Hot off the presses! May 15 Neurosci Lett

The May 15 issue of the Neurosci Lett is now up on Pubget (About Neurosci Lett): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

• Editorial Board
  - Neurosci Lett 455(2):iii (2009)
  
• Effects of treadmill running on spatial learning and memory in streptozotocin-induced diabetic rats
  - Neurosci Lett 455(2):79-83 (2009)
  Previous studies have shown an association between diabetes mellitus and impairments in learning and memory. These deficits were partially reversed by the use of insulin. Due to the fact that exercise has positive effects on many physiological systems, including the central nervous system, the present study, evaluated the effects of treadmill running on spatial learning and memory in streptozotocin (STZ)-induced diabetic rats. The exercise program was treadmill running at 17 meters per minute (m/min) at 0° inclination for 40 minutes per day (min/day), 7 days/week, for 12 weeks. Experimental groups were: the control-rest, the control-exercise, the diabetes-rest and the diabetes-exercise. Spatial learning and memory was investigated by Morris water maze test in the rats after 12 weeks of diabetes induction and the exercise period. Our data showed that spatial learning and memory was significantly impaired in the diabetes-rest group with respect to the control-rest group! . However, there were no differences between the other groups. The present results suggest that spatial learning and memory is affected under diabetic conditions and that treadmill running prevents these effects. The data correspond to the possibility that treadmill running is helpful in the prevention and alleviation of the cognitive decline in diabetes mellitus.
• Investigation of ethanol-induced impairment of spatial memory in γ2 heterozygous knockout mice
  - Neurosci Lett 455(2):84-87 (2009)
  GABAA receptors, the major inhibitory receptors in the mammalian central nervous system, are affected by a number of drug compounds, including ethanol. The pharmacological effects of certain drugs have been shown to be dependent upon specific GABAA receptor subunits. Because benzodiazepines and ethanol have similar effect signatures, it has been hypothesized that these drugs share the γ2-containing GABAA receptors as a mechanism of action. To probe the involvement of the γ2 subunit in ethanol's actions, spatial memory for the Morris water maze task was tested in γ2 heterozygous knockout mice and wild type littermate controls following ethanol administration at the following doses: 0.0, 1.25, 1.75, and 2.25 g/kg. While baseline learning and memory were unaffected by reduction of γ2 containing GABAA receptors, ethanol dose-dependently impaired spatial memory equally in γ2 heterozygous knockouts and wild type littermate controls.
• The PKC inhibitor Ro31-8220 blocks acute amphetamine-induced dopamine overflow in the nucleus accumbens
  - Neurosci Lett 455(2):88-92 (2009)
  Acute administration of the psychostimulant amphetamine increases extracellular levels of dopamine (DA) by reversing the DA transporter on ascending midbrain DA neurons. In vitro studies using striatal synaptosomal, slice and nucleus accumbens (NAcc) tissue preparations have implicated protein kinase C (PKC) in this effect. The present study further examined this effect in vivo by assessing the ability of the PKC inhibitor, Ro31-8220 (10 μM), to inhibit acute amphetamine-induced DA overflow when applied with this drug to the NAcc via reverse dialysis. Amphetamine was applied at a concentration of 30 μM, and the core and shell subregions of the NAcc were assayed separately in freely moving rats. These brain regions play a role in the acute locomotor-activating and motivational effects of amphetamine. Consistent with the findings of previous in vitro experiments, reverse dialysis of Ro31-8220 with amphetamine robustly attenuated the ability of this drug to increase ext! racellular levels of dopamine in both the core and shell subregions of the NAcc. These results confirm that amphetamine stimulates dopamine overflow via a PKC-dependent mechanism.
