longer lasting secondary consequences such as intermediate syndrome, or even permanent disability. Some esters produce a very specific syndrome of delayed peripheral neuropathy. This neuropathy is always preceded by severe acute intoxication, except in the case of a few specific agents such as tri-o-cresyl phosphate. All of these effects are reasonably well understood and show a dose threshold. Chronic low level exposure in non-poisoned subjects has been associated with impaired neurobehavioral performance in some, but not all, epidemiological studies. The mechanisms involved are not well understood, but if organophosphates do play a causal role, this will not necessarily be via acetylcholinesterase inhibition. Doses too low to produce cholinergic signs have been shown to produce a variety of effects in experimental animals ranging from enhanced maze learning to slowed nerve conduction. It is likely that other, more sensitive, brain proteins are the targets for such actions. Effects mediated via such target proteins would be expected to show very different structure-activity relationships to acute toxicity mediated by acetylcholinesterase. Hence epidemiological studies expecting similar (class) effects from low-dose exposure to different organophosphorus esters may produce variable results or false negatives.

Animals↗
PubMed2000

Distribution of angiotensin IV binding sites (AT4 receptor) in the human forebrain, midbrain and pons as visualised by in vitro receptor autoradiography.

Angiotensin IV and other AT4 receptor agonists, improve memory retention and retrieval in the passive avoidance and swim maze learning paradigms. Angiotensin IV binding sites (also known as the AT4 receptors) are widely distributed in guinea pig and monkey (Macaca fascicularis) brains where high densities of the binding sites have been detected in the hippocampus, neocortex and motor nuclei. However, the distribution of the binding sites in the human brain is not known. We have recently localised the angiotensin IV binding sites (AT4 receptors) in post-mortem human brain using iodinated Nle-angiotensin IV, a higher affinity and more stable analogue of angiotensin IV. This radioligand bound with relatively high affinity and specificity to angiotensin IV binding sites. In competition studies on consecutive sections through the prefrontal cortex and claustrum, angiotensin IV, Nle-angiotensin IV and LVV-hemorphin 7 competed for the binding of 125I[Nle]-angiotensin IV with nanomolar affinities. Angiotensin II and the AT1 and AT2 receptor antagonists were ineffective in competing for the binding at concentrations of up to 10 microM. We found high densities of 125I[Nle]-angiotensin IV binding sites throughout the cerebral cortex including the insular, entorhinal, prefrontal and cingulate cortices. Very high densities of the binding sites were observed in the claustrum, choroid plexus, hippocampus and pontine nucleus. Some thalamic nuclei displayed high densities of binding including the anteroprincipal, ventroanterior, anteromedial, medial dorsal and ventrolateral nuclei. The caudate nucleus, putamen, many amygdaloid nuclei and the red nucleus all displayed moderate densities of binding with a higher level detected in the substantia nigra pars compacta. In the hypothalamus, high densities binding sites were found in the ventromedial nucleus with lower levels in the dorsomedial and paraventricular nuclei. The distribution of 125I[Nle]-angiotensin IV binding sites in the human brain is similar to that found in other species and supports multiple roles for the binding sites in the central nervous system, including facilitation of memory retention and retrieval.

Aged↗
PubMed2004

The presynaptic active zone protein RIM1alpha is critical for normal learning and memory.

The active zone protein RIM1alpha is required both for maintaining normal probability of neurotransmitter release and for long-term presynaptic potentiation at brain synapses. We now demonstrate that RIM1alpha(-/-) mice exhibit normal coordination and anxiety-related behaviors but display severely impaired learning and memory. Mice with a synaptotagmin 1 mutation, which selectively lowers release probability, and mice with Rab3A deletion, which selectively abolishes presynaptic long-term potentiation, do not exhibit this abnormality. Our data suggest that a decrease in release probability or a loss of presynaptic LTP alone is not sufficient to cause major behavioral alterations, but the combination of presynaptic abnormalities in RIM1alpha(-/-) mice severely alters learning and memory.

Animals↗
PubMed2000

Role of maternal biochemistry in fetal brain development: effect of maternal thyroidectomy on behaviour and biogenic amine metabolism in rat progeny.

Few studies have addressed the role of biochemicals of maternal origin on fetal neurodevelopment and behavioural outcome. Thyroid deficiency in the thyroidectomized pregnant rat provides an excellent model to study fetal effects of maternal chemistry, as this condition is known to be associated with deficits in motor and cognitive behaviour in human offspring. Based on evidence that thyroid hormone of maternal origin may be an important determinant in regulating these behaviours, we assessed neurobehaviours and regional brain biogenic amine levels in offspring of rats thyroidectomized (Tx) prior to conception. Cross-fostering techniques were used to isolate fetal effects of maternal thyroid deficiency from possible neonatal effects during nursing by thyroid-deficient dams. The progeny of Tx dams showed significant deficits in maze learning, were less cautious in emotionality testing, and were more active in open-field exploration. Tx females appeared to be more vulnerable to the effects on learning. Learning in Tx males was only slightly impaired. Serotonin and dopamine metabolism was also affected in a brain region-specific manner in Tx progeny. Levels of 5-HIAA were reduced in the olfactory tubercle and cortex. HVA levels were lower in olfactory tubercle, but were elevated in the hippocampus. As these neurotransmitters play a functional role in activity, mood and learning, the findings may be pertinent to the observed behavioural impairments. The results are consistent with the hypothesis that an adequate in utero thyroid hormone environment may be essential for early fetal neurodevelopment even if the fetus is euthyroid.

