Same old: September 2007

Tuesday 11 September 2007

Untitled

Sleep-related eating disorder in a 29 year-old man: a case report with diagnostic polysomnographic findings.

Acta Neurol Taiwan. 2007 Jun;16(2):106-10

Authors: Yeh SB, Schenck CH

This is a case of a 29-year-old man with a 6 year history of sleep-related eating disorder (SRED) that occurred with partial consciousness on a nightly basis. His family or wife witnessed up to 5 episodes every night, with each eating episode lasting 8-16 minutes. Polysomnography documented 4 episodes of sleep-related eating arising from stage 2 Non-REM sleep, when he consumed cookies that he had brought to the sleep lab that night. While eating, his EEG remained in stage 2 sleep or else was a wakeful EEG, and the eating episodes lasted for a mean 13.3 minutes. There was no epileptiform EEG activity during the polysomnogrphic study with a seizure montage and fast paper speed. Therapy with clonazepam, 0.5 mg bedtime, did not control the nocturnal eating. The patient tried to limit access to food in his home before bedtime, and this had modest benefit. This case of SRED has both typical and atypical features, which are discussed.

PMID: 17685136 [PubMed - indexed for MEDLINE]

Autism

Is autism partly a consolidation disorder?

Is autism partly a consolidation disorder?

Behav Cogn Neurosci Rev. 2002 Dec;1(4):251-63

Authors: Femia LA, Hasselmo ME

Computational modeling has been useful for understanding processes of encoding and consolidation in cortical structures. In particular, this work suggests a role of neuromodulators in setting dynamics for consolidation processes during different stages of waking and sleep. Because autistic individuals show symptoms of a cognitive nature coupled with a high prevalence of comorbid conditions such as epileptiform discharge during sleep and sleep disorders, it is possible that autism could involve a breakdown in consolidation processes, which are essential to build effective cognitive representations of the environment on the basis of individual experiences. In this article, theories of consolidation during different stages of waking and sleep and the role of different neuromodulators in these consolidation processes are reviewed in conjunction with different features of autism, which may be understood in the context of these theories.

PMID: 17712983 [PubMed - in process]

Glutamate and development: seizures

The impact of chronic network hyperexcitability on developing glutamatergic synapses.

The impact of chronic network hyperexcitability on developing glutamatergic synapses.

Eur J Neurosci. 2007 Aug;26(4):975-991

Authors: Swann JW, Le JT, Lam TT, Owens J, Mayer AT

The effects recurring seizures have on the developing brain are an important area of debate because many forms of human epilepsy arise in early life when the central nervous system is undergoing dramatic developmental changes. To examine effects on glutamatergic synaptogenesis, epileptiform activity was induced by chronic treatment with GABAa receptor antagonists in slice cultures made from infant rat hippocampus. Experiments in control cultures showed that molecular markers for glutamatergic and GABAergic synapses recapitulated developmental milestones reported previously in vivo. Following a 1-week treatment with bicuculline, the intensity of epileptiform activity that could be induced in cultures was greatly diminished, suggesting induction of an adaptive response. In keeping with this notion, immunoblotting revealed the expression of NMDA and AMPA receptor subunits was dramatically reduced along with the scaffolding proteins, PSD95 and Homer. These effects could not be attributed to neuronal cell death, were reversible, and were not observed in slices taken from older animals. Co-treating slices with APV or TTX abolished the effects of bicuculline suggesting that effects were dependent on NMDA receptors and neuronal activity. Neurophysiological recordings supported the biochemical findings and demonstrated decreases in both the amplitude and frequency of NMDA and AMPA receptor-mediated miniature EPSCs (mEPSCs). Taken together these results suggest that neuronal network hyperexcitability interferes with the normal maturation of glutamatergic synapses, which could have implications for cognitive deficits commonly associated with the severe epilepsies of early childhood.

PMID: 17714191 [PubMed - as supplied by publisher]

Newly generated neurones in adult PC

Origin, migration and fate of newly generated neurons in the adult rodent piriform cortex.

Origin, migration and fate of newly generated neurons in the adult rodent piriform cortex.

