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Non-homogenous neural networks with chaotic recursive nodes: connectivity and multi-assemblies structures in recursive processing elements architectures.

This paper addresses recurrent neural architectures based on bifurcating nodes that exhibit chaotic dynamics, with local dynamics defined by first order parametric recursions. In the studied architectures, logistic recursive nodes interact through parametric coupling, they self organize, and the network evolves to global spatio-temporal period-2 attractors that encode stored patterns. The performance of associative memories arrangements is measured through the average error in pattern recovery, under several levels of prompting noise. The impact of the synaptic connections magnitude on architecture performance is analyzed in detail, through pattern recovery performance measures and basin of attraction characterization. The importance of a planned choice of the synaptic connections scale in RPEs architectures is shown. A strategy for minimizing pattern recovery degradation when the number of stored patterns increases is developed. Experimental results show the success of such strategy. Mechanisms for allowing the studied associative networks to deal with asynchronous changes in input patterns, and tools for the interconnection between different associative assemblies are developed. Finally, coupling in heterogeneous assemblies with diverse recursive maps is analyzed, and the associated synaptic connections are equated.

Algorithms↗

Cortical function: a view from the thalamus.

Neuroscientists from across the country gathered at the University of Wisconsin, Madison in September to honor Ray Guillery and his seminal work on the thalamus. The meeting focused on three timely research topics, each of which inspired new thinking about thalamic function. Presentations on the organization and dynamic nature of thalamocortical pathways, the role of the thalamus in communication between cortical areas, and the relationship between sensory and motor pathways of the brain, including cognitive aspects of thalamocortical processing, made for lively discussions. The meeting revealed that communication between thalamus and cortex is so rich that we should no longer consider the operations of either structure separately from the other. Proceedings of the meeting will be published in Progress in Brain Research in 2005. In this report, we provide a general overview of the main themes of the meeting.

Animals↗

Lhx6 delineates a pathway mediating innate reproductive behaviors from the amygdala to the hypothalamus.

In mammals, innate reproductive and defensive behaviors are mediated by anatomically segregated connections between the amygdala and hypothalamus. This anatomic segregation poses the problem of how the brain integrates activity in these circuits when faced with conflicting stimuli eliciting such mutually exclusive behaviors. Using genetically encoded and conventional axonal tracers, we have found that the transcription factor Lhx6 delineates the reproductive branch of this pathway. Other Lhx proteins mark neurons in amygdalar nuclei implicated in defense. We have traced parallel projections from the posterior medial amygdala, activated by reproductive or defensive olfactory stimuli, respectively, to a point of convergence in the ventromedial hypothalamus. The opposite neurotransmitter phenotypes of these convergent projections suggest a "gate control" mechanism for the inhibition of reproductive behaviors by threatening stimuli. Our data therefore identify a potential neural substrate for integrating the influences of conflicting behavioral cues and a transcription factor family that may contribute to the development of this substrate.

Aggression↗

Dynamics of memory representations in networks with novelty-facilitated synaptic plasticity.

The ability to associate some stimuli while differentiating between others is an essential characteristic of biological memory. Theoretical models identify memories as attractors of neural network activity, with learning based on Hebb-like synaptic modifications. Our analysis shows that when network inputs are correlated, this mechanism results in overassociations, even up to several memories "merging" into one. To counteract this tendency, we introduce a learning mechanism that involves novelty-facilitated modifications, accentuating synaptic changes proportionally to the difference between network input and stored memories. This mechanism introduces a dependency of synaptic modifications on previously acquired memories, enabling a wide spectrum of memory associations, ranging from absolute discrimination to complete merging. The model predicts that memory representations should be sensitive to learning order, consistent with recent psychophysical studies of face recognition and electrophysiological experiments on hippocampal place cells. The proposed mechanism is compatible with a recent biological model of novelty-facilitated learning in hippocampal circuitry.

Animals↗

Some certainty for the "zone of uncertainty"? Exploring the function of the zona incerta.

The zona incerta (ZI), first described over a century ago by Auguste Forel as a "region of which nothing certain can be said," forms a collection of cells that derives from the diencephalon. To this day, we are still not certain of the precise function of this "zone of uncertainty" although many have been proposed, from controlling visceral activity to shifting attention and from influencing arousal to maintaining posture and locomotion. In this review, I shall outline the recent advances in the understanding of the structure, connectivity and functions of the ZI. I will then focus on a possible and often neglected global role for the ZI, one that links its diverse functions together. In particular, I aim to highlight the idea that the ZI forms a primal center of the diencephalon for generating direct responses (visceral, arousal, attention and/or posture-locomotion) to a given sensory (somatic and/or visceral) stimulus. With this global role in mind, I will then address recent results indicating that abnormal ZI activity manifests in clinical symptoms of Parkinson disease.

Animals↗

Olfactory bulb networks revealed by lateral olfactory tract stimulation in the in vitro isolated guinea-pig brain.

