International Society For Neurochemistry Research Articles

RETRACTION: The oxysterol 27-hydroxycholesterol regulates α-synuclein and tyrosine hydroxylase expression levels in human neuroblastoma cells through modulation of liver X receptors and estrogen receptors-relevance to Parkinson's disease.

Retraction: G. Marwarha, T. Rhen, T. Schommer, and O. Ghribi, "The Oxysterol 27-Hydroxycholesterol Regulates α-Synuclein and Tyrosine Hydroxylase Expression Levels in Human Neuroblastoma Cells Through Modulation of Liver X Receptors and Estrogen Receptors-Relevance to Parkinson's Disease," Journal of Neurochemistry 119, no. 5 (2011): 1119-1136, https://doi.org/10.1111/j.1471-4159.2011.07497.x. The above article, published online on 23 September 2011 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Andrew Lawrence; the International Society for Neurochemistry; and John Wiley & Sons Ltd. The retraction has been agreed upon following an investigation by the authors' institution, the University of North Dakota, which determined that Figure2E was falsified by the corresponding author Othman Ghribi. Source data were not available for the article. The other authors were unaware of Ghribi's actions and not in any way involved. All authors were notified of the retraction decision, but did not respond.

Obituary-Abel Lajtha (1922-2024).

With sadness, the International Society for Neurochemistry (ISN) and the Journal of Neurochemistry (JNC) mourn the loss of one of the founding members of the neurochemistry field of science. Abel Lajtha, born in Budapest, Hungary on September 22, 1922, died on May 25, 2024. Abel had a long and distinguished record of service with ISN, having been a founding member of the Society, and served on the editorial board of the Society's journal, JNC.

An obituary to Yukio Yoneda (1950-2023).

Yukio Yoneda died on 31 December 2023, at 73 years old after a long fight against cancer. He was an eminent neurochemist in academia and industry and also had leadership roles within the International Society for Neurochemistry (ISN) and the Asian Pacific Society for Neurochemistry (APSN) and Japanese Society for Neurochemistry (JSN). Photo credit: Yukio Yoneda provided the APSN with the photo during his service to APSN.

In memoriam: Frode Fonnum (1937-2023).

Frode Fonnum died unexpectedly on 26th April 2023, at 86 years of age. He was a tower of strength-a primeval force-in neuroscience, neurochemistry and toxicology. His highly cited publications, comprised salient evidence for GABA and glutamate as brain neurotransmitters. He served as an expert, and as an organizer, including of European research cooperation and as President of the International Society for Neurochemistry (ISN). Photo credit: Per Kristian Opstad.

Neuronal actin cytoskeleton gain of function in the human brain

While advancements in imaging techniques have led to major strides in deciphering the human brain, successful interventions are elusive and represent some of the most persistent translational gaps in medicine. Human restricted CHRFAM7A has been associated with neuropsychiatric disorders. The physiological role of CHRFAM7A in human brain is explored using multiomics approach on 600 post mortem human brain tissue samples. The emerging pathways and mechanistic hypotheses are tested and validated in an isogenic hiPSC model of CHRFAM7A knock-in medial ganglionic eminence progenitors and neurons. CHRFAM7A is identified as a modulator of intracellular calcium dynamics and an upstream regulator of Rac1. Rac1 activation re-designs the actin cytoskeleton leading to dynamic actin driven remodeling of membrane protrusion and a switch from filopodia to lamellipodia. The reinforced cytoskeleton leads to an advantage to tolerate stiffer mechanical properties of the extracellular environment. CHRFAM7A modifies the actin cytoskeleton to a more dynamic and stiffness resistant state in an α7nAChR dependent manner. CHRFAM7A may facilitate neuronal adaptation to changes in the brain environment in physiological and pathological conditions contributing to risk or recovery. Understanding how CHRFAM7A affects human brain requires human studies in the areas of memory formation and erasure, cognitive reserve, and neuronal plasticity. This work is supported in part by the Community Foundation for Greater Buffalo (Kinga Szigeti). Also, in part by the International Society for Neurochemistry (ISN) and The Company of Biologists (Nicolas Rosas). ROSMAP is supported by NIA grants P30AG10161, P30AG72975, R01AG15819, R01AG17917. U01AG46152, and U01AG61356.