Brain Struct Funct. 2007 Sep 1;

Authors: Shapiro LA, Ng KL, Kinyamu R, Whitaker-Azmitia P, Geisert EE, Blurton-Jones M, Zhou QY, Ribak CE

Newly generated neurons are continuously added to the olfactory epithelium and olfactory bulbs of adult mammals. Studies also report newly generated neurons in the piriform cortex, the primary cortical projection site of the olfactory bulbs. The current study used BrdU-injection paradigms, and in vivo and in vitro DiI tracing methods to address three fundamental issues of these cells: their origin, migratory route and fate. The results show that 1 day after a BrdU-injection, BrdU/DCX double-labeled cells appear deep to the ventricular subependyma, within the white matter. Such cells appear further ventral and caudal in the ensuing days, first appearing in the rostral piriform cortex of mice at 2 days after the BrdU-injection, and at 4 days in the rat. In the caudal piriform cortex, BrdU/DCX labeled cells first appear at 4 days after the injection in mice and 7 days in rats. The time it takes for these cells to appear in the piriform cortex and the temporal distribution pattern suggest that they migrate from outside this region. DiI tracing methods confirmed a migratory route to the piriform cortex from the ventricular subependyma. The presence of BrdU/NeuN labeled cells as early as 7 days after a BrdU injection in mice and 10 days in the rat and lasting as long as 41 days indicates that some of these cells have extended survival durations in the adult piriform cortex.

PMID: 17764016 [PubMed - as supplied by publisher]

Novel FAAH inhibitors

Novel inhibitors of fatty acid amide hydrolase.

Novel inhibitors of fatty acid amide hydrolase.

Bioorg Med Chem Lett. 2007 Jun 15;17(12):3287-91

Authors: Sit SY, Conway C, Bertekap R, Xie K, Bourin C, Burris K, Deng H

A class of bisarylimidazole derivatives are identified as potent inhibitors of the enzyme fatty acid amide hydrolase (FAAH). Compound 17 (IC(50)=2 nM) dose-dependently (0.1-10mg/kg, iv) potentiates the effects of exogenous anandamide (1 mg/kg, iv) in a rat thermal escape test (Hargreaves test), and shows robust antinociceptive activity in animal models of persistent (formalin test) and neuropathic (Chung model) pain. Compound 17 (20 mg/kg, iv) demonstrates activity in the formalin test that is comparable to morphine (3mg/kg, iv), and is dose-dependently inhibited by the CB1 antagonist SR141716A. In the Chung model, compound 17 shows antineuropathic effects similar to high-dose (100 mg/kg) gabapentin. FAAH inhibition shows potential utility for the clinical treatment of persistent and neuropathic pain.

PMID: 17459705 [PubMed - indexed for MEDLINE]

Sex, cannabinoids and spatial WM

Sex differences in the effects of Delta9-tetrahydrocannabinol on spatial learning in adolescent and adult rats.

Sex differences in the effects of Delta9-tetrahydrocannabinol on spatial learning in adolescent and adult rats.

Behav Pharmacol. 2007 Sep;18(5-6):563-9

Authors: Cha YM, Jones KH, Kuhn CM, Wilson WA, Swartzwelder HS

Like other recreational drugs, cannabinoids may produce different effects in men and women. In this study we measured the effects of Delta-tetrahydrocannabinol (THC) on spatial learning in two groups that are underrepresented in drug research - females and adolescents. In the first experiment, adolescent (postnatal day 30) and adult (postnatal day 70) rats of both sexes were treated subchronically with 5.0 mg/kg THC or vehicle for five consecutive days. Thirty minutes after each daily injection, they were tested on the spatial version of the Morris water maze task. In the second experiment, a separate group of adolescent and adult rats of both sexes was treated with 5.0 mg/kg THC or vehicle daily for 21 days and tested, 4 weeks later, on the spatial version of the water maze. Subchronic THC impaired spatial learning, and this effect was dependent upon both the age and sex of the animals tested. Prior exposure to chronic THC, however, did not cause any long-lasting spatial learning deficits. On the basis of our previous studies in male rats the third experiment assessed the dose-response relationship for the effects of THC on spatial learning and memory in female animals. We found that subchronic THC treatment (2.5, 5.0, or 10.0 mg/kg, intraperitoneally) disrupted learning in both adolescents and adults, but with greater effects at higher doses in adolescents compared with adults. The developmental sensitivity to subchronic THC confirms previous work carried out in our laboratory, and the sex-dependent effects highlight the importance of including females in drug abuse and addiction research.