• Immunohistochemical localization of protein kinase C-alpha in the retina of pigs during postnatal development
  - Neurosci Lett 455(2):93-96 (2009)
  The cellular localization and protein expression level of protein kinase C (PKC)-alpha was examined in pig retina at different ages. Western blot analysis detected PKC-alpha in the retinas of 3-day-old piglets and indicated significantly increased expression in 6-month-old young adult and 2-year-old adult pigs. Immunohistochemistry of 3-day-old retinas revealed intense PKC-alpha reactivity in the inner plexiform and inner nuclear cell layers, weak reactivity in the ganglion cell layer, and few positive cells in the outer nuclear cell layer. The cellular localization of PKC-alpha in the adult retina was similar, with staining more intense than that in neonates. PKC-alpha was co-localized in some glial fibrillary acidic protein-positive cells and glutamine synthetase-positive cells in the retina. This study demonstrates that the protein level of retinal PKC-alpha is increased with maturation and suggests that PKC-alpha plays a role in signal transduction pathways for pos! tnatal development in porcine retina.
• No association between the promoter polymorphisms of PAI-1 gene and sporadic Alzheimer's disease in Chinese Han population
  - Neurosci Lett 455(2):97-100 (2009)
  Amyloid beta peptide (Aβ) accumulation is the major event in the brain of cases with Alzheimer's disease (AD). The serine protease plasmin, which is generated from the inactive zymogen plasminogen, could accelerate Aβ degradation, and thus may play a role in AD pathogenesis. It has been reported that the increasing of plasminogen activator inhibitor-1 (PAI-1) inhibits the activity of plasminogen activator and thus reduces the generation of plasmin in vivo. For seeking the correlation of the PAI-1 promoter with sporadic AD (SAD), we performed a case–control study in a group of Chinese Han population. In the study, we detected two polymorphisms, a G/A single base substitution polymorphism at −844 bp (rs2227631) and a single guanosine deletion/insertion 4G/5G polymorphism at −675 bp (rs1799889) upstream from the start of transcription. Direct sequencing was used for genotyping in 324 SAD patients and 278 controls. We failed to find any associations between these t! wo polymorphisms and SAD even after stratified by age of onset, gender and apolipoprotein E (APOE) var epsilon4 status. Our data do not support that there is an association between the PAI-1 promoter polymorphisms and SAD in the Chinese Han population.
• Association between promoter polymorphisms in anterior pharynx-defective-1a and sporadic Alzheimer's disease in the North Chinese Han population
  - Neurosci Lett 455(2):101-104 (2009)
  Amyloid β-peptide (Aβ) deposition in brain is important in the development of sporadic Alzheimer's disease (SAD) and Aβ is produced through sequential cleaving of amyloid precursor protein (APP) by β-secretase and γ-secrease. Anterior pharynx-defective-1 (APH-1) is an important subunit of the gamma-secretase complex, and its expression level was associated with the activity of γ-secrease. We hypothesized that alterations in the APH-1 promoter region might alter APH-1 expression and the activity of γ-secrease, thus be involved in the SAD process. In the present study, we sequenced APH-1a promoter region in 20 randomly selected controls and 20 SAD patients and detected two polymorphisms which were −980C/G (rs3754048) and −21C/A (rs2275780). Then, we investigated genotypes and allele of these two polymorphisms as well as apolipoprotein var epsilon4 (APOE var epsilon4) status in 256 SAD patients and 276 normal controls with restriction fragment length polymorphi! sms analysis and sequencing. Results showed the GG genotype and G allele of −980C/G polymorphism were more frequent in the SAD group than that in the controls not only in the whole subjects (genotype P = 0.038, allele P = 0.01 respectively) but also in the APOE var epsilon4 + subjects (genotype P = 0.048, allele P = 0.016 respectively). There was no statistical difference between SAD group and controls regarding to the frequency of alleles and genotypes of −21C/A whenever before or after stratification by APOE var epsilon4. Our results suggest that there is an association between −980C/G and the development of SAD in the Northern Han Chinese population and that allele G may interact synergistically with the APOE var epsilon4 allele to increase the risk of SAD.