Retraction: Cyclo(His-Pro) up-regulates heme oxygenase 1 via activation of Nrf2-ARE signalling.

The above article, published online on 16th October 2009 in Wiley Online Library (wileyonlinelibrary.com) and corrected in 2014 with a Corrigendum (JNeurochem 128(6): 975, URL: https://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2011.07368.x) correcting Figure 3 of the original publication, has been retracted by agreement between the journal's Editor-in-Chief, Andrew Lawrence, the International Society for Neurochemistry and John Wiley & Sons Ltd. The retraction has been agreed due to concerns raised regarding possible image manipulation of Figure 5b. Corresponding author Alba Minelli as well as all other authors have been contacted to clarify their respective contribution to the article, and provide the original scanned films upon request for the editorial team's review. Corresponding author Alba Minelli confirmed the following author contributions in the corrected version (J Neurochem. 2014 Mar;128(6):975) as the final version of the published manuscript which all authors had read and approved: A. Minelli (contact): substantial contribution to conception and design, drafting the article, data interpretation, C .Conte: real-time PCR and gene silencing experiments, data acquisition and analysis, S. Grottelli: data acquisition and analysis, I. Bellezza: drafting the article, data acquisition and analysis, C. Emiliani: revising the article critically for important intellectual content, J. Bolaños: revising the article critically for important intellectual content. Since the original data could not be retrieved to dispel the new concerns regarding Figure 5 of the original publication, the journal no longer has confidence in the results and conclusions drawn. REFERENCE Minelli, A., Conte, C., Grottelli, S., Bellezza, I., Emiliani, C., & Bolaños, J. P. (2009). Cyclo(his-pro) up-regulates heme oxygenase 1 via activation of Nrf2-ARE signalling. Journal of Neurochemistry, 111(4), 956-966. https://doi.org/10.1111/j.1471-4159.2009.06376.x.

Retraction: Differential effects of 24‐hydroxycholesterol and 27‐hydroxycholesterol on tyrosine hydroxylase and α‐synuclein in human neuroblastoma SH‐SY5Y cells

The above article, published online on 15 October 2008 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal's Editor-in-Chief Andrew J. Lawrence, the International Society for Neurochemistry and John Wiley & Sons Ltd. The retraction has been agreed due to identification of image manipulation in Figure 4a, showing duplications of the '27-OHC' and '24-OHC + 27-OHC' bands within the TH lane. The corresponding author and their institution failed to provide the original data upon request. As a result, the data and conclusions of the article are considered unreliable. The authors have been informed but did not respond to requests to approve the wording of this retraction notice. REFERENCE Rantham Prabhakara, J. P., Feist, G., Thomasson, S., Thompson, A., Schommer, E., & Ghribi, O. (2008). Differential effects of 24-hydroxycholesterol and 27-hydroxycholesterol on tyrosine hydroxylase and α-synuclein in human neuroblastoma SH-SY5Y cells. Journal of Neurochemistry, 107(6), 1722-1729. https://doi.org/10.1111/j.1471-4159.2008.05736.x.