PMID: 17762524 [PubMed - in process]

Opioids, cannabinoids and seizures!

Elevation of pentylenetetrazole-induced seizure threshold in cholestatic mice: Interaction between opioid and cannabinoid systems.

Elevation of pentylenetetrazole-induced seizure threshold in cholestatic mice: Interaction between opioid and cannabinoid systems.

J Gastroenterol Hepatol. 2007 Aug 30;

Authors: Shafaroodi H, Ghasemi M, Dehpour AR

Background and Aim: Several studies have reported that endogenous opioid and cannabinoid systems may be involved in some pathophysiological changes occurring in cholestatic liver disease. It is well known that endogenous opioids and cannabinoids alter the susceptibility of experimental animals to different models of seizure. Methods: The alterations in pentylenetetrazole-induced clonic seizure thresholds were evaluated from 1 to 6 days after bile duct ligation in mice. Whether the pretreatment of cholestatic mice with different doses of opioid receptor antagonist naltrexone or cannabinoid CB(1) receptor antagonist AM251 (AM251) would have changed the clonic seizure threshold was also examined. Results: Although the clonic seizure threshold was similar between sham-operated and unoperated mice, there was a time-dependent increase in the threshold in cholestatic mice, reaching a peak on day 3 after bile duct ligation and declining partially after day 4. Chronic pretreatment with naltrexone (2, 5, and 10 mg/kg) reversed the increased threshold in cholestatic mice on day 3 after operation in a dose-dependent manner with the highest doses used restoring the threshold to that of the control animals. A similar reversal of the increased threshold was observed after acute (0.5, 0.75, and 1 mg/kg) or chronic (0.5 mg/kg for 4 days) pretreatment with AM251. Moreover, concurrent administration of doses of AM251 and naltrexone that each separately induced a partial reversal of increased seizure threshold in cholestasis caused a complete restoring of the threshold to the control level. Conclusions: Both opioid and cannabinoid CB(1) receptors may be involved in the dramatic increase in pentylenetetrazole-induced seizure threshold in cholestasis.

PMID: 17764531 [PubMed - as supplied by publisher]

GPR55

Identification of GPR55 as a lysophosphatidylinositol receptor.

Identification of GPR55 as a lysophosphatidylinositol receptor.

Biochem Biophys Res Commun. 2007 Aug 24;

Authors: Oka S, Nakajima K, Yamashita A, Kishimoto S, Sugiura T

GPR55 is an orphan G protein-coupled receptor. In this study, we explored a possible endogenous ligand for GPR55 using HEK293 cells which expressed GPR55. We found that lysophosphatidylinositol induced rapid phosphorylation of the extracellular signal-regulated kinase in transiently or stably GPR55-expressing cells. On the other hand, lysophosphatidylinositol did not induce phosphorylation of the extracellular signal-regulated kinase in vector-transfected cells. Lysophosphatidic acid and sphingosine 1-phosphate also induced phosphorylation of the extracellular signal-regulated kinase in GPR55-expressing cells. However, these lipid phosphoric acids elicited similar responses in vector-transfected cells. Various types of other lysolipids as well as the cannabinoid receptor ligands did not induce phosphorylation of the extracellular signal-regulated kinase. We also found that lysophosphatidylinositol elicited a rapid Ca(2+) transient in GPR55-expressing cells. Lysophosphatidylinositol also stimulated the binding of GTPgammaS to the GPR55-expressing cell membranes. These results strongly suggest that GPR55 is a specific and functional receptor for lysophosphatidylinositol.

PMID: 17765871 [PubMed - as supplied by publisher]

Same old