Trematode parasites as indicators of an animal component in the diet of the Water Vole Arvicola amphibius.

The intestinal trematode fauna of the Water Vole Arvicola amphibius, (previously A. terrestris), was investigated to determine whether it might provide evidence of an animal component in the diet of this aquatic herbivorous small mammal. Interrogation of the electronic Host-Parasite Database of the Natural History Museum London revealed the presence of fourteen species of intestinal trematode in water voles, infection with each of which would require the ingestion of tissue from an animal intermediate host. The results obtained using these parasite indicators provide convincing evidence of animal components in the diet of A. amphibius and support anecdotal reports of water voles feeding on animal material in the field.

Trophodynamics of Protomyctophum (Myctophidae) in the Scotia Sea (Southern Ocean).

This study investigated spatial and temporal patterns in distribution, population structure and diet of Bolin's lanternfish Protomyctophum bolini, Tenison's lanternfish Protomyctophum tenisoni and gaptooth lanternfish Protomyctophum choriodon in the Scotia Sea using data collected by midwater trawl during spring, summer and autumn. Protomyctophum bolini was the most abundant species of the genus encountered throughout the Scotia Sea with the greatest concentrations occurring around the Antarctic Polar Front (APF). This species had a life cycle of 2+ years, but spatial differences in population structure were apparent as the I-group was absent from all regions south of the APF, suggesting that the species does not recruit in the Scotia Sea. Protomyctophum tenisoni occurred mostly in waters characteristic of the APF and was absent from the southern Scotia Sea. It had a limited size range, but there was clear size-related sexual dimorphism with males significantly larger than females. The species had a life cycle of c. 2 years, but the I-group (c. 1 year old, 1 November to 31 October the next year) occurred only in regions close to the APF suggesting that recruitment is restricted to these waters. A seasonal southward migration for P. choriodon is likely as the species occurred mostly to the south-west of South Georgia in summer, but extended to the sea-ice sectors in autumn. Protomyctophum choriodon had a life cycle of 4+ years in the Scotia Sea and the population was dominated by age classes >3 years old. Larval stages were absent during the surveys for all species. Diurnal variations in vertical distribution were apparent for all three species. Interspecific variations in diet were evident, but all species were primarily copepod feeders, with Metridia spp., Rhincalanus gigas and Calanus simillimus generally dominating their diet. Small euphausiids, principally Thysanoessa spp., were also an important component of their diets, particularly for P. choriodon which had the largest body size. The spatial and temporal variations in diet for both P. bolini and P. tenisoni were broadly consistent with underlying abundance patterns within the mesozooplankton community.

Long-term changes in deep-water fish populations in the northeast Atlantic: a deeper reaching effect of fisheries?

A severe scarcity of life history and population data for deep-water fishes is a major impediment to successful fisheries management. Long-term data for non-target species and those living deeper than the fishing grounds are particularly rare. We analysed a unique dataset of scientific trawls made from 1977 to 1989 and from 1997 to 2002, at depths from 800 to 4800 m. Over this time, overall fish abundance fell significantly at all depths from 800 to 2500 m, considerably deeper than the maximum depth of commercial fishing (approx. 1600 m). Changes in abundance were significantly larger in species whose ranges fell at least partly within fished depths and did not appear to be consistent with any natural factors such as changes in fluxes from the surface or the abundance of potential prey. If the observed decreases in abundance are due to fishing, then its effects now extend into the lower bathyal zone, resulting in declines in areas that have been previously thought to be unaffected. A possible mechanism is impacts on the shallow parts of the ranges of fish species, resulting in declines in abundance in the lower parts of their ranges. This unexpected phenomenon has important consequences for fisheries and marine reserve management, as this would indicate that the impacts of fisheries can be transmitted into deep offshore areas that are neither routinely monitored nor considered as part of the managed fishery areas.

First-principles theory for the H + H2O, D2O reactions.

A full quantum dynamical study of the reactions of a hydrogen atom with water, on an accurate ab initio potential energy surface, is reported. The theoretical results are compared with available experimental data for the exchange and abstraction reactions in H + D2O and H + H2O. Clear agreement between theory and experiment is revealed for available thermal rate coefficients and the effects of vibrational excitation of the reactants. The excellent agreement between experiment and theory on integral cross sections for the exchange reaction is unprecedented beyond atom-diatom reactions. However, the experimental cross sections for abstraction are larger than the theoretical values by more than a factor of 10. Further experiments are required to resolve this.