PMON12 Effects of Endocrine Disruptors on Autophagy Markers Gene Expression in Immortalized GnRH Neurons and Hypothalami of Adult Male Mice

Abstract Benzophenones (BP) and Bisphenol A (BPA) are endocrine disrupting chemicals (EDC). Previously, we showed that the in-vitro exposure to EDC inhibited Kiss-induced gene expression in GT1-7 and GN11 cells (donated by Pamela Mellon, UCSD), and altered expression of inflammatory markers in GT1-7 cells and hypothalami of adult male mice.In the present study, we evaluated the effects of the in-vivo exposure to BP2 and BP3 (250 µg/kg/day, orally, for 5 days) on the expression of autophagy markers in hypothalamic nuclei in C57Bl/6 adult male mice, and the in-vitro exposure to BPA, BP2 or BP3 in immortalized GnRH neurons. Animals were sacrificed, brains rapidly dissected and conserved -80°C until processed. Micropunches containing Anteroventral Periventricular (AVPV) or Arcuate (ARC) nucleus were obtained. Effects of the in-vitro exposure for 12 or 24 hours to BPA, BP2 or BP3 (1×10-9M, Sigma), or DMSO as control, were evaluated in GT1-7 and GN11 cell lines, mature and immature GnRH neurons. ARN was obtained using Tri-Reagent (Molecular Research Center, Inc), reverse-transcribed and gene expression analyzed by qPCR, using Ppib as control gene. Results were presented as Media±SE and analyzed by ANOVA (Statistica, StatSoft Inc, USA).In-vivo, five-day exposure to BP2 or BP3 did not alter Lamp2 or p62 gene expression in the AVPV or ARC in adult male mice (ANOVA: ns). In GT1-7 cells, Ulk1 was not significantly altered by any of the stimuli (ANOVA: ns; n=5), whereas in GN11 cells, BP3 significantly increased Ulk1 gene expression after 12 and 24 h exposure [DMSO-24h: 0.93±0.21, DMSO-12h: 0.73± 0.19, BPA-24h: 1.78±0.31, BPA-12h: 1.47±0.33, BP2-24h: 1.51±0.49, BP2-12h: 1.06±0.23, BP3-24h: 2.41±0.89, BP3-12h: 2.45±0.82, Repeated Measures ANOVA: Main effect "TREATMENT" p<0.05, BP3 different from DMSO, p<0.05, n=4]. Our results reinforce the notion that the exposure to EDC have different effects depending on the experimental model and time of exposure, with developing cells being more susceptible to disruption that mature cells. We need more experiments to fully understand if exposure to EDC alters other markers of the autophagy process in mouse hypothalamus and GnRH neurons.Funding: CONICET, ANPCYT, International Society for Neurochemistry, Fund. Williams, Fund. R. Barón. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

In-Vitro Exposure to Endocrine Disruptors Alters Inflammatory Markers in Whole Hypothalami and Immortalized GnRH Neurons

