2011
, 2011
Modeling associative retrieval from long-term memory
Lecture
Tuesday, December 27, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Modeling associative retrieval from long-term memory
Prof. Misha Tsodyks
Department of Neurobiology, WIS
The question I will address in the lecture is how information is retrieved from memory when there are no precise item-specific cues. Real life examples are when you try to recall the names of your class-mates, or your favorite writers, or places to see in Rome. I hypothesize that in this situation, retrieval occurs in an associative manner, i.e. each recalled item is triggering the retrieval of a subsequent one. Mathematically this problem can be reduced to random graphs, and general results about the retrieval capacity of the recall can be derived. The main conclusion of the analysis is that retrieval capacity is severely limited, such that only a small fraction of items can be recalled, with characteristic power-law scaling with the total number of items in memory. Theoretical results can be compared to free recall experiments and surprisingly good agreement is observed
Modeling associative retrieval from long-term memory
Lecture
Tuesday, December 27, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Modeling associative retrieval from long-term memory
Prof. Misha Tsodyks
Department of Neurobiology, WIS
The question I will address in the lecture is how information is retrieved from memory when there are no precise item-specific cues. Real life examples are when you try to recall the names of your class-mates, or your favorite writers, or places to see in Rome. I hypothesize that in this situation, retrieval occurs in an associative manner, i.e. each recalled item is triggering the retrieval of a subsequent one. Mathematically this problem can be reduced to random graphs, and general results about the retrieval capacity of the recall can be derived. The main conclusion of the analysis is that retrieval capacity is severely limited, such that only a small fraction of items can be recalled, with characteristic power-law scaling with the total number of items in memory. Theoretical results can be compared to free recall experiments and surprisingly good agreement is observed.
Local brain oscillations of sleep and sleepiness
Lecture
Wednesday, December 21, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Local brain oscillations of sleep and sleepiness
Dr. Yuval Nir
Dept of Psychiatry,
University of Wisconsin-Madison
Slow waves and sleep spindles are the two fundamental brain oscillations of NREM sleep, yet they have been mostly studied in vitro, under anesthesia, within few brain regions or with scalp EEG recordings. We examined intracranial depth EEG and single-unit activity recorded simultaneously in up to 12 brain regions in neurosurgical patients to better characterize regional diversity in these sleep oscillations. First, we found changes in spindle occurrence, frequency, and timing between regions and across sleep, reflecting anatomical projections and thalamocortical hyperpolarization levels that change with sleep depth. We further show that both slow waves (and the underlying active and silent neuronal states) and sleep spindles occur mostly locally, thereby showing that constrained intracerebral communication is an important feature of sleep. Next, we confirmed that in freely behaving rats, slow waves and silent periods in sleep likewise occur predominantly locally. Moreover, after a long period of being awake, while both EEG and behavior indicate wakefulness, local populations of neurons go offline, exhibiting "local sleep". We are now exploring whether such local sleep may lead to cognitive consequences, such as lapses of attention, in awake people who are sleep deprived
Another line of research focuses on disconnection from the external environment - conditions in which sensory stimuli fail to be incorporated into our perceptual stream. To this end, we are examining neuronal responses to sounds in rats across spontaneous vigilance states with an emphasis on comparing wakefulness with REM sleep. Responses of individual neurons in primary auditory cortex are comparable in wake and sleep, calling into question the proposal that the thalamus does not relay peripheral signals effectively to the cortex in sleep. Important differences between waking and sleep may lie in how signals propagate across cortical regions and layers.