Dopamine-related tetrahydroisoquinolines: significant urinary excretion by alcoholics after alcohol consumption.

Concentrations of dopamine-related tetrahydroisoquinolines (salsolinol and O-methylated salsolinol) were significantly higher in the daily urine samples of alcoholic subjects admitted for alcohol detoxification than in the daily urine samples of nonalcoholic control subjects. Salsolinol concentrations in alcoholic subjects appeared to drop to trace (control) values 2 to 3 days after admission, following the disappearance of ethanol and its reactive metabolite acetaldehyde from the blood. These results indicate that physiologically active tetrahydroisoquinolines increase in humans during long-term alcohol consumption, presumably because of acetaldehyde's direct condensation with catecholamines. The presence of these or similar condensation products in the urine could be useful as clinical indicators of prior blood acetaldehyde concentrations in chronic alcoholics.

Jugular venous neurone specific enolase (NSE) increases following carotid endarterectomy under general, but not local, anaesthesia.

INTRODUCTION: Previous studies indicate that local (LA) rather than general anaesthesia (GA) for carotid endarterectomy (CEA) is associated with reflex hypertension and preservation of cerebral cytochrome oxidase after carotid clamping. The hypothesis that LA offers protection against ischaemic cerebral injury has been investigated by measuring ipsilateral jugular venous neurone specific enolase (NSE: neuronal glycolytic enzyme) and S-100B (glial cell protein) during and after CEA. METHODS: 27 patients with symptomatic carotid artery disease (70-99% stenosis) underwent CEA, 14 under LA and 13 under GA. Jugular venous blood samples were assayed for NSE and S-100B before carotid clamping and at 5min before and 5min, 2, 4, 6, 8, 12 and 24h after clamp release. RESULTS: No neurological complications occurred. S-100B levels were low and did not increase from baseline in either group. Pre-clamp NSE levels were similar in both groups (LA: 17.6 (15.2-20.7)microg/l, GA: 21.5 (11.3-26.2)microg/l; p=0.37) but increased significantly 2h after clamp release in GA patients (LA: 25.5 (16.6-27.8)microg/l, GA: 48.2 (31.4-61.3)microg/l, p=0.05) with a significant rise from baseline in GA patients (p=0.04). CONCLUSIONS: CEA performed under GA is associated with greater rises in jugular venous NSE, and hence cerebral injury, than CEA performed under LA.

Effects of different feed additives alone or in combination on broiler performance, gut microflora and ileal histology.

1. The objectives of this experiment were to investigate the effects of different xylanases, alone or in combination with different organic acid and oligosaccharide sources, on bird performance, gut microflora and ileal histology. 2. Birds were given a diet based on a commercial formulation, which was split into 8 batches. Batch 1 contained the antibiotic growth promoter Avilamycin and acted as the positive control. To batch 2 the enzyme Allzyme PT was added and to batch 3 Allzyme PT was added with the organic acid and oligosaccharide mixture Avimos. To batch 4, Allzyme PT was added with the oligosaccharide mixture Biomos. To batch 5, yeast extract 2012 was added with the organic acid mixture Gustor and the enzyme xylanase XP20. To batch 6, yeast extract 2012 and feed acidifier Gustor were added as before, with the enzyme Avizyme 1300. Batches 7 and 8 both acted as negative experimental controls, with no added growth promoters. 3. A total of 64 birds were housed in individual wire cages in each of three consecutive experimental replicates (24 birds/treatment). Birds were fed ad libitum from 7 to 28 d and a 7-d excreta collection was carried out to determine apparent metabolisable energy (AME) content. 4. At 28 d, the birds were killed and viscosity of jejunal digesta supernatant and gizzard weight were determined. Samples were taken from the crop, ileum and caecum and analysed for viable presumptive lactic acid bacteria and coliforms. The overall microbial flora was determined using denaturing gradient gel electrophoresis of 16S ribosomal DNA followed by DNA sequence analysis in order to assign amplicons to a bacterial species. Ileal sections were also collected for histological analysis. 5. Total live weight gain (12%) and gain:feed (9%) were significantly improved for all diets containing additives, compared to the negative control diets. All diets containing xylanases gave significantly lower in vivo viscosity values than the positive and negative controls. Diet treatment significantly affected viable coliform numbers in the ileum and also viable lactobacilli in the ileum and caecum. A substantial proportion of the bacteria present in the GI tract (40%) belong to unknown species. No effects of diet treatment on histological measurements were observed in this study. 6. All the additive combinations studied were at least as effective as the antibiotic growth promoter and the results for Allzyme PT suggest that xylanase alone is as effective as any of the combinations studied.