• Contribution of syntaxin 1A to the genetic susceptibility to migraine: A case–control association study in the Spanish population
  - Neurosci Lett 455(2):105-109 (2009)
  Migraine is a common neurological disorder with a complex inheritance pattern. Mutations in genes encoding proteins that are involved in ion transport across the neuronal membrane have been linked to rare monogenic variants of migraine. These or other related genes and proteins are also candidates to be involved in the inherited predisposition to the more common forms of migraine without aura (MO) or migraine with aura (MA). One of these proteins, syntaxin 1A, encoded by the STX1A gene, is a key molecule in ion channel regulation and synaptic exocytosis. We assessed the contribution of STX1A to migraine by analyzing three SNPs that cover the entire gene (rs6951030–rs941298–rs4363087), in a case–control association study in 210 migraine patients (102 MO, 86 MA, 22 hemiplegic migraine) and 210 sex-matched unrelated controls. The single-marker analysis revealed significant differences in both allele frequencies (P = 0.0087, OR = 1.48) and genotype distributions (P =! 0.0133) of the rs941298 SNP between migraineurs and controls, with an overrepresentation of T-allele carriers in the migraine sample (OR = 1.78). We subsequently performed a haplotype-based analysis and observed evidence of an overrepresentation of the A–T–G (rs6951030–rs941298–rs4363087) allelic combination in migraine patients and an increased frequency of carriers of this risk haplotype (P = 0.008, OR = 1.71). These differences remained significant when patients were subdivided into MO and MA. When the control series was enlarged for rs941298, we confirmed the association only with the whole migraine group.
• Neural activities underlying environmental and personal risk identification tasks
  - Neurosci Lett 455(2):110-115 (2009)
  The present study examined domain specific neural activities associated with the identification of environmental and personal risks. We recorded neural activities from subjects, using functional magnetic resonance imaging and event-related brain potential, when they identified risky and safe environmental and personal events. We found that, relative to the semantic control task, both environmental and personal risk identification tasks were associated with increased sustained activities in the medial frontal and supramarginal gyrus. Moreover, relative to the personal risk identification task, the environmental risk identification task resulted in greater transient activity in the posterior cingulate cortex and precuneus. ERPs recorded over the parietal area associated with the environmental risk identification task occurred earlier than that linked to the personal risk identification task. Our findings suggest that the extent of involvement and temporal courses of retr! ieval of emotional experiences may distinguish between the environmental and personal risk identification tasks.
• Resolving the relationship between ApolipoproteinE and depression
  - Neurosci Lett 455(2):116-119 (2009)
  Several studies have reported an association between the ApolipoproteinE-var epsilon4 (APOE4) allele and depression among elders. However others have failed to find an association. Since APOE4 is a well recognized risk factor for Alzheimer dementia, cognitive status may represent an important confounder between APOE4 and depression. In this investigation, we examined the relationship between the ApolipoproteinE-var epsilon4 allele and depression among elders accounting for cognitive status. Using a case-control design (n = 1052), we investigated the association between ApolipoproteinE-var epsilon4 and depression in Alzheimer disease patients (n = 528) and in cognitively intact controls (n = 524). We demonstrated an apparent association between the APOE4 allele and depression in the combined dataset (p = 0.001) when not controlling for cognitive status. However, once stratified by the presence of Alzheimer disease, there was no association in either the Alzheimer group ! (p = 0.290) or the cognitively intact controls (p = 0.494). In this dataset there is no association between the ApolipoproteinE-var epsilon4 allele and depression among those with Alzheimer disease or among cognitively intact elders. However there is a significant association between female gender and depression in the cognitively intact (p = 0.003) but not among those with Alzheimer disease. Additionally, individuals with Alzheimer disease and depression had a significantly younger age of onset for their Alzheimer disease than those without depression (p = 0.017).
