Neural competition via lateral inhibition between decision processes and not a STOP signal accounts for the antisaccade performance in healthy and schizophrenia subjects

A commentary on Re-starting a neural race: anti-saccade correction by Noorani, I., and Carpenter, R. H. S. (2014). Eur. J. Neurosci. 39, 159–164. doi: 10.1111/ejn.12396 Decision making is the process of accumulating evidence about the world and the utility of possible outcomes (Cutsuridis, 2010). A paradigm often used by behavioral neuroscientists to investigate decision processes is the antisaccade paradigm (see Figure 1A; Hallett, 1978). In the antisaccade paradigm subjects are required to suppress an erroneous saccade (error prosaccade) toward a peripheral stimulus and instead make an eye movement to a position in the opposite hemifield (antisaccade). The response repertoire of a subject performing the antisaccade task has been reported to be: (1) the subject makes an erroneous response (i.e., looking toward the peripheral stimulus), (2) the subject makes the antisaccade (i.e., looking in the opposite direction of the peripheral stimulus, and (3) the subject makes an erroneous response followed by a corrected antisaccade (Evdokimidis et al., 2002)

Bradykinesia models of Parkinson’s disease

This entry describes a plethora of experimental observations from PD bradykinesia in humans and animals ranging across neuronal, electromyographic and behavioral levels and discusses related theoretical and computational models developed to reproduce and explain these findings. Some computational models of bradykinesia have focused entirely on the effects of dopamine depletion in the basal ganglio-thalamo-cortical relations, whereas others emphasize dopamine depletion in cortico-spino-muscular interactions. Future models will have to produce a more comprehensive and detailed neural model of basal ganglia-thalamo-cortico-spino-muscular interactions, in order to study more systematically the effects of dopamine depletion in these nuclei and integrate into a ‘unified theory’ all the known neurophysiological, EMG and behavioral observations associated with parkinsonism

Memory processes in medial temporal lobe: experimental, theoretical and computational approaches

The medial temporal lobe (MTL) includes the hippocampus, amygdala and parahippocampal regions, and is crucial for episodic and spatial memory. MTL memory function consists of distinct processes such as encoding, consolidation and retrieval. Encoding is the process by which perceived information is transformed into a memory trace. After encoding, memory traces are stabilized by consolidation. Memory retrieval (recall) refers to the process by which memory traces are reactivated to access information previously encoded and stored in the brain. Although underlying neural mechanisms supporting these distinct functional stages remain largely unknown, recent studies have indicated that distinct oscillatory dynamics, specific neuron types, synaptic plasticity and neuromodulation, play a central role. The theta rhythm is believed to be crucial in the encoding and retrieval of memories. Experimental and computational studies indicate that precise timing of principal cell firing in the hippocampus, relative to the theta rhythm, underlies encoding and retrieval processes. On the other hand, sharp-wave ripples have been implicated in the consolidation through the “replay” of memories in compressed time scales. The neural circuits and cell types supporting memory processes in the MTL areas have only recently been delineated using experimental approaches such as optogenetics, juxtacellular recordings, and optical imaging. Principal (excitatory) cells are crucial for encoding, storing and retrieving memories at the cellular level, whereas inhibitory interneurons provide the temporal structures for orchestrating the activities of neuronal populations of principal cells by regulating synaptic integration and timing of action potential generation of principal cells as well as the generation and maintenance of network oscillations (rhythms). In addition, neuromodulators such as acetylcholine alter dynamical properties of neurons and synapses, and modulate oscillatory state and rules of synaptic plasticity and their levels might tune MTL to specific memory processes. The research topic offers a snapshot of the current state of-the-art on how memories are encoded, consolidated, stored and retrieved in MTL structures. Accepted papers to the research topic include studies (experimental or computational) focusing on the structure and function of neural circuits, their cellular components (principal cell and inhibitory interneurons) and their properties, synaptic plasticity rules involved in these memory processes, network oscillations such as theta, gamma and sharp-wave ripples, and the role of neuromodulators in health and in disease (Alzheimer's disease and schizophrenia)

A simulation study on the effects of dendritic morphology on layer V prefrontal pyramidal cell firing behaviour

Pyramidal cells, the most abundant neurons in neocortex, exhibit significant structural variability across different brain areas and layers in different species. Moreover, in response to a somatic step current, these cells display a range of firing behaviors, the most common being (1) repetitive action potentials (Regular Spiking—RS), and (2) an initial cluster of 2–5 action potentials with short interspike interval (ISIs) followed by single spikes (Intrinsic Bursting—IB). A correlation between firing behavior and dendritic morphology has recently been reported. In this work we use computational modeling to investigate quantitatively the effects of the basal dendritic tree morphology on the firing behavior of 112 three-dimensional reconstructions of layer V PFC rat pyramidal cells. Particularly, we focus on how different morphological (diameter, total length, volume, and branch number) and passive [Mean Electrotonic Path length (MEP)] features of basal dendritic trees shape somatic firing when the spatial distribution of ionic mechanisms in the basal dendritic trees is uniform or non-uniform. Our results suggest that total length, volume and branch number are the best morphological parameters to discriminate the cells as RS or IB, regardless of the distribution of ionic mechanisms in basal trees. The discriminatory power of total length, volume, and branch number remains high in the presence of different apical dendrites. These results suggest that morphological variations in the basal dendritic trees of layer V pyramidal neurons in the PFC influence their firing patterns in a predictive manner and may in turn influence the information processing capabilities of these neurons

Dendritic Inhibition Effects in Memory Retrieval of a Neuromorphic Microcircuit Model of the Rat Hippocampus

Background: Studies have shown that input comparison in the hippocampus between the Schaffer collateral (SC) input in apical dendrites and the perforant path (PP) input in the apical tufts dramatically changes the activity of pyramidal cells (PCs). Equally, dendritic inhibition was shown to control PC activity by minimizing the depolarizing signals in their dendritic trees, controlling the synaptic integration time window, and ensuring temporal firing precision. Objectives: We computationally investigated the diverse roles of inhibitory synapses on the PC dendritic arbors of a CA1 microcircuit model in mnemonic retrieval during the co-occurrence of SC and PP inputs. Results: Our study showed inhibition in the apical PC dendrites mediated thresholding of firing during memory retrieval by restricting the depolarizing signals in the dendrites of non-engram cells, thus preventing them from firing, and ensuring perfect memory retrieval (only engram cells fire). On the other hand, inhibition in the apical dendritic tuft removed interference from spurious EC during recall. When EC drove only the engram cells of the SC input cue, recall was perfect under all conditions. Removal of apical tuft inhibition had no effect on recall quality. When EC drove 40% of engram cells and 60% of non-engram cells of the SC input cue, recall was disrupted, and this disruption was worse when the apical tuft inhibition was removed. When EC drove only the non-engram cells of the cue, then recall was perfect again but only when the population of engram cells was small. Removal of the apical tuft inhibition disrupted recall performance when the population of engram cells was large. Conclusions: Our study deciphers the divers