Chyle leak following an axillary sentinel lymph node biopsy for breast cancer in a patient with superior vena caval thrombosis - a case report and review of the literature.

Chyle leak is a very rare complication following an axillary lymph node dissection. We report a case of chyle leak following sentinel lymph node biopsy in a patient with breast cancer with superior vena caval thrombosis. To our knowledge, this is the first case report of chyle leakage following axillary sentinel lymph node biopsy. We describe the aetiology, prevention and treatment strategy that can be adopted in these patients.

Combinatorial Preconditioning of Rat Brain Cultures with Subprotective Ethanol and Resveratrol Concentrations Promotes Synergistic Neuroprotection.

Preconditioning brain cultures with moderate concentrations of ethanol (EtOH) or trans-resveratrol (RES), key red wine constituents, can prevent amyloid-ß (Aß) neurotoxicity. Past studies have indicated that moderate EtOH activates synaptic N-methyl-D-aspartate receptors (NMDAR) that, in part, signal via protein kinase C (PKC) to increase protective antioxidant proteins such as peroxiredoxin-2 (Prx2). RES preconditioning also is reported to involve NMDAR and PKC. However, although moderate, the EtOH and RES concentrations used have been noticeably above circulating levels from two glasses of wine, a daily intake linked to reduced risk of cognitive decline among older social drinkers. Given their mechanistic parallels, we speculated that subprotective EtOH and RES concentrations in a combinatorial preconditioning paradigm might elicit synergistic neuroprotection. To examine this notion, rat cerebellar cultures were pretreated with 10 mM EtOH (circulating concentration after ~ 2 drinks), 5 µM RES, EtOH + RES combinatorially, or media alone (controls). After 3 days, media were removed, and fresh media aliquots containing Aß25-35 (25 µM) were added. Assessing apoptosis 24 h later with Hoescht 33342, neurodegeneration did not differ from controls in cultures separately preconditioned with 10 mM EtOH or 5 µM RES. However, apoptosis was prevented in combinatorially preconditioned cultures. Also, immunoblotting revealed elevated Prx2 levels due to combinatorial pretreatment that correlated with subsequent neuroprotection, whereas Prx2 was unchanged in separately pretreated cultures. Although the protective mechanisms require clarification, synergistically upregulated NMDAR-PKC-Prx2 (and other antioxidant proteins) is a reasonable component. These findings imply that EtOH + RES antioxidant synergy could be involved in neurobenefits attributed to low-moderate wine consumption.

Tamoxifen effect on L-DOPA induced response complications in parkinsonian rats and primates.

The contribution of striatal protein kinase C (PKC) isoform changes in levodopa (L-DOPA) induced motor response complications in parkinsonian rats was investigated and the ability of tamoxifen, an antiestrogen with a partial PKC antagonist property, to prevent these response alterations in 6-hydroxydopamine (6-OHDA) lesioned rats as well as in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treated cynomologous monkeys was studied. Following treatment of adult male rats with L-DOPA twice daily for 3 weeks, protein levels of left (lesioned) and right (intact) striatal PKC isoforms were measured. Western blot analysis showed increased protein expression of both the novel PKC epsilon isoform and the atypical PKC lambda isoform ipsilateral to the lesion (174+/-17% for epsilon, 140+/-9% for lambda, of intact striatum in 6-OHDA lesioned plus chronic L-DOPA treated animals) in acute L-DOPA treated rats. No enhancement was observed in PKC immunoreactivity for other isoforms. Tamoxifen (5.0 mg/kg p.o.) significantly attenuated the L-DOPA induced augmentation of protein expression of PKC epsilon and PKC lambda, but had no effect on immunoreactivity for other PKC isoforms. In chronic L-DOPA treated parkinsonian rats, tamoxifen prevented (5.0 mg/kg p.o.) as well as ameliorated (5.0 mg/kg p.o.) the characteristic shortening in duration of motor response to L-DOPA challenge. In MPTP lesioned primates, similar to the ameliorative effect seen in rats, tamoxifen (1 and 3 mg/kg p.o) reduced the appearance of L-DOPA induced dyskinesia by 61% and 55% respectively (p<0.05). These results suggest that changes in specific striatal PKC isoforms contribute to the pathogenesis of L-DOPA induced motor complications and further that drugs able to selectively inhibit these signaling kinases might provide adjunctive benefit in the treatment of Parkinson's disease.

