PubMed Health⌕ Search

Biomedical subjects

G M Rose

Publications and source records attributed to G M Rose.

At least 55 records · Page 3Linked to original sources
PubMed1995

Enduring effects of chronic corticosterone treatment on spatial learning, synaptic plasticity, and hippocampal neuropathology in young and mid-aged rats.

Prolonged treatment with stress levels of corticosterone has been reported to produce changes in the hippocampus. In the experiments reported here, we examined for functional and morphological consequences of this treatment. First, young adult or mid-aged male Long-Evans rats were treated for either 1 or 3 months with corticosterone, at a dose sufficient to mimic the elevated hormone levels observed following exposure to mild stress. Two weeks following the termination of treatment, the animals were tested in the Morris water maze to assess spatial learning. No behavioral deficits were observed after 1 month of treatment. A 3 month treatment period also had no effect in young rats, but produced a learning impairment in the mid-aged rats. We then examined whether the effect of elevated corticosterone in mid-aged animals could be produced by a physiological stressor. Mid-aged rats were maintained for 6 months under conditions of low or high social stress. Six months of exposure to high social stress produced significant spatial learning impairments in the Morris water maze. These effects were absent in high social stress animals that had been previously adrenalectomized (with low-level corticosterone replacement), suggesting that elevated glucocorticoid levels mediate the effects of stress on spatial memory in older animals. In a final experiment, mid-aged rats were treated with corticosterone at levels that mimicked those naturally occurring at the diurnal peak (medium-B: 12-17 micrograms/dl) or in response to stress (high-B: 25-32 micrograms/dl). Only rats exposed to high levels of corticosterone demonstrated impaired performance in the Morris water maze.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1994

Psychological stress repeatedly blocks hippocampal primed burst potentiation in behaving rats.

Primed burst (PB) potentiation is a long-term increase in CA1 population spike amplitude produced by brief physiologically patterned electrical stimulation of the hippocampal commissure. Exposure of rats to a novel environment resulted in a blockade of short-term (Post-tetanic potentiation, PTP) and long-term (PB potentiation) plasticity in all cases (n = 6). When the animals had extensive exposure to the environment (14 consecutive days), PTP and PB potentiation occurred. With placement of the rats in a second novel environment, once again, neither PTP nor PB potentiation was observed. Placement of rats in each of the two novel environments produced a significant increase in serum corticosterone levels, while placement in the familiar environment produced no increase in response. These findings support the hypothesis that hippocampal plasticity is repeatedly susceptible to modulation by the stress of forced exposure to a novel environment.

Animals↗
PubMed1994

The use of ephemera with particular reference to blood and organ donation: a review of sources.

Emphasis has been placed upon a study of the use made of ephemera such as leaflets, pamphlets and booklets by non-professional staff working in British statutory organizations such as health authorities, community health councils and family health services authorities as well as voluntary organizations such as charities, citizens' advice bureaux and patient participation groups. Publicity methods and the use made of ephemeral materials by those statutory and voluntary organizations involved in recruiting and retaining blood and organ donors is highlighted. Research findings confirm that patients, carers and others, wish to receive comprehendable and appropriate health information. Ephemera provided in support of this need are not comprehensive in subject coverage and lack any standardization of format. In particular, great care needs to be taken with the design of leaflets, pamphlets and booklets. Ephemeral materials are difficult to locate and obtain, and no bibliographical centre exists to coordinate and support existing activity by identifying, acquiring, storing, advertising and distributing such health care material. Marketing and publicity skills, and much time and effort are required to rectify this deficiency, and thus to satisfy the needs of consumers.

Blood Donors↗
PubMed1993

Hippocampal plasticity induced by primed burst, but not long-term potentiation, stimulation is impaired in area CA1 of aged Fischer 344 rats.

The effect of two types of electrical stimulation designed to induce long-lasting plasticity of the Schaffer/commissural inputs to CA1 pyramidal neurons was investigated using in vitro hippocampal slices made from young (3-6 month) and old (24-27 month) Fischer 344 rats. The first stimulation paradigm, primed burst (PB) stimulation, consisted of a total of five physiologically patterned stimuli: a single priming pulse followed 170 ms later by a burst of four pulses at 200 Hz. The second stimulation paradigm, long-term potentiation (LTP) stimulation, consisted of a 200 Hz/1 second train (a total of 200 stimuli). Primed burst and LTP stimulation were equally effective at inducing a lasting increase in the population spike recorded from slices made from young rats. However, the enhancement of population spike amplitude produced by PB, but not LTP, stimulation was significantly less in slices made from old rats. These results suggest that the capacity of the hippocampus to demonstrate long-lasting synaptic plasticity is not altered with age, but that engaging plasticity-inducing mechanisms becomes more difficult. Furthermore, these data suggest that physiologically patterned paradigms for inducing long-lasting synaptic plasticity may more accurately assess the functional status of hippocampal memory encoding mechanisms than does conventional LTP stimulation.