Bisphenol A (BPA), a monomer of polycarbonate plastics, and Benzophenones (BPs), used as UV-filters, are endocrine disrupting chemicals (EDC) found in everyday products. Previously, we showed that the in-vitro exposure to BPA decreased Kiss-induced GnRH expression in GN11 cells (donated by Dr. Susan Wray, NIH), immature GnRH neurons, and that exposure to all the EDC decreased Kiss-induced GnRH gene expression in GT1-7 cells (donated by Dr. Pamela Mellon, UCSD), mature GnRH neurons. In this study, we analyzed the effect of in-vitro exposure to the same EDC (BPA, BP2 or BP3, Sigma, 1x10-9 M) or medium as control (C) in mature GnRH neurons (GT1-7 cells), and isolated hypothalami from adult Balb/c males on Glial fibrillary acidic protein (GFAP) and cytokine gene expression. Cells were exposed to the compounds for 12 or 24 h, in DMEM (high glucose) with charcoal-stripped FBS, and the hypothalami for 6 h to the EDC, in Krebs-Ringer buffer. After the incubations, RNA was extracted using Tri-Reagent (Molecular Research Center, OH, USA), 1-2 µg RNA was reverse transcribed and Real-Time PCR performed using specific primers. Results were expressed as Mean±SE and analyzed by T-test or ANOVA using Statistica v12 (StatSoft Inc, USA) Twenty-four hour BPA exposure increased il18 in GT1-7 cells (C=1.0±0.04, BPA=1.2±0.1, T-test p<0.05, n=7), whereas neither BP2 nor BP3 had an effect on il18 expression (ANOVA: ns, n=7). When il6 was analyzed, 24-hour BPA decreased its expression relative to C and to 12-hour BPA, whereas BP3 had a dual effect depending on the time-point analyzed, increasing the expression at 12-hour stimulation and decreasing it after 24-hour stimulation (DMSO-12h=0.82±0.08, DMSO-24h= 1.01±0.13, BPA-12h=1.00±0.11, BPA-24h=0.68±0.06, BP2-12h=0.75±0.12, BP2-24h=0.82±0.18, BP3-12h=1.20±0.10, BP3-24h=0.83±0.05; Repeated Measures Two-way ANOVA: BPA-24h different from DMSO-24h and BPA-12h p<0.05, BP3-12h different from DMSO-12h and from BP3-24h p<0.05, n=4). In the hypothalami, 6-hour BPA exposure increased gfap gene expression (C=0.8±0.2, BPA=1.7±0.4; T-test p<0.05, n=9), whereas neither BP2 nor BP3 had any significant effect (C=0.8±0.2, BP2=1.4±0.3, BP3=1.0±0.3, ANOVA ns, n=9). There was no significant change in il18, il6 or il1b gene expression in whole hypothalami with any of the EDC tested (ANOVA ns). Our results show that the EDC herein studied have the potential to alter the inflammatory state of mature GnRH neurons and to activate astrocytes in the hypothalamus. The pattern for cytokine expression in the whole tissue could be different from the one observed in GnRH neurons, as the hypothalamus contain multiple cell types, and effects can be different in the different cells. More experiments are needed to dissect the mechanisms involved in the effects observed. Funding: CONICET, ANPCyT, UBA, International Society for Neurochemistry, Asoc. ORT Arg., Fund. R. Barón, Fund. Williams.

Reflections on motherhood and the impact of COVID 19 pandemic on women's scientific careers.

I am writing this piece in a bit of an impulse. It has been several months now since life was normal. I used to have childcare support and I could often go outside to work, to run errands or for any other reason. Now, my two-year-old daughter wakes me up at about 6:30 AM and I play with her until lunchtime. She takes a two-hour nap in the afternoon, a period I use for remote work meetings. When she wakes up, I stay with her until around 7:00 PM. Then it is TV and dinnertime for her and work time for me again. She typically goes to bed at 8:30 PM, and I stay in her room until about 9:30 PM. At that point, I am exhausted. I can rarely work at that time. I have been in self-isolation at home with my elderly mother, who is at high risk for SARS-CoV-2 infection. Of course, it does not help that I no longer can count on external childcare and that in my country the response to COVID-19 has been the second worst in the world, with potential to become the worst soon.

Construction and reconstruction of brain circuits: normal and pathological axon guidance.

Perception of our environment entirely depends on the close interaction between the central and peripheral nervous system. In order to communicate each other, both systems must develop in parallel and in coordination. During development, axonal projections from the CNS as well as the PNS must extend over large distances to reach their appropriate target cells. To do so, they read and follow a series of axon guidance molecules. Interestingly, while these molecules play critical roles in guiding developing axons, they have also been shown to be critical in other major neurodevelopmental processes, such as the migration of cortical progenitors. Currently, a major hurdle for brain repair after injury or neurodegeneration is the absence of axonal regeneration in the mammalian CNS. By contrasts, PNS axons can regenerate. Many hypotheses have been put forward to explain this paradox but recent studies suggest that hacking neurodevelopmental mechanisms may be the key to promote CNS regeneration. Here we provide a seminar report written by trainees attending the second Flagship school held in Alpbach, Austria in September 2018 organized by the International Society for Neurochemistry (ISN) together with the Journal of Neurochemistry (JCN). This advanced school has brought together leaders in the fields of neurodevelopment and regeneration in order to discuss major keystones and future challenges in these respective fields.