Contrasting effects of catecholic and O-methylated tetrahydroisoquinolines on hydroxyl radical production.

Tetrahydroisoquinolines (TIQs) are intraneuronal, catecholamine-derived alkaloids that have been implicated in the etiology of Parkinson's disease and in alcohol related disorders. The in vitro production of the cytotoxic hydroxyl radical (*OH) was recorded during the autoxidation of salsolinol (SAL) and salsolinol-1-carboxylic acid (SAL-1C), but not when these two catecholic TIQs were oxidized by tyrosinase. Significantly higher levels of the radical were produced when these catecholic TIQs were incubated with *OH generating complexes, or with chelated iron. In contrast, mono-O-methylated TIQs such as salsoline (SLN) and salsoline-1-carboxylic acid (SLN-1C) did not generate *OH during autoxidation or when incubated with chelated iron or tyrosinase. Radical production by *OH-generating complexes was reduced in the presence of O-methylated TIQs. The neurotoxicity of TIQs may result from their propensity to autoxidize and generate reactive quinoids and ensuing oxygen radicals. The functional significance of the replacement of a hydroxyl group attached to C-7 of SAL or SAL-1C with a methoxyl group remains to be determined. This single structural modification may prevent mono-O-methylated TIQs from participating in catalytic redox cycling reactions that would otherwise augment *OH production. If true, then O-methylation and other cellular mechanisms that circumvent the autoxidation of catecholamine-derived TIQs may reduce the likelihood of these substances forming cytotoxic quinoids and influencing endogenous *OH-generating reactions.

Trends in body size across an environmental gradient: a differential response in scavenging and non-scavenging demersal deep-sea fish.

Body size trends across environmental gradients are widely reported but poorly understood. Here, we investigate contrasting relationships between size (body mass) and depth in the scavenging and predatory demersal ichthyofauna (800-4800 m) of the North-east Atlantic. The mean size of scavenging fish, identified as those regularly attracted to baited cameras, increased significantly with depth, while in non-scavengers there was a significant decline in size. The increase in scavenger size is a consequence of both intra and inter-specific effects. The observation of opposing relationships, in different functional groups, across the same environmental gradient indicates ecological rather than physiological causes. Simple energetic models indicate that the dissimilarity can be explained by different patterns of food distribution. While food availability declines with depth for both groups, the food is likely to be in large, randomly distributed packages for scavengers and as smaller but more evenly distributed items for predators. Larger size in scavengers permits higher swimming speeds, greater endurance as a consequence of larger energy reserves and lower mass specific metabolic rate, factors that are critical to survival on sporadic food items.

Mutations to antibiotic resistance occur during the stationary phase in Lactobacillus plantarum ATCC 8014.

When Lactobacillus plantarum ATCC 8014 was maintained in LCM broth (which consists of buffered tryptone and is sufficient to support the growth of some species of Lactobacillus ) for long periods (120 d), viable bacteria persisted. Rifampicin-, streptomycin- and sodium-fusidate-resistant mutants were recovered from parallel LCM broth cultures following a stochastic pattern. Individual cultures appeared to yield mutants intermittently. One culture in particular yielded rifampicin-resistant colonies at a frequency of 1 in 100 viable bacteria after 20 d incubation and these persisted until the experiment was terminated at 115 d. In a separate experiment two parallel cultures yielded mutants resistant to low concentrations of streptomycin at a similar frequency. Using a chemostat it was shown that in continuous culture in LCM at slow growth rates the highest frequency of recovery of antibiotic-resistant mutants was achieved when the bacteria exhibited doubling times of 90 h or greater. The frequency of recovery of mutants was as high as 1 in 1000 viable bacteria. Thus, mutations to antibiotic resistance in L. plantarum ATCC 8014 can take place in the absence of measurable cell division. The data are consistent with the notion that populations of starved bacteria in stationary phase can be genetically dynamic.

