Society For Neuroscience 2014
Report by Haley Peckham
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In 1969, the Committee of Brain Sciences in the US wanted to set up a formal society for scientists studying the brain with a goal to “help direct attention to the importance of neurosciences for the future intellectual and emotional well-being of this country”. After some considerable discussion about a name, The Society for Neuroscience was born, having at its heart three missions: “1) To advance understanding of nervous systems and their role in behaviour; 2) To promote education in the neurosciences; 3) To inform the general public on results and implications of current research”. For the last 44 years, the annual meeting of the Society has been reliably delivering on these goals for increasingly large numbers of attendees.
The first Society for Neuroscience (SfN) meeting was held in Washington, DC, in October 1971 and attracted 1,396 attendees. This year, also in Washington, DC, the 44th SfN had 30,056 registrants by 5 p.m. on the first day of the conference, and featured an overwhelming 15,000 presentations by neuroscientists and 854 poster topics (each home to 10–25 posters) over five days. Happily, SfN also provided an app which, in lieu of a Dr Who-style Tardis, was the only way to personalise and efficiently organise a schedule between concurrently running lectures, symposia and poster sessions.
As the SfN is geared towards sharing cutting-edge neuroscience with other scientists, any non-neuroscientist—or even a neuroscientist from a different field—would likely be out of their depth looking at the posters, but the lectures, presented by outstanding leaders in their fields, and the symposia, usually presented by experienced lab-heads, offer a clarifying view of the relevant and interesting findings in the field and their implications for treatments or future research.
Psychotherapists may have found the Albert and Ellen Grass lecture, “Cellular and Molecular Mechanisms of Explicit Learning in the Hippocampus”, an extremely helpful introduction to the critical elements required for induction of LTP, the accepted cellular model of learning and memory first described by Tim Bliss and Terje Lømo in 1972.
Roger Nicoll from the University of California in his lecture pared the elements involved in (early) LTP down to the absolutely necessary NMDA receptor activation, consequent activation of the calcium-dependent enzyme calmodulin kinase II (CaMKII), and the recruitment of AMPA receptors to the synapse. The NMDA receptor is a coincidence detector, detecting information from both the presynaptic cell (glutamate) and the postsynaptic cell (depolarisation), and only opening to allow influx of calcium ions to the postsynaptic neuron if those two conditions are simultaneously met. Firstly, depolarisation of the postsynaptic membrane must be sufficient to remove the magnesium ion block from the NMDA channel; secondly, the glutamate released following depolarisation of the presynaptic cell must bind to the NMDA receptor; finally, the channel opens so that ions including calcium will flow in, activating the CaMKII enzyme. This enzyme phosphorylates a store of AMPA receptors that are trafficked to the membrane and also open in response to glutamate binding, letting more calcium ions into the postsynaptic cell and initiating further signalling events that drive late LTP events such as protein synthesis which modify the strength of the synapse.
Happily, the Presidential Special Lecture, “The Living Record of Memory: Genes, Neurons and Synapses”, given by Kelsey Martin (UCLA, who studied with Eric Kandel), also focused on mechanisms of LTP. The lecture addressed the question of how neurons that have one nucleus but make many synapses can selectively strengthen stimulated synapses. The late LTP formation that requires both transcription (DNA to mRNA) and translation (mRNA to protein) has to be specific to a stimulated synapse and not apply to every synapse formed by the neuron. The take-home message of the lecture was that gene expression within the neuron is decentralised. The nucleus sets the tone of readiness for all synapses, and mRNA transcribed from genes in the nucleus is transported throughout the neuronal arbour, poised for a local signal from a stimulated synapse to drive local mRNA translation into protein. The calcium influx from early LTP at a particular synapse activates Netrin1, which drives translation of mRNA into the proteins required at that synapse for induction of late LTP and strengthening of the synapse. Another related question is how the transcription required for late LTP is triggered at the nucleus following synaptic stimulation at a particular synapse up to 50 µm away, and again, the messenger, CREB-regulated transcriptional coactivator 1 (CRTC1) is distributed in its inactive form over the neuronal arbour in readiness for synaptic stimulation. When the synapse is stimulated, the calcium influx drives the immediate translocation of CRTC1 to the nucleus, where it binds CREB, a transcription factor that regulates expression of plasticity-related genes, thus driving the transcription required for late LTP.
Finally, a wonderful symposium, a gift to psychotherapists, entitled Nature, Nurture and Trajectories to Mental Health took place, featuring four 30-minute talks. The first, by Richard Davidson (Psychology and Psychiatry Professor and Founder of the Center for Investigating Healthy Minds at the Waisman Center at the University of Wisconsin–Madison) focused on his Nature Neuroscience paper in 2012, which described a sequence of events in females, beginning with early-life stressors leading to increased cortisol levels, and predicted reduced resting-state functional connectivity between their amygdala and ventro-medial prefrontal cortex some 14 years later. Next, the Director of the Sackler Center for Developmental Psychobiology, BJ Casey, shared her findings on fear extinction learning conducted in both humans and rodents. As might be suspected, teens have heightened sensitivity to threat cues and also heightened emotional reactivity. The behavioural modification programs designed to treat anxiety may sensitise the adolescent further due to their developmentally reduced ability to respond to fear extinction learning. A very refreshing input from Dr. Casey was her evident commitment to finding empowering and therapeutic alternatives to drug treatments for adolescents. Dr. Casey’s group also found evidence that early-life stress in humans leads to hypoactivity in the nucleus accumbens, which correlated with increased depression scores. This could mean that early-life stress leads to premature closing of a developmental window of neuroplasticity in certain circuits or brain regions. This point was elaborated on beautifully by the next speaker, Takao Hensch, who spoke about balancing plasticity and stability across brain development. Essentially, our genes interact with our environment, but there are multiple critical periods throughout development where the window for the brain to be shaped by the environment is open, but after which it shuts. The most obvious example of this is in language development. “Genie”, a survivor of extreme neglect, did not have an environment that allowed her to learn language, and although she was discovered by services at the age of 13, it was too late for her to learn language, as the developmental opportunity window had closed. The critical windows themselves are plastic, and it is inhibitory circuits that orchestrate this brain plasticity. Professor Hensch’s group has manipulated critical windows in the visual system by either reducing or enhancing inhibitory tone through limiting gaba-aminobutyric acid (GABA) protein synthesis or enhancing GABA signalling with the drug diazepam. Knowledge of the critical periods for particular aspects of development will help inform policymakers, as well as those on the front line working with children and families, to help ensure a safe, positive, and rich environmental impact on these beautifully impressionable but vulnerable minds.
I have come away from SfN enriched and exhausted. I would have preferred a Tardis to the app. Too many sessions that I wanted to see I could not. At times, SfN became an incoherent assault on my capacity for concentration; at other times it was a most deliciously complete immersion in the puzzle that holds all of my intellectual and emotional attention. I continue to ask and learn: How can neuroscience supplement and inform the work we do with the troubled and distressed minds of our clients?