COGNITIVE DYSFUNCTION AND CHOLINERGIC ALTERATIONS PRIOR TO DOPAMINE LOSS IN MICE OVER-EXPRESSING WILD-TYPE HUMAN ALPHA-SYNUCLEIN
Lecture
Tuesday, December 20, 2011
Hour: 12:15
Location:
Gerhard M.J. Schmidt Lecture Hall
COGNITIVE DYSFUNCTION AND CHOLINERGIC ALTERATIONS PRIOR TO DOPAMINE LOSS IN MICE OVER-EXPRESSING WILD-TYPE HUMAN ALPHA-SYNUCLEIN
Dr. Iddo Magen
Dept of Neurology,
University of California at Los Angeles
Parkinson’s disease (PD) is a characterized, in addition to loss of dopaminergic neurons in the substantia nigra, by loss of cholinergic neurons in the basal nucleus (Zarow et al., 2003) and pathology of alpha-synuclein, a protein implicated in familial PD, in this region concurrently with pathology of alpha-synuclein pathology in the substantia nigra (Braak et al., 2003), as well as decrease in the activity of choline acetyltransferase, the rate limiting enzyme in the synthesis of acetylcholine (Ziabreva et al., 2006). Mild cognitive deficits are also observed in the early stages of PD (Elgh et al., 2009; Mamikonyan et al., 2009). Mice over-expressing the human wild-type alpha-synuclein under the Thy1 promoter (Thy1-aSyn) present progressive sensorimotor and non-motor behavioral abnormalities reminiscent of the pre-manifest early stages of PD (Magen and Chesselet, ’10) and subsequently exhibit a loss of striatal DA (Lam et al. ’11). We now examined whether these mice also exhibit cognitive deficits in tests sensitive to cholinergic function, and whether they present cholinergic deficits.
Thy1-aSyn mice on a mixed C57BL/6-DBA/2 background presented spatial working memory deficits in the Y-maze which showed progression from 3-4 to 5-6 months and to 7-9 months. Thy1-aSyn mice also showed spatial memory deficits in the novel place recognition test and recognition memory deficits in the novel object recognition test at 4-5 months of age. In a reversal learning task at 4-5 months, Thy1-aSyn mice learned the initial contingency rule as equally well as WT littermates, but were impaired in learning a reversal of this rule, mirroring the cognitive inflexibility displayed by early PD patients in similar tasks. Expression of both proteinase-K resistant and non-resistant alpha-synuclein in the medial septum and the basal nucleus, two major regions of cholinergic input into the forebrain, was increased in Thy1-aSyn mice at 5 months of age, and cholinergic neurons in both regions expressed both human and mouse alpha-synuclein in Thy1-aSyn mice, while endogenous (murine) alpha-synuclein expression was either lower or absent in cholinergic neurons in WT mice. However, morphological features of the cholinergic neurons such as cell body diameter did not change in either the basal nucleus or the septum. Acetylcholine levels decreased by 30% in the cortex of Thy1-aSyn mice at 6 months, further suggesting a link between acetylcholine pathology and the cognitive deficits.
Our data indicate that Thy1-aSyn mice display cognitive dysfunction at an early age, which is associated with decreased acetylcholine levels. As the cognitive tests used are sensitive to cholinergic function (Barker et al., 2008; Yang et al., 2009; Botton et al., 2010), future pharmacological studies will attempt to reverse these deficits using cholinergic agonists and/or acetylcholinesterase inhibitors. A study with an acute nicotine treatment is to be performed soon, to determine whether nicotine can reverse the cognitive deficits, which might point to a causal relation between the cognitive deficits and the compromised cholinergic system. In addition, the cognitive phenotype faithfully reproduces the early cognitive deficits in PD, whereas the lack of any neuropathology in cholinergic neurons suggests that the Thy1-aSyn models mild cognitive deficits rather than dementia, which is mostly associated with a gross neuropathology. Thus, it can serve as a basis for the testing of cognitive enhancers other than cholinergic agents.
Natural Vision Improvement
Lecture
Monday, December 19, 2011
Hour: 11:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Natural Vision Improvement
Meir Schneider
School for Self-Healing
San Francisco, CA
Toward a scientific understanding of subjective experience:an open discussion
Lecture
Thursday, December 15, 2011
Hour: 14:30
Location:
Camelia Botnar Building
Toward a scientific understanding of subjective experience:an open discussion
Prof. Giulio Tononi
Dept of Psychiatry,
University of Wisconsin
An integrated information theory of consciousness
Lecture
Wednesday, December 14, 2011
Hour: 14:30
Location:
Dolfi and Lola Ebner Auditorium
An integrated information theory of consciousness
Prof. Giulio Tononi
Department of Psychiatry
University of Wisconsin
Over the past decades, studies have investigated the neural correlates of consciousness with increasing precision. However, why experience is generated by the cortex and not the cerebellum, why it fades during certain stages of sleep and returns in others, or why some cortical areas endow experience with colors and others with sound, remains unexplained. Moreover, key questions remain unanswered. For example, how much consciousness is there when only a few brain 'islands' remain active? How much during sleepwalking or psychomotor seizures? Are newborns conscious, and to what extent?
