SFN Neuroblogging: Send Sci Your Info!

So yay, Sci’s one of the SFN Neurobloggers!!! And this means she will be blogging, every day, about the cool and possibly weird stuff that she sees at the meeting (I hope there will be weird stuff…). Exciting, right?
Of course right!
Well, Sci will be making up her meeting planner in the next few days. She’s got a few major themes in mind, but she’s open to anything. So if you’d like a special blog post to be all about YOU, email Sci your poster info! Sci might stop by. She might chat you up. And she might be wowed by your totally awesome findings!
So email me your poster info, ya’ll know you wanna be famous.

2 Responses

  1. Session Number 38
    Session Title: Synaptic Integration
    Date and Time: Saturday Oct 17, 2009 1-5PM
    Location: South Hall A
    Synaptic mechanisms of action explaining carbon dioxide induced paralysis
    S.M. Bierbower and R.L. Cooper. Dept of Biology, Univ of KY.
    Carbon dioxide (CO2) is universally found and impacts all organisms throughout their lifetime. Interestingly, invertebrates and vertebrates are very different systemically, yet the effect of CO2 is not. Crayfish serve as an excellent model since these animals possess the complex ability to integrate sensory information, relay the information into motor output to target tissues and allow the ‘sympathetic-like’ autonomic response to be easily studied. It is through this motor output (i.e., locomotor activity, heart and ventilatory measures) that we can assess the internal state of the organism. The effects previously identified in Drosophila melanogaster larvae were also shown in the crayfish with acute CO2 exposure. While attraction to low levels of CO2 has been documented in insects, this is a foundation study showing attraction/repellent behavioral responses in crustaceans. The identified effect (i.e., immobilization, cardiac arrest) is characterized by a cessation heart (HR) and ventilatory (VR) rates after approximately 10 minutes, a steady decrease in locomotor activity, as well as unresponsiveness to stimuli prior to HR and VR cessation. To identify mechanisms of action, we examined synaptic transmission (EPSPs) at the skeletal NMJ by introducing an excitatory neurotransmitter (glutamate). Results indicate that the anesthetic effect is characterized by a decrease in synaptic transmission resulting from CO2 induced glutamate receptor block; thus this should be considered a paralytic effect. Due to glutamatergic insensitivity, the site of action was identified as post-synaptic at NMJs. Furthermore, to identify the effect of CO2 on chemical synapses within a complete circuit, the ‘sensory-ganglia-motor nerve-muscle’ of the abdominal superficial flexor muscle was used. Results show a knockout of neural activity from the CNS; therefore this research proposes a glutamatergic drive from the CNS to the motor nerve root. Thus, nicotine was used to further explain the CO2 effect on glutamatergic receptors shown to be inhibited at NMJs.

  2. Hey, I want to be famous!
    Program#/Poster#: 147.7/I9
    Title: The transcriptional repressor NRSF/REST mediates acquired HCN channelopathy in the epileptogenic process
    Location: South Hall A
    Presentation Time: Sunday, Oct 18, 2009, 10:00 AM -11:00 AM
    Authors: *S. MCCLELLAND1, C. FLYNN2, C. DUBE1, C. RICHICHI1, J. MUNDY1, R. PETROSYAN1, Q. ZHA1, C. BERNARD2, T. Z. BARAM1;
    1UC Irvine, Irvine, CA; 2Univ. de la Méditerranée, Marseille, France
    Abstract: –
    Rationale:
    Abnormal expression and function of ion channels is associated with neurological disorders, including temporal lobe epilepsy (TLE; Bender et al., J Neurosci, 2003). In experimental models of TLE dysfunction of the current mediated by the HCN chanels, Ih, is found and accompanied by repression of HCN type 1 (HCN1) subunit expression. Here we studied the molecular basis of this repression, and the underlying mechanisms.

    Methods:
    Experimental TLE was provoked using kainic-acid-induced status epilepticus (KA-SE). Levels of HCN1 and of the transcriptional repressor NRSF were assayed using Western blot, the binding of NRSF to the regulatory region of the hcn1 gene was examined using Chromatin Immunoprecipitation (ChIP). Finally, the role of NRSF regulation of gene expression in the epileptogenic process was assessed by administering oligodeoxynucleotides (ODNs) comprising either the NRSE sequence (as a ‘decoy’ preventing NRSF bidning to its cognate DNA -binding sequence) or a scrambled sequence, to KA-SE or control rats. In all cases, the CA1 region of the hippocampus was resected three days later for analysis of HCN1, HCN2, Kv4.2 and NRSF expression.

    Results:
    (1) The hcn1 gene was found to contain a functional NRSF DNA-binding sequence (NRSE). (2) Levels of NRSF, a transcriptional repressor, were increased in nuclear extracts from KA-SE rats, compared to controls. (3) HCN1 levels were reduced in KA-SE rats, and (4) this reduction was abrogated by administration of NRSE ODNs, but not scrambled ODNs. (5) Using ChIP, binding of NRSF to the hcn1 gene was augmented specifically in KA-SE-rats, and was abolished by administration of NRSE ODNs, but not scrambled ones. (6) The expression of HCN2 and Kv4.2 were not affected by KA-SE or ODN administration.

    Conclusions:
    NRSF regulated HCN1 expression via interactions with the hcn1 gene chromatin, and this persistent (>a week) suppression is involved in circuit dysfunction (Flynn et al., adjacent poster). Preventing the interaction of NRSF with the hcn1 gene prevents the repression of HCN1 expression and the associated circuit dysfunction and epileptogenic process. Therefore, understanding and controlling this regulatory mechanism may have major clinical implications.

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