Journal Article↗
PubMed1992

Effects of transplantation of fetal hippocampal or hindbrain tissue into the brains of adult rats with hippocampal lesions on water maze acquisition.

Rats were given bilateral aspiration lesions of the hippocampus. Some of these rats then received bilateral transplants of fetal hippocampal or dorsal ventricular ridge tissue that was dissected from embryonic rat brains at 16 or 17 days of gestation. The remaining rats with hippocampal lesions did not receive fetal brain transplants. Rats with neocortical aspiration lesions, but without transplants, and rats without brain damage were also included in the study. All of the rats were trained to find a submerged platform in a Morris water maze. Rats with the fetal brain transplants were more impaired in some measures of maze learning than were rats with hippocampal lesions only. The results indicate that transplants of fetal brain tissue are not always associated with recovery of behavioral function after brain damage and may even increase a lesion-induced behavioral impairment in tasks that require complex cognitive functioning.

Animals↗
PubMed1983

An association between granule cell density in the dentate gyrus and two-way avoidance conditioning in the house mouse.

Mice with genetically associated variations in the number and density of granule cells in the dentate gyrus were tested for open-field activity, spatial maze learning, and two-way avoidance conditioning. The number of granule cells was not associated with any behavior measured. Only avoidance conditioning was related to granule cell density, which had a negative correlation with performance on the shuttle box task. This result was replicated in two genetically different stocks of mice. Density of the more caudal portion of the dentate was associated with early stages of avoidance learning, whereas the more rostral portion was associated with later stages. The results are discussed in relation to theories of functional dissociation within the hippocampus.

Animals↗
PubMed1975

Locomotor, avoidance,and maze behavior in rats with selective disruption of hippocampal output.

Behavioral correlates of selective disruption of hippocampal output were investigated in a series of five experiments. In two experiments an attempt was made through behavioral investigation to determine whether the CA1 neurons project to the fimbria or to the subiculum. The results supported recent views that the subiculum is the recipient of CA1 axons. Disruption of the CA1 output in the dorsal hippocampus of rats produced increased open-field activity, whereas passive avoidance and spontaneous alternation behaviors remained unchanged. No differentiation was obtained between CA1 damage and neocortical lesions in maze learning. Blocking of the fimbrial CA3 output from the dorsal hippocampus improved passive avoidance performance and impaired active avoidance performance, whereas open-field and spontaneous alternation behaviors were unaffected. Interruption of the CA3 output from the ventral hippocampus improved active avoidance performance and reduced spontaneous alternation behavior. Open-field behavior and passive avoidance performance remained unchanged. Total fimbrial sections increased open-field activity, improved passive and active avoidance, and reduced spontaneous alternation. The results are discussed in terms of functional differentiation between the CA1 and CA3 of the dorsal hippocampus and in terms of functional differences in the fimbrial CA3 output from the dorsal and ventral hippocampus.

Animals↗
PubMed2001

The concepts of 'sameness' and 'difference' in an insect.

Insects process and learn information flexibly to adapt to their environment. The honeybee Apis mellifera constitutes a traditional model for studying learning and memory at behavioural, cellular and molecular levels. Earlier studies focused on elementary associative and non-associative forms of learning determined by either olfactory conditioning of the proboscis extension reflex or the learning of visual stimuli in an operant context. However, research has indicated that bees are capable of cognitive performances that were thought to occur only in some vertebrate species. For example, honeybees can interpolate visual information, exhibit associative recall, categorize visual information and learn contextual information. Here we show that honeybees can form 'sameness' and 'difference' concepts. They learn to solve 'delayed matching-to-sample' tasks, in which they are required to respond to a matching stimulus, and 'delayed non-matching-to-sample' tasks, in which they are required to respond to a different stimulus; they can also transfer the learned rules to new stimuli of the same or a different sensory modality. Thus, not only can bees learn specific objects and their physical parameters, but they can also master abstract inter-relationships, such as sameness and difference.

Animals↗
PubMed2005

Pathogenic bacteria induce aversive olfactory learning in Caenorhabditis elegans.

Food can be hazardous, either through toxicity or through bacterial infections that follow the ingestion of a tainted food source. Because learning about food quality enhances survival, one of the most robust forms of olfactory learning is conditioned avoidance of tastes associated with visceral malaise. The nematode Caenorhabditis elegans feeds on bacteria but is susceptible to infection by pathogenic bacteria in its natural environment. Here we show that C. elegans modifies its olfactory preferences after exposure to pathogenic bacteria, avoiding odours from the pathogen and increasing its attraction to odours from familiar nonpathogenic bacteria. Particular bacteria elicit specific changes in olfactory preferences that are suggestive of associative learning. Exposure to pathogenic bacteria increases serotonin in ADF chemosensory neurons by transcriptional and post-transcriptional mechanisms. Serotonin functions through MOD-1, a serotonin-gated chloride channel expressed in sensory interneurons, to promote aversive learning. An increase in serotonin may represent the negative reinforcing stimulus in pathogenic infection.