Are animals conscious, how much, and in which way? Can a conscious machine be built? To address such questions, empirical observations need to be complemented by a principled theoretical approach. The information integration theory (IIT) has several related aims: to characterize, starting from phenomenology, what consciousness is and how each experience is structured; to account for several neurobiological observations about its neural substrate; and to develop measures of consciousness that can be applied, at least in principles, to humans, animals, and machines.
Automated In-vivo Phenotyping of Rodents – Towards PhenoWorld
Lecture
Wednesday, December 7, 2011
Hour: 12:15
Location:
Nella and Leon Benoziyo Building for Brain Research
Automated In-vivo Phenotyping of Rodents – Towards PhenoWorld
Dr. Walter Förster
TSE Systems International Group
Sculpting the mature nervous system:Nuclear receptors shape connections by controlling degeneration and regeneration during development
Lecture
Tuesday, December 6, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Sculpting the mature nervous system:Nuclear receptors shape connections by controlling degeneration and regeneration during development
Prof. Oren Schuldiner
Dept of Molecular Cell Biology, WIS
Adult neurons in the CNS undergo little or no regeneration following insults such as spinal cord injury. Their inability to regenerate results from both non-cell autonomous negative signals as well as from reduced internal growth capabilities. In contrast, developing neurons are capable of extensive growth, extension and reorganization. However, it has long been challenged whether growth events during development resemble the regenerative process following injury. In my talk I will present unpublished data regarding a new pathway that we discovered, consisting of a nuclear receptor complex regulating the mTor kinase, as crucial for a regenerative process during neuronal remodeling of the Drosophila mushroom body (MB) neurons. Importantly, these nuclear receptors are not important for the initial growth of these or other types of neurons. Therefore, we discovered a pathway that is selectively required for regeneration during development. I will also provide evidence that the worm ortholog of Hr51, one of the nuclear receptors we identified, is required for injury induced regeneration following axotomy. Therefore, our data uncover a novel pathway regulating regeneration during development and following injury and suggest that developmental and injury induced axon regeneration share molecular similarities.
Odor coding in awake mice
Lecture
Thursday, December 1, 2011
Hour: 12:15
Location:
Gerhard M.J. Schmidt Lecture Hall
Odor coding in awake mice
Dr. Roman Shusterman
Janelia Farm Research Campus, HHMI
Olfaction is traditionally considered a ‘slow’ sense, but recent evidence demonstrates that rodents are capable of making extremely difficult odor discriminations rapidly, in as little as a single sniff. To understand the temporal aspects of olfactory information processing, we studied how sniffing shapes the responses of mitral/tufted cells in awake mice. We found that odorants evoked precisely sniff-locked activity in mitral/tufted (M/T) cells in the olfactory bulb of awake mouse. The trial- to-trial response jitter averaged 12 ms, a precision comparable to other sensory systems. Individual cells expressed odor-specific temporal patterns of activity and responses were more tightly time-locked to the sniff phase than to the time after inhalation onset. Precise locking to sniff phase may facilitate ensemble coding by making synchrony relationships across neurons robust to variation in sniff rate. Additional feature that olfactory system should encode is odor intensity. Psychophysical experiments in humans demonstrate that perceived odor intensity falls rapidly with repeated sampling. Changes in perceived intensity can also be due to changes in odor concentration. We show that activity of M/T cells is a neural corelate of psychophysical phenomena.
Pages
2011
, 2011
Modeling associative retrieval from long-term memory
Lecture
Tuesday, December 27, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Modeling associative retrieval from long-term memory
Prof. Misha Tsodyks
Department of Neurobiology, WIS
The question I will address in the lecture is how information is retrieved from memory when there are no precise item-specific cues. Real life examples are when you try to recall the names of your class-mates, or your favorite writers, or places to see in Rome. I hypothesize that in this situation, retrieval occurs in an associative manner, i.e. each recalled item is triggering the retrieval of a subsequent one. Mathematically this problem can be reduced to random graphs, and general results about the retrieval capacity of the recall can be derived. The main conclusion of the analysis is that retrieval capacity is severely limited, such that only a small fraction of items can be recalled, with characteristic power-law scaling with the total number of items in memory. Theoretical results can be compared to free recall experiments and surprisingly good agreement is observed.