Action Potentials↗
PubMed1992

Inverted-U relationship between the level of peripheral corticosterone and the magnitude of hippocampal primed burst potentiation.

Studies have shown that peripheral levels of corticosterone correlate with the magnitudes of two well-described physiological models of memory, long-term potentiation (LTP) and primed burst (PB) potentiation. In the present experiments, the authors investigated the effects of experimenter-controlled manipulations of the levels of corticosterone on the magnitude of hippocampal PB potentiation in urethane-anesthetized rats. Primed burst potentiation is a long-lasting (at least 30 minutes) increase in the amplitude of the CA1 population spike and EPSP slope in response to physiologically patterned stimulation of the hippocampal commissure. The levels of serum corticosterone were controlled by implanting corticosterone pellets in adrenalectomized rats (ADX/PELLET). In the first experiment, a significant negative linear correlation between elevated (stress) levels of serum corticosterone (greater than 20 micrograms/dL) and the magnitude of PB potentiation in ADX/PELLET subjects (r = 0.60, P < .05) was found. In the second experiment, the shape of the corticosterone-PB potentiation function was different at low and intermediate levels of corticosterone than it was at high levels of corticosterone: There was a positive correlation at low levels (0-10 micrograms/dL), a peak response at intermediate levels (11-20 micrograms/dL), and a negative correlation at high levels (21-93 micrograms/dL) of corticosterone. Thus, the overall relationship between corticosterone and PB potentiation is an inverted-U function. These findings provide strong support for the hypothesis that corticosterone exerts a concentration-dependent biphasic influence on the expression of hippocampal plasticity.

Adrenalectomy↗
PubMed1992

Chronic sodium azide treatment impairs learning of the Morris water maze task.

A reduction in the activity of cytochrome oxidase, a respiratory chain enzyme, has been recently identified in mitochondria from blood platelets and postmortem brain tissue from Alzheimer's disease (AD) patients. We have developed an animal model of this deficit in rats by chronic subcutaneous infusion of sodium azide, a selective inhibitor of cytochrome oxidase, delivered via Alzet 2ML4 osmotic minipumps. In previous work, azide-treated rats were impaired in an appetitively motivated spatial learning task, the radial arm maze. In the present investigation, we tested male Sprague-Dawley rats (350-400 g), which were tonically infused with azide or saline, on an aversively motivated spatial task, the Morris water maze. Azide-treated rats were impaired on both acquisition and retention of this task, without showing evidence of a motor impairment. Thus, the present results are consistent with previous findings showing that chronic azide treatment produces a learning and memory deficit. These findings strengthen the hypothesis that azide treatment in rats produces a useful animal model of some aspects of AD.

Animals↗
PubMed1991

Electrically-evoked release of norepinephrine in the rat cerebellum: an in vivo electrochemical and electrophysiological study.

Norepinephrine (NE) release from the locus coeruleus (LC) afferents to the cerebellar cortex of urethane anesthetized rats was achieved by electrical stimulation of the locus coeruleus or by local administration of potassium into the cerebellum. Both methods evoked an overflow of NE-like electroactive species. Electrically-evoked and potassium-induced overflow of NE-like responses were found to be reversible and reproducible. Releases were not observed in cerebellar white matter, an area which is relatively devoid of monoamine containing terminals. Systemic administration of desipramine, a potent and selective norepinephrine re-uptake blocker, significantly augmented the electrically-evoked electrochemical responses. Measurements of evoked release taken using high-speed chronoamperometry support the idea that a predominant contributor to electrically-induced signals was NE. Electrophysiological recordings of single Purkinje cells were performed with the same Nafion-coated single carbon fiber electrodes used for electrochemical recordings. Electrical stimulation of the LC was seen to depress Purkinje cell firing rates; an increase in electroactive species was detected at the same site that paralleled the time course of the electrophysiological response. These studies provide further direct evidence that the LC norepinephrine-containing cells have a direct inhibitory effect on Purkinje cells in the cerebellum, and that both pre- and postsynaptic events can be measured with the same recording sensor.

Animals↗
PubMed1991

Dopaminergic and noradrenergic modulation of amphetamine-induced changes in auditory gating.