(1S,2S)-1-(4-hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)-1-propanol: a potent new neuroprotectant which blocks N-methyl-D-aspartate responses.

(1S,2S)-1-(4-Hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)-1-propanol (20, CP-101,606) has been identified as a potent and selective N-methyl-D-aspartate (NMDA) antagonist through a structure activity relation (SAR) program based on ifenprodil, a known antihypertensive agent with NMDA antagonist activity. Sites on the threo-ifenprodil skeleton explored in this report include the pendent methyl group (H, methyl, and ethyl nearly equipotent; propyl much weaker), the spacer group connecting the C-4 phenyl group to the piperidine ring (an alternating potency pattern with 0 and 2 carbon atoms yielding the greatest potency), and simple phenyl substitution (little effect). While potent NMDA antagonists were obtained with a two atom spacer, this arrangement also increased alpha 1 adrenergic affinity. Introduction of a hydroxyl group into the C-4 position on these piperidine ring resulted in substantial reduction in alpha 1 adrenergic affinity. The combination of these observations was instrumental in the discovery of 20. This compound potently protects cultured hippocampal neurons from glutamate toxicity (IC50 = 10 nM) while possessing little of the undesired alpha 1 adrenergic affinity (IC50 approximately 20 microM) of ifenprodil. Furthermore, 20 appears to lack the psychomotor stimulant effects of nonselective competitive and channel-blocking NMDA antagonists. Thus, 20 shows great promise as a neuroprotective agent and may lack the side effects of compounds currently in clinical trials.

(3R,4S)-3-[4-(4-fluorophenyl)-4-hydroxypiperidin-1-yl]chroman-4,7-diol: a conformationally restricted analogue of the NR2B subtype-selective NMDA antagonist (1S,2S)-1-(4-hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)- 1-propanol.

(1S,2S)-1-(4-Hydroxyphenyl)-2-(4-hydroxy-4-phenylpiperidino)-1-propanol (CP-101,606, 1) is a recently described antagonist of N-methyl-D-aspartate (NMDA) receptors containing the NR2B subunit. In the present study, the optimal orientation of compounds of this structural type for their receptor was explored. Tethering of the pendent methyl group of 1 to the phenolic aromatic ring via an oxygen atom prevents rotation about the central portion of the molecule. Several of the new chromanol compounds have high affinity for the racemic [3H]CP-101,606 binding site on the NMDA receptor and protect against glutamate toxicity in cultured hippocampal neurons. The new ring caused a change in the stereochemical preference of the receptor-cis (erythro) compounds had better affinity for the receptor than the trans isomers. Computational studies suggest that steric interactions between the pendent methyl group and the phenol ring in the acyclic series determine which structures can best fit the receptor. The chromanol analogue, (3R,4S)-3-[4-(4-fluorophenyl)-4-hydroxypiperidin-1- yl]chroman-4,7-diol (12a, CP-283,097), was found to possess potency and selectivity comparable to CP-101,606. Thus 12a is a new tool to explore the function of the NR2B-containing NMDA receptors.

Ethanol pre-exposure suppresses HIV-1 glycoprotein 120-induced neuronal degeneration by abrogating endogenous glutamate/Ca2+-mediated neurotoxicity.