Animals↗
PubMed1997

Functional screening of 2 Mb of human chromosome 21q22.2 in transgenic mice implicates minibrain in learning defects associated with Down syndrome.

Using Down syndrome as a model for complex trait analysis, we sought to identify loci from chromosome 21q22.2 which, when present in an extra dose, contribute to learning abnormalities. We generated low-copy-number transgenic mice, containing four different yeast artificial chromosomes (YACs) that together cover approximately 2 megabases (Mb) of contiguous DNA from 21q22.2. We subjected independent lines derived from each of these YAC transgenes to a series of behavioural and learning assays. Two of the four YACs caused defects in learning and memory in the transgenic animals, while the other two YACs had no effect. The most severe defects were caused by a 570-kb YAC; the interval responsible for these defects was narrowed to a 180-kb critical region as a consequence of YAC fragmentation. This region contains the human homologue of a Drosophila gene, minibrain, and strongly implicates it in learning defects associated with Down syndrome.

Animals↗
PubMed2001

Executive function in traumatic brain injury and obsessive-compulsive disorder: an overlap?

Thirteen individuals with traumatic brain injury, 13 individuals with obsessive-compulsive disorder (OCD) and 10 normal controls were compared on neuropsychological measures of executive function. Individuals with a traumatic brain injury performed significantly poorer than the other two groups on a test measuring visuo-spatial strategy. Although the traumatic brain injury group made more errors on a test of maze learning and the OCD group less than the control group, this did not reach statistical significance. No support for an overlap in executive dysfunction in traumatic brain injury and OCD was found. It may be that the 'error prevention system' in the brain was influenced in a contrasting way by executive dysfunction in these disorders. This difference may reveal itself clinically in impulsivity/perseveration and slowness, respectively. Further studies were needed to test this hypothesis.

Adolescent↗
PubMed1969

Studies on memory: evidence for a widespread memory trace in the neocortex after the suppression of recent memory by puromycin.

Intracerebral injections of puromycin in mice have provided evidence that the hippocampal area of the brain contains the memory trace of recently learned maze behavior and that, with time, the trace is also found in the neocortex. The present experiments were planned to determine whether this enlargement of locus would develop after the blockage of recent memory in the hippocampus by puromycin, i.e., whether the neocortical locus is established if hippocampal memory is suppressed. The experiments depend upon our earlier finding that the memory blockage caused by puromycin can be removed by small intracerebral injections of saline. Control experiments showed that saline injected into the frontal cortex three days after training did not release the puromycin blockage of memory in the hippocampal area. Injections of saline into the frontal cortex 6 and 11 days after training did, however, release memory in mice whose recent memory had been suppressed by puromycin; we interpret this result to mean that the memory trace appears widely in the cortex despite the suppression of recent memory in the hippocampus. The theoretical implications of this finding are briefly discussed.

Animals↗
PubMed1970

Adrenalectomy and the suppression of memory by puromycin.

It has previously been shown that expression of memory of maze-learning in mice is blocked by puromycin injected intracerebrally one or more days after the training experience. Bilateral adrenalectomy before training has now been found to protect memory against the effects of puromycin. This protection is absent when adrenalectomy follows training. In view of control experiments, we conclude that adrenalectomy before training modifies factors necessary for the expression of memory and that this alteration makes puromycin ineffective in blocking memory.

Adrenal Glands↗
PubMed1970

Some evidence for the involvement of adrenergic sites in the memory trace.

Puromycin was injected bitemporally in mice one day after training in a Y-maze. Eight days later various psychotropic drugs were injected intraperitoneally or subcutaneously at maximum tolerable doses. Ten days after the drug injection the mice were tested for their memory of the maze-learning. Memory was lost in control animals injected with saline but restored in most of the animals injected with imipramine, tranylcypromine, or D-amphetamine. Some indication of restoration was observed after injection of reserpine or L-dopa. These results suggest that the blockage caused by puromycin is due to adsorption of peptidyl-puromycin to adrenergic sites and that these sites may be involved in the memory trace.

Animals↗
PubMed1971

Pituitary peptides and the suppression of memory by puromycin.

It has previously been shown that the expression of memory of maze-learning in mice is blocked by intracerebrally-injected puromycin one or more days after the training experience, and that bilateral adrenalectomy before training protects memory against this effect of puromycin. Purified cortrophin gel, injected subcutaneously up to 3 days before training, has now been found to give results like those obtained with adrenalectomy and, additionally, to provide a high degree of protection when injected up to 16 hr after training. Several possible explanations for these effects have been considered and found to be inadequate.

Adrenalectomy↗