The origins and early history of neurochemistry and its societies.

At the 2017 joint meeting of the International Society for Neurochemistry (ISN) and the European Society for Neurochemistry, 150years of neurochemistry - the 50th anniversary of ISN, 40years of European Society for Neurochemistry, and 60years of the Journal of Neurochemistry (JNC) - was celebrated with a historical symposium that explored the foundations of neurochemical societies, key international figures in the discipline of neurochemistry, and the pre-eminent role of the JNC. The foundations of neurochemistry were laid in Europe, notably France and Germany, in the late 18th and early 19th centuries. Neurochemists in the United Kingdom made globally relevant contributions before and after the Second World War, and Swedish contributions were especially prominent in the 1950s and 1960s. As neurochemistry is a truly international branch of neuroscience, the important contributions of neurochemists in the Americas and the Asia-Pacific were also recognized, as were the seminal roles of the American, Asia-Pacific, and Japanese Societies of Neurochemistry. Although ISN was only formed in 1967, earlier international meetings in Europe and the Americas reflected the growing recognition of the importance of chemistry and biochemistry for understanding and responding to the pathophysiology of clinical conditions and diseases of the central and peripheral nervous systems. JNC was first published in 1956, but the ISN only assumed complete ownership of the journal under tempestuous circumstances in 1970. The ISN-JNC interface and the sterling work of the JNC Editors has meant that the income generated by the journal has allowed the ISN Council to implement diverse programs for supporting neurochemistry internationally, including sustaining regional neurochemical societies, and supporting neurochemists in the developing world and schools of neurochemistry.

Preface: The energetic brain - a review from students to students.

This Review article 'The energetic brain - A review from students to students' has been written by a group of students following the 14th International Society for Neurochemistry Advanced School held in 2018. Comprehensively written by students for students, it provides both an excellent educational opportunity and a state-of-the-art insight into the field of brain energy metabolism specifically targeted to young researchers, fulfilling an important aspect of the International Society for Neurochemistry's educational mission. The current Review continues a series of similar student-authored articles that Journal of Neurochemistry has published since 2016.

MON-031 In Vitro Exposure to Bisphenol A, Benzophenones 2 or 3, Have Different Effects on GnRH Gene Expression and Secretion in Mature and Immature GnRH Neurons