Modeling associative retrieval from long-term memory
Lecture
Tuesday, December 27, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Modeling associative retrieval from long-term memory
Prof. Misha Tsodyks
Department of Neurobiology, WIS
The question I will address in the lecture is how information is retrieved from memory when there are no precise item-specific cues. Real life examples are when you try to recall the names of your class-mates, or your favorite writers, or places to see in Rome. I hypothesize that in this situation, retrieval occurs in an associative manner, i.e. each recalled item is triggering the retrieval of a subsequent one. Mathematically this problem can be reduced to random graphs, and general results about the retrieval capacity of the recall can be derived. The main conclusion of the analysis is that retrieval capacity is severely limited, such that only a small fraction of items can be recalled, with characteristic power-law scaling with the total number of items in memory. Theoretical results can be compared to free recall experiments and surprisingly good agreement is observed
Local brain oscillations of sleep and sleepiness
Lecture
Wednesday, December 21, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Local brain oscillations of sleep and sleepiness
Dr. Yuval Nir
Dept of Psychiatry,
University of Wisconsin-Madison
Slow waves and sleep spindles are the two fundamental brain oscillations of NREM sleep, yet they have been mostly studied in vitro, under anesthesia, within few brain regions or with scalp EEG recordings. We examined intracranial depth EEG and single-unit activity recorded simultaneously in up to 12 brain regions in neurosurgical patients to better characterize regional diversity in these sleep oscillations. First, we found changes in spindle occurrence, frequency, and timing between regions and across sleep, reflecting anatomical projections and thalamocortical hyperpolarization levels that change with sleep depth. We further show that both slow waves (and the underlying active and silent neuronal states) and sleep spindles occur mostly locally, thereby showing that constrained intracerebral communication is an important feature of sleep. Next, we confirmed that in freely behaving rats, slow waves and silent periods in sleep likewise occur predominantly locally. Moreover, after a long period of being awake, while both EEG and behavior indicate wakefulness, local populations of neurons go offline, exhibiting "local sleep". We are now exploring whether such local sleep may lead to cognitive consequences, such as lapses of attention, in awake people who are sleep deprived
Another line of research focuses on disconnection from the external environment - conditions in which sensory stimuli fail to be incorporated into our perceptual stream. To this end, we are examining neuronal responses to sounds in rats across spontaneous vigilance states with an emphasis on comparing wakefulness with REM sleep. Responses of individual neurons in primary auditory cortex are comparable in wake and sleep, calling into question the proposal that the thalamus does not relay peripheral signals effectively to the cortex in sleep. Important differences between waking and sleep may lie in how signals propagate across cortical regions and layers.
COGNITIVE DYSFUNCTION AND CHOLINERGIC ALTERATIONS PRIOR TO DOPAMINE LOSS IN MICE OVER-EXPRESSING WILD-TYPE HUMAN ALPHA-SYNUCLEIN
Lecture
Tuesday, December 20, 2011
Hour: 12:15
Location:
Gerhard M.J. Schmidt Lecture Hall
COGNITIVE DYSFUNCTION AND CHOLINERGIC ALTERATIONS PRIOR TO DOPAMINE LOSS IN MICE OVER-EXPRESSING WILD-TYPE HUMAN ALPHA-SYNUCLEIN
Dr. Iddo Magen
Dept of Neurology,
University of California at Los Angeles
Parkinson’s disease (PD) is a characterized, in addition to loss of dopaminergic neurons in the substantia nigra, by loss of cholinergic neurons in the basal nucleus (Zarow et al., 2003) and pathology of alpha-synuclein, a protein implicated in familial PD, in this region concurrently with pathology of alpha-synuclein pathology in the substantia nigra (Braak et al., 2003), as well as decrease in the activity of choline acetyltransferase, the rate limiting enzyme in the synthesis of acetylcholine (Ziabreva et al., 2006). Mild cognitive deficits are also observed in the early stages of PD (Elgh et al., 2009; Mamikonyan et al., 2009). Mice over-expressing the human wild-type alpha-synuclein under the Thy1 promoter (Thy1-aSyn) present progressive sensorimotor and non-motor behavioral abnormalities reminiscent of the pre-manifest early stages of PD (Magen and Chesselet, ’10) and subsequently exhibit a loss of striatal DA (Lam et al. ’11). We now examined whether these mice also exhibit cognitive deficits in tests sensitive to cholinergic function, and whether they present cholinergic deficits.