• An association study of monoamine oxidase A (MAOA) gene polymorphism in methamphetamine psychosis
  - Neurosci Lett 455(2):120-123 (2009)
  Methamphetamine continues to be the most widely abused drug in Japan. Chronic methamphetamine users show psychiatric signs, including methamphetamine psychosis. Monoamine oxidase A (MAOA) is one of the major enzymes responsible for the degradation of neurotransmitters. Abnormalities in MAO levels have been related to a wide range of psychiatric disorders. We examined whether or not the MAOA-u variable-number tandem repeat (VNTR) has a functional polymorphism in methamphetamine psychosis and whether or not such a polymorphism is related to the prolongation of psychosis. As expected, there was a significant difference in the MAOA-u VNTR between males with persistent versus transient methamphetamine psychosis (p = 0.018, odds ratio (OR) = 2.76, 95% CI: 1.18–6.46). Our results suggest that the high-activity allele class of MAOA-u VNTR in males may be involved in susceptibility to a persistent course of methamphetamine psychosis. We found no differences among females. The! sample size of females with methamphetamine psychosis was too small to have significant analysis.
• The pseudohomophone effect: Evidence for an orthography–phonology-conflict
  - Neurosci Lett 455(2):124-128 (2009)
  The standard pseudohomophone effect in the lexical decision task, i.e. longer response times and higher error rates for pseudohomophones compared with spelling controls, is commonly explained by an orthography–phonology-conflict. This study tested this conflict account, using a multi-method approach including participant's behavioral responses, confidence ratings, pupillary responses and event-related potentials (ERPs). The classic pseudohomophone effect was replicated using relatively long, multi-syllabic stimuli. Pseudohomophones were rated less confidently as being nonwords than spelling controls, and they affected the pupillary response by increasing the peak pupil diameter. Both findings are interpreted in terms of increased conflict and higher cognitive demands leading to uncertainty while solving the task. The ERP revealed an N400 component for spelling controls, showing a graded effect: word < pseudohomophone < spelling control. This can be seen as evidence f! or (partial) semantic activation through pseudohomophones. Taken together, the results provide strong multi-method evidence for the conflict account of the pseudohomophone effect.
• Crossmodal transfer of emotion by music
  - Neurosci Lett 455(2):129-133 (2009)
  Music is one of the most powerful elicitors of subjective emotion, yet it is not clear whether emotions elicited by music are similar to emotions elicited by visual stimuli. This leads to an open question: can music-elicited emotion be transferred to and/or influence subsequent vision-elicited emotional processing? Here we addressed this question by investigating processing of emotional faces (neutral, happy and sad) primed by short excerpts of musical stimuli (happy and sad). Our behavioural experiment showed a significant effect of musical priming: prior listening to a happy (sad) music enhanced the perceived happiness (sadness) of a face irrespective of facial emotion. Further, this musical priming-induced effect was largest for neutral face. Our electrophysiological experiment showed that such crossmodal priming effects were manifested by event related brain potential components at a very early (within 100 ms post-stimulus) stages of neuronal information processing! . Altogether, these results offer new insight into the crossmodal nature of music and its ability to transfer emotion to visual modality.
• Decreased levels of disrupted-in-schizophrenia 1 (DISC1) are associated with expansion of the dentate granule cell layer in normal and kindled rats
  - Neurosci Lett 455(2):134-139 (2009)
  Disrupted-in-schizophrenia 1 (DISC1) is a candidate gene involved in the pathogenesis of schizophrenia. DISC1 expression is particularly abundant in the adult dentate gyrus, in which decreased levels lead to aberrant growth, impaired migration, and accelerated integration of adult generated neurons. Because seizures can also result in similar changes, we tested the hypothesis that DISC1 expression may be altered in an animal model of epilepsy. We found that extended amygdala kindling (i.e., 99-electrical stimulations) significantly decreased DISC1 labeling in the dentate granule cell layer and subgranular zone. Extended kindling also led to an increase in the number of ectopic granule cells in the hilus. In addition, although the width of the granule cell layer was not generally affected by kindling, decreased levels of DISC1 in the subgranular zone and granule cell layer were associated with an expansion of the upper blade and crest of the dentate gyrus in both normal! and kindled rats. These novel findings suggest that seizure activity affects DISC1 signaling in the dentate gyrus and that DISC1 expression may regulate the cytoarchitectural organization of the granule cell layer.