Bisphenol A, (BPA), a component of polycarbonate plastics, and Benzophenones (BPs), UV filters, are endocrine disrupting chemicals (EDC). Previously we showed that the in vitro exposure to BPA decreased Kiss-induced GnRH expression in GN11 cells (Dr. Susan Wray, NIH), immature GnRH neurons (1). In this study, we analyzed the in vitro effects of BPA, BP2 and BP3 (1x10-9M), or medium as control (C) in mature GnRH neurons (GT1-7 cells, donated by Dr Pamela Mellon, UCSD, USA, and isolated hypothalami from adult Balb/c males). Effects of BP2 and BP3 (1x10-9M) were also analyzed in GN11 cells. We exposed the cell lines for 24 h and the hypothalami for 6 h to the EDC. GT1-7 and GN11 cells were further incubated with Kiss (1x10-9M, Phoenix Pharmaceuticals, Inc, CA, USA) for 4 h to analyze gene expression (qPCR) and for 1 h to analyze GnRH secretion (RIA). Hypothalami exposed to BPA showed increased GnRH expression compared to C (Relative expression: C:1.0±0.2; BPA:2.2±0.5; Student T-test: BPA vs C p<0.05, n=9), whereas neither BP2 nor BP3 had any effect (ANOVA: ns). There was no effect on GnRH secretion (ANOVA: ns). GT1-7 cells exposed to C showed Kiss-induced GnRH gene expression, while the exposure to the EDC abolished this response (Relative expression: C-Basal:1.0±0.1, C-Kiss:1.6±0.3, BPA-Basal:1.3±0.2, BPA-Kiss:1.1±0.2, BP2-Basal:1.2±0.1, BP2-Kiss:1.4±0.2, BP3-Basal:1.3±0.3, BP3-Kiss:1.1±0.2; Repeated measures Two-way ANOVA: Interaction p<0.05, n=6). There was no difference in Kiss-stimulated GnRH release in EDC-exposed cells vs C-exposed cells (Repeated measures Two-way ANOVA: Interaction ns; Main Effect: Time of Kiss exposure: p<0.01, n=7). In GN11 cells, exposure to BP2 inhibited Kiss-induced GnRH gene expression, whereas there was no such effect in cells exposed to BP3 (Relative Expression: C-Basal:1.1±0.02, C-Kiss:1.3±0.1, BP2-Basal:1.2±0.1, BP2-Kiss:1.0±0.1, BP3-Basal:1.0±0.1, BP3-Kiss:1.3±0.1; Repeated measures Two-way ANOVA: Interaction p<0.01, n=8). Exposure to BP3 significantly increased GnRH secretion and abolished the response to Kiss, whereas BP2 significantly decreased Kiss-stimulated release [GnRH (pg/ml): C-Basal: 8.5±1.3, C-Kiss: 32.9±8.8, BP2-Basal: 16.5±4.9, BP2-Kiss: 16.9±5.1, BP3-Basal: 18.0±3.2, BP3-Kiss: 20.8±5.6, Repeated measures Two-way ANOVA: Interaction p<0.05; C-Kiss vs C-Basal, BP3-Basal vs C-Basal, BP2-Kiss vs C-Kiss p<0.05, n=9]. Our results show that EDC exposure alters the physiology of mature and immature GnRH neurons, although effects are different in the two cell lines, and they also differ in mature GnRH neurons vs hypothalamus. Further studies are needed to dissect the mechanisms involved. 1- Endoc. Rev. 38(3S), SAT-256, 2017. Nothing to disclose. Funding: CONICET, ANPCyT, UBA, International Society for Neurochemistry, Asoc. ORT Arg., Fund. R. Barón, Fund. Williams.

Notes on the Recent History of Neuroscience in Africa.

Neuroscience began with neuroanatomy and neurosurgery in Egypt more than 5000 years ago. Knowledge grew over time and specialized neurosurgery centers were established in north Africa in the eleventh century. However, it was not until the twentieth century that neuroscience research became established in sub-Saharan Africa. In most African countries, clinical research focused on understanding the rationale and improving treatment of epilepsy, infections, nutritional neuropathies, stroke and tumors. Significant advances were made. In the twenty-first century, African knowledge expanded to include all branches of neuroscience, contributing to genetic, biochemical and inflammatory determinants of brain disorders. A major focus of basic neuroscience research has been, and is, investigation of plant extracts, drugs and stress in animal models, providing insight and identifying potential novel therapies. A significant event in the history of African neuroscience was the founding of the Society of Neuroscientists of Africa (SONA) in 1993. The International Brain Research Organization (IBRO) supported SONA conferences, as well as workshops and neuroscience training schools in Africa. Thanks to their investment, as well as that of funding agencies, such as the National Institutes of Health (NIH), International Society for Neurochemistry (ISN), World Federation of Neurosurgical Societies (WFNS), World Federation of Neurology (WFN) and the International League Against Epilepsy (ILAE), neuroscience research is well-established in Africa today. However, in order to continue to develop, African neuroscience needs continued international support and African neuroscientists need to engage in policy and decision-making to persuade governments to fund studies that address the unique regional needs in Africa.

