Diagrams and diaries. How neural modeling of language acquisition took off

Date and Time: Thursday 12 April, 4.30 pm
Location: Faculty of Social and Behavioural Sciences, Pieter de la Court gebouw, Wassenaarseweg 52, 2333 AK  Leiden, room SB45
Abstract:  Charles Darwin boosted the study of language acquisition in 1877 by publishing the diary he had kept of his son William's first speech between 1839 and 1841. Three years earlier, Carl Wernicke had brilliantly published his neuropsychological diagrams of the language network in the brain. Such diagram making soon became an industry. Physiologist William Preyer absorbed both developments, the diary approach to early language acquisition and neuropsychological diagram making. In 1881 he published his classical Die Seele des Kindes, in which both approaches were combined in the construction of the very first neuropsychological model of language acquisition. In this lecture I will go back to the two historical roots of these developments. They are, first, the chain of discoveries about language in the brain, leading from Franz Joseph Gall too the so-called "diagram makers" and, second, the scattered pedagogical efforts to keep diaries of early cognitive development, which had been triggered by Jean-Jacques Rousseau.
 

Consciousness: The radical plasticity thesis

Date and Time: Thursday 15 March 2012, 4.30 pm
Location: Faculty of Social and Behavioural Sciences, Pieter de la Court gebouw, Wassenaarseweg 52, 2333 AK Leiden, room SB45
Abstract: Here, I explore the idea that consciousness is something that the brain learns to do rather than an intrinsic property of certain neural states and not others. Starting from the idea that neural activity is inherently unconscious, the question thus becomes: How does the brain learn to be conscious? I suggest that consciousness arises as a result of the brain's continuous attempts at predicting not only the consequences of its actions on the world and on other agents, but also the consequences of activity in one cerebral region on activity in other regions. By this account, the brain continuously and unconsciously  learns to redescribe its own activity to itself, so developing systems of meta-representations that characterise and qualify the target first-order representations. Such learned redescriptions, enriched by the emotional value associated with them,  form the basis of conscious experience. Learning and plasticity are thus central to consciousness, to the extent that experiences only occur in experiencers that have learned to know they possess certain first-order states and that have learned to care more about certain states than about others. This is what I call the ³Radical Plasticity Thesis². In a sense thus, this is the enactive perspective, but turned both inwards and
(further) outwards. Consciousness involves ³signal detection on the mind²; the mind is the brain's (non-conceptual, implicit) theory about itself. I illustrate these ideas through neural network models that simulate the relationships between performance and awareness in different tasks.

The clock in our brain: circadian rhythms, aging and Alzheimer's disease

Date and Time: Monday 6 February 2012, 5.00 pm
Location: Faculty of Social and Behavioural Sciences, Pieter de la Court gebouw, Wassenaarseweg 52, 2333 AK  Leiden, room SC01
Abstract: Our brain produces biological rhythms of about a year, a month, a week and a day that are important for survival of the individual and the species. An age-related decrease in circadian modulation has been observed in many rhythms. Elderly people start napping during the day and often complain of disturbed sleep during the night. In Alzheimer's disease (AD), this fragmented sleep–wake pattern is even more pronounced. In aging, and even more so in AD, a marked reduction in vasopressin, the main neuropeptide was found in the biological clock of the brain, the suprachiasmatic nucleus (SCN). We have tried a number of strategies designed to stimulate the circadian timing system in order to enhance the functionality of the clock.
Increased input to the circadian timing system can be effectuated by bright environmental light, peripheral nerve stimulation, melatonin and increased levels of physical activity. We demonstrated that the decreased amplitude of the circadian sleep–wake pattern in old rats could be restored to the level of young rats by increasing the intensity of daytime environmental light, and that such increased light-input counteracted the age-related decrease in the number of AVP neurons in the SCN. In humans, we found that additional bright light, fitness training, repeated transcutaneous electric nerve stimulation (TENS) and melatonin improved the coupling of rest–activity rhythms to stable environmental cues (so-called Zeitgebers). The SCN coordinates also the peripheral clocks in the body, including the pineal clock that receives SCN input via a multisynaptic noradrenergic pathway. Rhythmic pineal melatonin production is disrupted already early in AD, probably secondary to a functional disruption of the SCN.  In order to determine whether the progression of symptoms may be ameliorated by long-term application of the two major synchronizers of the circadian timing system: bright light and melatonin, a long-term, double-blind, placebo controlled, randomized trial was performed with 189 residents from which 87% had dementia. The interventions were randomly assigned to long-term daily treatment with whole day bright (±1000 lx) or dim (±300 lx) light, plus evening melatonin (2.5 mg) or placebo for a maximum period of 3.5 years. Light attenuated cognitive deterioration by 3 points on the MMSE test, it addition, it ameliorated depressive symptoms and the increase in functional limitations over time. Melatonin shortened sleep onset latency and increased sleep duration, although it adversely affected mood. Combined treatment of light and melatonin also attenuated aggressive behavior, increased sleep efficiency, and improved nocturnal restlessness. To counteract the adverse effect of melatonin on mood, it is recommended only in combination with light. The anatomical and functional findings from the reported studies indicate that the SCN retains considerable plasticity in healthy and demented older individuals. The reactivation of the SCN is, of course, not a therapy for AD, it is rather a therapy for the SCN. However, it is also a proof of principle which shows that even if neurons are affected by AD, they can still be reactivated if the right stimuli are applied. Therefore, the SCN appears to be a suitable structure to illustrate the potentials of our ‘use it or lose it’ concept, besides its clinical relevance of manipulating circadian rhythms.
 

Perception and action
Exploring representational underpinnings of Action Simulation

Date and Time: 10 november 2011, 4.30 pm
Location: Faculty of Social and Behavioural Sciences, Pieter de la Court gebouw, Wassenaarseweg 52, 2333 AK  Leiden, room SB45
Abstract: In this talk I discuss experimental evidence concerning the perception of occluded action and the putative role of simulation (of unseen action) as a substitute of perception (of unseen action). Experiments address four major issues: transition from perception to simulation, time course of simulation, competition between true and pseudo-simulation, and motor contributions to simulation. In the upshot I conclude that short-term simulation may be grounded in processes subserving top-down control of action prediction and production.

Imaging the effects of antidepressant treatment in patients with major depression

The Literate Brain; Reading: Cognitive processes and neural pathways

Stress, genes and memory

Neural signatures of word production

The human reward system: some basic findings and clinical implications