Dopaminergic and noradrenergic mediation of central sensory gating were assessed in Sprague-Dawley rats using a condition-test paradigm in which auditory evoked potentials were recorded. In this paradigm, unmedicated rats 'gate', i.e. suppress the response to the second of a pair of clicks delivered at a 0.5 s interval. Amphetamine-treated rats fail to gate; in this respect, they resemble schizophrenic humans. Previous studies had indicated noradrenergic involvement in the mediation of auditory gating in rats. In this study, we used selective antagonists to assess the contribution of alpha- and beta-adrenergic receptors, and dopamine D1- and D2-receptors, to amphetamine-induced alterations in gating. Both the alpha-antagonist, phentolamine, and the beta-antagonist, timolol, normalized gating by potentiating amphetamine-induced decreases in the amplitude of the test response. SCH 23390, a D1-receptor antagonist, also normalized gating, but by elevating the amphetamine-reduced amplitude of the conditioning response. Sulpiride did not significantly alter amphetamine-induced changes in gating. Thus, both noradrenergic alpha- and beta-receptors and dopamine D1-receptors appear to modulate gating. However, their dissimilar means of normalizing gating suggests that noradrenergic and dopaminergic drugs act via different mechanisms and possibly different neuroanatomical loci.

Adrenergic alpha-Antagonists↗
PubMed1990

Modulation of hippocampal primed burst potentiation by anesthesia.

This study demonstrates that the anesthetics urethane and pentobarbital differentially affect a low threshold form of long-lasting synaptic plasticity, termed primed burst (PB) potentiation, in the CA1 area of rat hippocampus. PB potentiation was generated by the delivery of a 5-pulse patterned stimulus train, consisting of one priming pulse followed 170 ms later by a burst of 4 pulses at 200 Hz. PB potentiation could not be reliably generated in urethane-anesthetized rats unless stimulus currents were raised to 150% of baseline levels during the stimulus train. In pentobarbital-anesthetized rats, PB potentiation could always be evoked at baseline stimulus intensities. Differences between the anesthetics which could contribute to their varying effects upon PB potentiation are discussed.

Action Potentials↗
PubMed1990

Auditory sensory gating in hippocampal neurons: a model system in the rat.

Diminished evoked response to repeated auditory stimuli, an example of sensory gating normally present in human subjects, is often absent in schizophrenics. To examine the mechanism of the normal response and to delineate possible sites of its abnormality in psychosis, it would be desirable to reproduce the phenomenon in laboratory animals. In this study, we show that the pattern of diminished response to the second of paired auditory stimuli is found in activity recorded from the CA3 region of the hippocampus of anesthetized rats. The evoked potential recorded from this area is predominantly an N40 wave, at identical latency to the prominent negative wave recorded from the skull surface of unanesthetized rats. Similar responses were not found in other areas, including the auditory neocortex and the medial geniculate nucleus. Amphetamine, which diminished sensory gating in both animals and humans, diminished the gating of the evoked potential recorded in the hippocampus. The effect of amphetamine was reversed by haloperidol. The rat hippocampus may therefore contain neurons that can be used to study the neurobiology of sensory gating.

Action Potentials↗
PubMed1989

The effects of cholecystokinin (CCK-8) on dopamine-containing nerve terminals in the caudate nucleus and nucleus accumbens of the anesthetized rat: an in vivo electrochemical study.

The action of cholecystokinin (CCK) on presynaptic function of dopaminergic nerve terminals has been the subject of much debate in the literature. In efforts to resolve some of the reported ambiguities, high speed in vivo electrochemical recordings were carried out in the caudate nucleus and nucleus accumbens of the urethane anesthetized rat, to determine effects of locally applied sulfated (CCK-8S) and unsulfated (CCK-8US) CCK octapeptide. Locally-applied CCK-8S and CCK-8US caused no increase in the baseline electrochemical signals recorded from either brain region. However, locally applied CCK-8S potentiated the potassium-evoked overflow of dopamine (DA) into the extracellular space in both the caudate and nucleus accumbens. In contrast, pressure ejection of CCK-8US produced no significant effects on the potassium-evoked overflow of DA in either structure. These data support a facilitatory effect of CCK-8S on potassium-evoked overflow from DA-containing nerve terminals in the urethane anesthetized rat that is likely mediated through a peripheral type CCK receptor.

Anesthesia↗
PubMed1989

Adrenalectomy reduces the threshold for hippocampal primed burst potentiation in the anesthetized rat.