Issue Cover (September 2017)

Front cover: This review originated from the first International Society for Neurochemistry (ISN) and Journal of Neurochemistry (JNC) Flagship School held in Alpbach, Austria (Sep 2016), and uses its curriculum and discussions as a framework to review some of the current knowledge in the field of synaptic plasticity. The cover image depicts the pathways and mediators of synapse-to-nucleus communication and local proteostasis in synaptic plasticity. 1. Long-term potentiation (LTP) induces a cascade of events via increased Ca2+ levels and glutamate receptor activity. This, in turn, leads to proteasomal protein turnover and hence synaptic plasticity. The elevated Ca2+ levels also lead to increased CREB-dependent transcription of LTP-enhancing genes and their local synaptic translation. 2. Conversely, long-term depression (LTD) leads to decreased Ca2+ influx through glutamate receptors, LTD-dependent transcription in turn reducing pro-LTP gene expression. Read the full article ‘The malleable brain: plasticity of neural circuits and behavior – a review from students to students’ by N. Schaefer, C. Rotermund, E.-M. Blumrich, M. V. Lourenco, P. Joshi, R. U. Hegemann, S. Jamwal, N. Ali, E. M. García Romero, S. Sharma, S. Ghosh, J. K. Sinha, H. Loke, V. Jain, K. Lepeta, A. Salamian, M. Sharma, M. Golpich, K. Nawrotek, R. K. Paidi, S. M. Shahidzadeh, T. Piermartiri, E. Amini, V. Pastor, Y. Wilson, P. A. Adeniyi, A. K. Datusalia, B. Vafadari, V. Saini, E. Suárez-Pozos, N. Kushwah, P. Fontanet and A. J. Turner (J. Neurochem. 2017, vol. 142 (6), pp. 790–811) on doi: 10.1111/jnc.14107

The malleable brain: plasticity of neural circuits and behavior - a review from students to students.

One of the most intriguing features of the brain is its ability to be malleable, allowing it to adapt continually to changes in the environment. Specific neuronal activity patterns drive long-lasting increases or decreases in the strength of synaptic connections, referred to as long-term potentiation and long-term depression, respectively. Such phenomena have been described in a variety of model organisms, which are used to study molecular, structural, and functional aspects of synaptic plasticity. This review originated from the first International Society for Neurochemistry (ISN) and Journal of Neurochemistry (JNC) Flagship School held in Alpbach, Austria (Sep 2016), and will use its curriculum and discussions as a framework to review some of the current knowledge in the field of synaptic plasticity. First, we describe the role of plasticity during development and the persistent changes of neural circuitry occurring when sensory input is altered during critical developmental stages. We then outline the signaling cascades resulting in the synthesis of new plasticity-related proteins, which ultimately enable sustained changes in synaptic strength. Going beyond the traditional understanding of synaptic plasticity conceptualized by long-term potentiation and long-term depression, we discuss system-wide modifications and recently unveiled homeostatic mechanisms, such as synaptic scaling. Finally, we describe the neural circuits and synaptic plasticity mechanisms driving associative memory and motor learning. Evidence summarized in this review provides a current view of synaptic plasticity in its various forms, offers new insights into the underlying mechanisms and behavioral relevance, and provides directions for future research in the field of synaptic plasticity. Read the Editorial Highlight for this article on page 788. Cover Image for this issue: doi: 10.1111/jnc.13815.

The malleable brain - An educational review from students to students.

The Review "The malleable brain: plasticity of neural circuits and behavior - A review from students to students" has been written by a group of students following the International Society for Neurochemistry and Journal of Neurochemistry Flagship School. Comprehensively written by students for students, it provides both an excellent educational opportunity and a state-of-the-art insight into the field of neuronal plasticity specifically targeted to young researchers, and thus fulfills an important aspect of the ISN's educational mission. Read the highlighted article 'The malleable brain: plasticity of neural circuits and behavior - a review from students to students' on page 790.

Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students.