• The evaluation of effects of lipoic acid on the lipid peroxidation, nitrite formation and antioxidant enzymes in the hippocampus of rats after pilocarpine-induced seizures
  - Neurosci Lett 455(2):140-144 (2009)
  It has been suggested that pilocarpine-induced seizures is mediated by increases in oxidative stress. Current researches have suggested that antioxidant compounds may afford some level of neuroprotection against the neurotoxicity of seizures in cellular level. The objective of the present study was to evaluate the neuroprotective effects of lipoic acid (LA) in rats, against the observed oxidative stress during seizures induced by pilocarpine. Wistar rats were treated with 0.9% saline (i.p., control group), LA (10 mg/kg, i.p., LA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of LA (10 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before of administration of LA (LA plus pilocarpine group). After the treatments all groups were observed for 6 h. The enzyme activities as well as the lipid peroxidation and nitrite concentrations were measured using spectrophotometric methods and the results compared to values obtained from saline and! pilocarpine-treated animals. Protective effects of LA were also evaluated on the same parameters. In pilocarpine group there was a significant increase in lipid peroxidation and nitrite level. However, no alteration was observed in superoxide dismutase and catalase activities. Antioxidant treatment significantly reduced the lipid peroxidation level and nitrite content as well as increased the superoxide dismutase and catalase activities in hippocampus of rats after seizures induced by pilocarpine. Our findings strongly support the hypothesis that oxidative stress in hippocampus occurs during seizures induced by pilocarpine, proving that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and also imply that strong protective effect could be achieved using lipoic acid as an antioxidant.
• Circadian control of neural excitability in an animal model of temporal lobe epilepsy
  - Neurosci Lett 455(2):145-149 (2009)
  We provide experimental evidence for the emerging imbalance in the firing activity of two distinct classes (type 1 and type 2) of population spikes recorded from the hippocampal area CA1 in an animal model of temporal lobe epilepsy. We show that during the latent period of epileptogenesis following status epilepticus inducing brain injury, there is a sustained increase in the firing rate of type 1 population spikes (PS1) with a concurrent decrease in the firing rate of type 2 population spikes (PS2). Both PS1 and PS2 firing rates are observed to follow a circadian rhythm and are in-phase in control rats. Following brain injury there is an abrupt phase shift in the circadian activity of the PS firing rates. We hypothesize that this abrupt phase shift is the underlying cause for the emergence of imbalance in the firing activity of the two PS. We test our hypothesis in the framework of a simple two-dimensional Wilson–Cowan model that describes the interaction between fi! ring activities of populations of excitatory and inhibitory neurons.
• Effectiveness of riluzole in suppressing spasticity in the spinal cord injured rat
  - Neurosci Lett 455(2):150-153 (2009)
  Spasticity poses a major detrimental impact on the quality of life in a significant number of people with spinal cord injury (SCI). Recent observations in our laboratory suggest that spinal transection at the sacral S2 level induces a significant increase in glutamatergic input to sacrocaudal motoneurons during the time spasticity is present in the tail muscles. The present study examined the effectiveness of riluzole, an agent that has been shown to reduce glutamate release, in managing spasticity within the tail musculature. In this blinded, cross-over study animals with S2 spinal transections were tested behaviorally for the progression of spasticity in the tail musculature using our established system. When the animals demonstrated a significant level of spastic behavior (e.g. increased response to quick stretch, noxious and non-noxious cutaneous stimuli), they received either saline or riluzole (8 or 10 mg/kg i.p.) and assessed behaviorally at 1, 3, 6, and 12 post! -injection. Results: riluzole at 8 mg/kg significantly decreased the response of the tail muscle to noxious and non-noxious cutaneous stimuli for the first 3 h post-administration, while administration of riluzole at 10 mg/kg significantly decreased the responsiveness of the tail to all of the behavioral assessments. However, a significant percentage of the animals displayed motor impairments at this higher dosage. Conclusion: suppression of glutamate release by the administration of riluzole can reduce several, but not all, aspects of spastic activity in the tail muscles at concentrations that do not elicit negative side-effects.
• Contents
  - Neurosci Lett 455(2):CO4 (2009)