Previously we demonstrated that the threshold for inducing hippocampal long-term potentiation (LTP) was reduced when the pattern of electrical stimulation mimicked physiological activity. This form of LTP, termed primed burst (PB) potentiation, is blocked by stress. In the present study, we tested the possibility that adrenal hormones contribute to the stress-related inhibition of PB potentiation. Our primary finding is that the amount of stimulation current necessary to induce PB potentiation was lower in adrenalectomized rats than in controls. This finding indicates that adrenal hormones exert an inhibitory influence on the induction of physiological plasticity in the hippocampus.

Action Potentials↗
PubMed1989

Differential effect of norepinephrine upon granule cells and interneurons in the dentate gyrus.

The effect of locally applied norepinephrine upon dentate granule cells and neighboring interneurons was examined in urethane-anesthetized rats. Norepinephrine inhibited the spontaneous firing of physiologically identified granule cells, but excited interneurons. These results demonstrate that two coexisting hippocampal cell types, which have many physiological properties and behavioral correlates in common, may be differentiated using a pharmacological criterion.

Action Potentials↗
PubMed1989

Unilateral hydrothorax in small children on chronic continuous peritoneal dialysis.

Three small children whose weights were under 15 kg and who were on continuous ambulatory peritoneal dialysis or continuous cycling peritoneal dialysis developed massive unilateral hydrothorax. The occurrence of hydrothorax was late, 3-22 months after the initiation of dialysis. Two of the three fluid collections were left-sided. Each episode was preceded by retention of dialysate. After drainage of the hydrothorax a modified peritoneal dialysis regimen was successful in sustaining patients for a few weeks until further therapy for end-stage renal disease could be pursued.

Female↗
PubMed1989

Differential effects of methionine5-enkephalin on hippocampal pyramidal cells and interneurons.

While the excitatory action of opioids and opiate drugs upon pyramidal neurons in the hippocampus is well known, the mechanism by which this excitation is achieved is still argued. A popular hypothesis is that opiates reduce the activity of inhibitory interneurons, thereby indirectly exciting the pyramidal cells. To validate this idea, it is necessary to show that opiates selectively affect the population of interneurons. The present study therefore examined the effects of met-enkephalin upon pyramidal cells and interneurons located in area CA1. Extracellular action potentials were recorded using multibarrelled micropipettes. Drugs were applied locally by either pressure micro-ejection or microiontophoresis. Met-enkephalin (10(-5) M) elevated the spontaneous discharge of pyramidal cells, while interneurons were inhibited. The responses of both types of cell were blocked by the opiate antagonist naloxone. When the synaptic connections between the pyramidal cells and interneurons were disrupted by local application of magnesium or bicuculline, met-enkephalin had no effect on the pyramidal cells. However, neither magnesium nor bicuculline altered the enkephalin-induced inhibition of theta neurons. These results support the hypothesis that opioids of the enkephalin subclass, excite pyramidal cells in the hippocampus through a disinhibition mechanism.

Action Potentials↗
PubMed1988

The effects of delta 9-tetrahydrocannabinol on potassium-evoked release of dopamine in the rat caudate nucleus: an in vivo electrochemical and in vivo microdialysis study.

The effect of systemically administered delta 9-tetrahydrocannabinol (THC), the psychoactive ingredient in marijuana, on the potassium-evoked release of dopamine (DA) was examined in the neostriatum of the chloral hydrate anesthetized rat. Both in vivo electrochemical and in vivo microdialysis techniques were employed. A low dose of THC (0.5 mg/kg, i.p.) increased the time course of potassium-evoked in vivo electrochemical signals corresponding to released extracellular DA. In vivo microdialysis showed an increase in potassium-evoked DA release following 0.5 and 2.0 mg/kg doses of THC. Potassium-evoked electrochemical signals corresponding to released extracellular DA were augmented in time course following i.p. administration (5.0 mg/kg) of nomifensine, a recognized and potent catecholaminergic reuptake blocker. In addition, in vivo brain microdialysis studies of nomifensine (5.0 mg/kg i.p.) on neostriatal potassium-evoked DA release showed that DA levels were augmented in magnitude over the time course of the microdialysis. Taken together, these studies indicate that THC has a potent presynaptic augmenting effect on at least the neostriatal portions of the mesotelencephalic DA system in the rat, although the possibility that this effect could be mediated transsynaptically cannot be ruled out. Given the previous extensive evidence for an involvement of portions of the mesotelencephalic DA system in mediating the reinforcing and euphorigenic properties of many classes of abused drugs, and in mediating direct electrical brain stimulation reward, we suggest that the presently demonstrated effects of THC on forebrain dopamine function may be related to marijuana's euphorigenic properties and, thus, to its abuse potential.

Caudate Nucleus↗