Thy1-aSyn mice on a mixed C57BL/6-DBA/2 background presented spatial working memory deficits in the Y-maze which showed progression from 3-4 to 5-6 months and to 7-9 months. Thy1-aSyn mice also showed spatial memory deficits in the novel place recognition test and recognition memory deficits in the novel object recognition test at 4-5 months of age. In a reversal learning task at 4-5 months, Thy1-aSyn mice learned the initial contingency rule as equally well as WT littermates, but were impaired in learning a reversal of this rule, mirroring the cognitive inflexibility displayed by early PD patients in similar tasks. Expression of both proteinase-K resistant and non-resistant alpha-synuclein in the medial septum and the basal nucleus, two major regions of cholinergic input into the forebrain, was increased in Thy1-aSyn mice at 5 months of age, and cholinergic neurons in both regions expressed both human and mouse alpha-synuclein in Thy1-aSyn mice, while endogenous (murine) alpha-synuclein expression was either lower or absent in cholinergic neurons in WT mice. However, morphological features of the cholinergic neurons such as cell body diameter did not change in either the basal nucleus or the septum. Acetylcholine levels decreased by 30% in the cortex of Thy1-aSyn mice at 6 months, further suggesting a link between acetylcholine pathology and the cognitive deficits.
Our data indicate that Thy1-aSyn mice display cognitive dysfunction at an early age, which is associated with decreased acetylcholine levels. As the cognitive tests used are sensitive to cholinergic function (Barker et al., 2008; Yang et al., 2009; Botton et al., 2010), future pharmacological studies will attempt to reverse these deficits using cholinergic agonists and/or acetylcholinesterase inhibitors. A study with an acute nicotine treatment is to be performed soon, to determine whether nicotine can reverse the cognitive deficits, which might point to a causal relation between the cognitive deficits and the compromised cholinergic system. In addition, the cognitive phenotype faithfully reproduces the early cognitive deficits in PD, whereas the lack of any neuropathology in cholinergic neurons suggests that the Thy1-aSyn models mild cognitive deficits rather than dementia, which is mostly associated with a gross neuropathology. Thus, it can serve as a basis for the testing of cognitive enhancers other than cholinergic agents.
Natural Vision Improvement
Lecture
Monday, December 19, 2011
Hour: 11:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Natural Vision Improvement
Meir Schneider
School for Self-Healing
San Francisco, CA
Toward a scientific understanding of subjective experience:an open discussion
Lecture
Thursday, December 15, 2011
Hour: 14:30
Location:
Camelia Botnar Building
Toward a scientific understanding of subjective experience:an open discussion
Prof. Giulio Tononi
Dept of Psychiatry,
University of Wisconsin
An integrated information theory of consciousness
Lecture
Wednesday, December 14, 2011
Hour: 14:30
Location:
Dolfi and Lola Ebner Auditorium
An integrated information theory of consciousness
Prof. Giulio Tononi
Department of Psychiatry
University of Wisconsin
Over the past decades, studies have investigated the neural correlates of consciousness with increasing precision. However, why experience is generated by the cortex and not the cerebellum, why it fades during certain stages of sleep and returns in others, or why some cortical areas endow experience with colors and others with sound, remains unexplained. Moreover, key questions remain unanswered. For example, how much consciousness is there when only a few brain 'islands' remain active? How much during sleepwalking or psychomotor seizures? Are newborns conscious, and to what extent?