The neurotoxic mechanism of HIV-1 envelope glycoprotein 120 (gp120) involves glutamatergic (NMDA) receptor/Ca2+-dependent excitotoxicity, mediated in part via glia. Pro-inflammatory cytokines also may have roles. We have reported that pre-exposure of brain cultures to 'physiological' ethanol concentrations (20-30 mM) protects against neuronal damage from HIV-1 gp120, but not from the direct receptor agonist, NMDA. Using lactate dehydrogenase assays and propidium iodide staining of rat organotypic hippocampal-entorhinal cortical slice cultures we determined that ethanol's suppression of gp120 neurotoxicity required at least 4 days of pretreatment. The gp120-induced neurotoxicity was accompanied by interleukin-6 elevations that were not affected by the pretreatment. However, gp120 induced substantial, early increases in extracellular glutamate levels that were blocked by ethanol pretreatment, conceivably abrogating excitotoxicity. Consistent with abrogation of excitotoxic pathways, fura-2 imaging showed selective deficits in gp120-dependent intracellular Ca2+ responses in ethanol-pretreated slices. Gp120 is believed to increase glutamate levels by both stimulating release and inhibiting (re)uptake. Results with a labeled glutamate analog, D-[3H]aspartate, revealed that gp120's inhibition of glutamate uptake, rather than its stimulation of release, was abolished after ethanol. Further studies indicated that two converging effects of ethanol pretreatment may underlie the abolishment of gp120-mediated glutamate uptake inhibition: (a) blockade of gp120-induced release (ostensibly from glia) of arachidonic acid, an inhibitor of astroglial glutamate reuptake, and (b) modest proliferation and activation of astroglia upon gp120 stimulation--which are likely to augment glutamate transporters. Thus, as with gp120 itself, glia and glutamate/arachidonic acid regulation appear to be important targets for ethanol. Since moderate ethanol consumption is as common among HIV-infected individuals as in the general population, this newly recognized neuroprotective (and apparently anti-excitotoxic) effect of ethanol withdrawal in vitro could be important, but it requires further study before its significance, if any, is understood.

Metrifonate improves associative learning and retention in aging rabbits.

The cholinergic system is known to show deterioration during aging and Alzheimer's disease (AD). In response, a therapeutic approach to AD has been to attempt to compensate for the decrease in central cholinergic function by potentiating the activity of the remaining intact cholinergic cells with cholinesterase (ChE) inhibitors. In this study treatment with the long-lasting ChE inhibitor metrifonate facilitated acquisition and retention of eyeblink conditioning in aging rabbits. Metrifonate treatment resulted in steady-state, dose-dependent acetylcholinesterase (AChE) inhibition in red blood cells. Maximal behavioral efficacy was achieved with AChE inhibition of approximately 40%, with no further improvements resulting from increased levels of inhibition. Metrifonate was behaviorally effective in the absence of the severe side effects that can plague ChE inhibitors, supporting metrifonate as a possible treatment for the cognitive deficits resulting from normal aging and AD.

Studies on the effects of pyrogallol and the structurally related dopa decarboxylase inhibitor RO4-4602 on acetaldehyde metabolism.

Microanalytic procedures for the determination of AcH in whole blood from EtOH-intoxicated animals given PG or related drugs should utilize a hemolysis step in 0.5 N PCA in order to inhibit PG-dependent AcH production in vitro. Thiourea may also be included as an added protective measure. RO4-4602, a clinically important drug that contains a PG ring structure, is a moderate in vitro inhibitor of AldDH activity, comparable in potency to PG, chloral hydrate, or diethyldithiocarbamate.

HIV-I gpI20 neurotoxicity in brain cultures is prevented by moderate ethanol pretreatment.

The HIV-1 coat protein gp 20, a potent neurotoxin that may underlie AIDS dementia, activates glia to cause neurotoxicity via the NMDA receptor and perhaps other routes. We find that pretreating cultures of rat organotypic cortical/hippocampal slices or cerebellar granule cells subchronically with ethanol in physiological concentrations (20-30 mM; 6 days) largely or even completely inhibits neurodegeneration due to gp120. However, NMDA-induced neurotoxicity appears unaffected by moderate ethanol pretreatment, indicating that ethanol's neuroprotection against gp120 is upstream of the NMDA receptor, possibly at a glial activation stage. The results could lead to a better understanding of relationships between ethanol, glia and neurodegeneration, particularly in AIDS.

Associative learning down-regulates PKC beta 2- and gamma-immunoreactivity in astrocytes.

We showed previously that associative learning induced a twofold increase in protein kinase C gamma-immunoreactivity (PKC gamma-ir) in rabbit CA1 pyramidal neurons, whereas subicular neurons remained unchanged. Here, we investigated the effects of associative learning on PKC-positive astrocytes by determining their numerical density in the CA1 region and the subiculum of naive, pseudoconditioned and trace eyeblink conditioned rabbits. Associative learning induced a 70-80% reduction in the number of PKC beta 2- and gamma-positive astrocytes in the CA1 region, but not in the subiculum. No changes were found in the number of PKC alpha- or beta 1-positive astrocytes in either hippocampal subregion. These results suggest a conditioning-specific downregulation of PKC beta 2 and gamma in a subset of astrocytes in a brain region where a simultaneous alteration in neuronal PKC gamma was evident.