Synapses are essential components of neurons and allow information to travel coordinately throughout the nervous system to adjust behavior to environmental stimuli and to control body functions, memories, and emotions. Thus, optimal synaptic communication is required for proper brain physiology, and slight perturbations of synapse function can lead to brain disorders. In fact, increasing evidence has demonstrated the relevance of synapse dysfunction as a major determinant of many neurological diseases. This notion has led to the concept of synaptopathies as brain diseases with synapse defects as shared pathogenic features. In this review, which was initiated at the 13th International Society for Neurochemistry Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental disorders (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer and Parkinson disease). We finally discuss the appropriateness and potential implications of gathering synapse diseases under a single term. Understanding common causes and intrinsic differences in disease‐associated synaptic dysfunction could offer novel clues toward synapse‐based therapeutic intervention for neurological and neuropsychiatric disorders. In this Review, which was initiated at the 13th International Society for Neurochemistry (ISN) Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer's and Parkinson's diseases), gathered together under the term of synaptopathies.Read the Editorial Highlight for this article on page 783.

A Learned Society's Perspective on Publishing.

Scientific journals that are owned by a learned society, like the Journal of Neurochemistry (JNC), which is owned by the International Society for Neurochemistry (ISN), benefit the scientific community in that a large proportion of the income is returned to support the scientific mission of the Society. The income generated by the JNC enables the ISN to organize conferences as a platform for members and non-members alike to share their research, supporting researchers particularly in developing countries by travel grants and other funds, and promoting education in student schools. These direct benefits and initiatives for ISN members and non-members distinguish a society journal from pure commerce. However, the world of scholarly publishing is changing rapidly. Open access models have challenged the business model of traditional journal subscription and hence provided free access to publicly funded scientific research. In these models, the manuscript authors pay a publication cost after peer review and acceptance of the manuscript. Over the last decade, numerous new open access journals have been launched and traditional subscription journals have started to offer open access (hybrid journals). However, open access journals follow the general scheme that, of all participating parties, the publisher receives the highest financial benefit. The income is generated by researchers whose positions and research are mostly financed by taxpayers' or funders' money, and by reviewers and editors, who frequently are not reimbursed. Last but not least, the authors pay for the publication of their work after a rigorous and sometimes painful review process. JNC itself has an open access option, at a significantly reduced cost for Society members as an additional benefit. This article provides first-hand insights from two former Editors-in-Chief, Kunihiko Suzuki and Leslie Iversen, about the history of JNC's ownership and about the difficulties and battles fought along the way to its current success and reputation. Scientific journals that are owned by a learned society, like the Journal of Neurochemistry (JNC) which is owned by the International Society for Neurochemistry (ISN), benefit the scientific community in that a large proportion of the income is returned to support the scientific mission of the Society. The income generated by the JNC enables the ISN to organize conferences as a platform for members and non-members alike to share their research, supporting researchers particularly in developing countries by travel grants and other funds, and to promote education in student schools. These direct benefits and initiatives for ISN members and non-members distinguish a society journal from pure commerce. However, the world of scholarly publishing is changing rapidly. Open access models have challenged the business model of traditional journal subscription and hence provide free access to publicly funded scientific research. In these models, the manuscript authors pay a publication cost after peer review and acceptance of the manuscript. Over the last decade, numerous new open access journals have been launched and traditional subscription journals have started to offer open access (hybrid journals). However, open access journals pertain to the general scheme that, of all participating parties, the publisher receives the highest financial benefit. The income is generated by researchers whose positions and research are mostly financed by tax payers' or funders' money, reviewers and editors, who frequently are not reimbursed. Last but not least, the authors pay for the publication of their work after a rigorous and sometimes painful review process. JNC itself has an open access option, at a significantly reduced cost for Society members as an additional benefit. This article provides first-hand insights from a long-standing Editor-in-Chief, Kunihiko Suzuki, about the history of JNC's ownership and about difficulties and battles fought on the way to its current success and reputation today. This article is part of the60th Anniversary special issue.