Are animals conscious, how much, and in which way? Can a conscious machine be built? To address such questions, empirical observations need to be complemented by a principled theoretical approach. The information integration theory (IIT) has several related aims: to characterize, starting from phenomenology, what consciousness is and how each experience is structured; to account for several neurobiological observations about its neural substrate; and to develop measures of consciousness that can be applied, at least in principles, to humans, animals, and machines.
Automated In-vivo Phenotyping of Rodents – Towards PhenoWorld
Lecture
Wednesday, December 7, 2011
Hour: 12:15
Location:
Nella and Leon Benoziyo Building for Brain Research
Automated In-vivo Phenotyping of Rodents – Towards PhenoWorld
Dr. Walter Förster
TSE Systems International Group
Sculpting the mature nervous system:Nuclear receptors shape connections by controlling degeneration and regeneration during development
Lecture
Tuesday, December 6, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Sculpting the mature nervous system:Nuclear receptors shape connections by controlling degeneration and regeneration during development
Prof. Oren Schuldiner
Dept of Molecular Cell Biology, WIS
Adult neurons in the CNS undergo little or no regeneration following insults such as spinal cord injury. Their inability to regenerate results from both non-cell autonomous negative signals as well as from reduced internal growth capabilities. In contrast, developing neurons are capable of extensive growth, extension and reorganization. However, it has long been challenged whether growth events during development resemble the regenerative process following injury. In my talk I will present unpublished data regarding a new pathway that we discovered, consisting of a nuclear receptor complex regulating the mTor kinase, as crucial for a regenerative process during neuronal remodeling of the Drosophila mushroom body (MB) neurons. Importantly, these nuclear receptors are not important for the initial growth of these or other types of neurons. Therefore, we discovered a pathway that is selectively required for regeneration during development. I will also provide evidence that the worm ortholog of Hr51, one of the nuclear receptors we identified, is required for injury induced regeneration following axotomy. Therefore, our data uncover a novel pathway regulating regeneration during development and following injury and suggest that developmental and injury induced axon regeneration share molecular similarities.
Odor coding in awake mice
Lecture
Thursday, December 1, 2011
Hour: 12:15
Location:
Gerhard M.J. Schmidt Lecture Hall
Odor coding in awake mice
Dr. Roman Shusterman
Janelia Farm Research Campus, HHMI
Olfaction is traditionally considered a ‘slow’ sense, but recent evidence demonstrates that rodents are capable of making extremely difficult odor discriminations rapidly, in as little as a single sniff. To understand the temporal aspects of olfactory information processing, we studied how sniffing shapes the responses of mitral/tufted cells in awake mice. We found that odorants evoked precisely sniff-locked activity in mitral/tufted (M/T) cells in the olfactory bulb of awake mouse. The trial- to-trial response jitter averaged 12 ms, a precision comparable to other sensory systems. Individual cells expressed odor-specific temporal patterns of activity and responses were more tightly time-locked to the sniff phase than to the time after inhalation onset. Precise locking to sniff phase may facilitate ensemble coding by making synchrony relationships across neurons robust to variation in sniff rate. Additional feature that olfactory system should encode is odor intensity. Psychophysical experiments in humans demonstrate that perceived odor intensity falls rapidly with repeated sampling. Changes in perceived intensity can also be due to changes in odor concentration. We show that activity of M/T cells is a neural corelate of psychophysical phenomena.
Pages
2011
, 2011
There are no events to display
2011
, 2011
Neurodegenerative diseases, stem cells and inflammation-new prospects for therapy
Conference
Thursday, December 1, 2011
Hour:
Location:
Dolfi and Lola Ebner Auditorium
Neurodegenerative diseases, stem cells and inflammation-new prospects for therapy
Metabolism and the Metabolic Disorder
Conference
Tuesday, October 25, 2011
Hour:
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
The enigma of inflammation in A.L.S: What can be learned from other
Conference
Sunday, March 6, 2011
Hour:
Location:
Dolfi and Lola Ebner Auditorium
Measuring Behavior and Physiology: Bridging the Genotype Phenotype Gap
Conference
Thursday, March 3, 2011
Hour: 08:00 - 16:30
Location:
Dolfi and Lola Ebner Auditorium
Olfaction: from receptors to behavior
Conference
Thursday, February 10, 2011
Hour: 08:00 - 16:30
Location:
Dolfi and Lola Ebner Auditorium