Olfactory information processing is mediated by synaptic connections between the olfactory bulbs (OBs) and piriform-limbic cortices. Limited accessibility using common in vivo and in vitro preparations has hindered previous attempts to define these synaptic interactions. We utilized the isolated guinea-pig brain preparation to overcome these experimental limitations. Previous studies demonstrated extensive functional preservation in this preparation maintained in vitro by arterial perfusion. Field potential laminar profiles were performed with multi-channel probes in the OB following stimulation of both the lateral olfactory tract (LOT) and the anterior piriform cortex (APC). Current-source density analysis was carried out on laminar profiles to reconstruct current sinks/sources associated with intrinsic synaptic activities. LOT stimulation induced sequentially i) an antidromic population spike (at 2.66+/-0.39 ms) located in the mitral cell layer that was resistant to 100 Hz high-frequency stimulation (HFS) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM), ii) a component located in the external plexiform layer at 3.85+/-0.63 ms that was unaffected by HFS, iii) a large amplitude potential (peak amplitude at 5.84+/-0.58 ms) generated in the external plexiform layer, abolished by HFS and CNQX, but not by bicuculline (50 microM), iv) a late response (onset at 20.00+/-2.94 ms) abolished by CNQX and enhanced by bicuculline. Stimulation of the APC also induced a late potential abolished by HFS and CNQX. Both APC-evoked and late LOT-evoked responses were abolished by a transverse cut to separate OB from APC. These results demonstrate in an isolated mammalian brain preparation the presence of reciprocal synaptic interactions between the OB and piriform cortical structures.

2-Amino-5-phosphonovalerate↗

Metabotropic glutamate receptors and striatal synaptic plasticity: implications for neurological diseases.

Long- and short-term changes in the efficacy of synaptic transmission are known as synaptic plasticity. Phenomena such as long-term depression (LTD) and long-term potentiation (LTP) are two classical forms of synaptic plasticity that are expressed in several brain areas, including the striatum. Bi-directional changes in corticostriatal synaptic transmission, i.e. LTD and LTP, have been proposed to represent the cellular mechanisms underlying the physiological processes of motor learning and behavior. In parallel, other forms of synaptic plasticity induced by different experimental pathological conditions have been described in the striatum; these changes are presumed to represent the cellular processes underlying several neurological disorders, including Parkinson's disease and Huntington's chorea. A considerable number of receptor and post-receptor systems participate in the mechanisms of synaptic plasticity in the striatum, where glutamate plays a primary role through its ionotropic and metabotropic receptors (mGluRs). These latter constitute a group of recently characterized molecules, which have been shown to modulate synaptic transmission by acting on cellular excitability, ionic conductances and neurotransmitter release. These receptors have also been involved in several neuronal pathophysiological processes. The role of mGluRs in synaptic transmission and synaptic plasticity has been recently deeply studied and characterized in the striatum, in both physiological and pathological conditions. These findings open new and interesting perspectives in the study of basal ganglia function, and introduce new possible pharmacological approaches for the treatment of neurological disorders in which mGluRs have been experimentally involved.

Acetylcholine↗

Pontine cholinergic mechanisms and their impact on respiratory regulation.

Activation of pontomedullary cholinergic neurons may directly and indirectly cause depression of respiratory motoneuronal activity, activation of respiratory premotor neurons and acceleration of the respiratory rate during REM sleep, as well as activation of breathing during active wakefulness. These effects may be mediated by distinct subpopulations of cholinergic neurons. The relative inactivity of cholinergic neurons during slow-wave sleep also may contribute to the depressant effects of this state on breathing. Cholinergic muscarinic and nicotinic receptors are expressed in central respiratory neurons and motoneurons, thus allowing cholinergic neurons to act on the respiratory system directly. Additional effects of cholinergic activation are mediated indirectly by noradrenergic, serotonergic and other neurons of the reticular formation. Excitatory and suppressant respiratory effects with features of natural states of REM sleep or active wakefulness can be elicited in urethane-anesthetized rats by pontine microinjections of the cholinergic agonist, carbachol. Carbachol models help elucidate the neural basis of respiratory disorders associated with central cholinergic activation.

Acetylcholine↗

Rhythmic and dysrhythmic thalamocortical dynamics: GABA systems and the edge effect.

Brain function is fundamentally related in the most general sense to the richness of thalamocortical interconnectivity, and in particular to the rhythmic oscillatory properties of thalamocortical loops. Such rhythmicity is involved in the genesis of cognition, in the sleep-wake cycle, and in several neurological and psychiatric disorders. The role of GABA-mediated transmission in regulating these functional states is addressed here. At the cortical level, inhibition determines the spread of cortical activation by sculpting the precise activity patterns that underlie the details of cognition and motor control. At the thalamic level, GABA-mediated inhibition modulates and resets distribution of the ongoing thalamocortical rhythmic oscillations that bind multisensory inputs into a single cognitive experience and regulate arousal levels.

Animals↗

Microcircuits in action--from CPGs to neocortex.

To understand the interface between global brain function and molecular neuroscience--that is, the microcircuit level--a major challenge. Such understanding is prerequisite if we are to account for neural function in cellular terms. Very few vertebrate microcircuits are yet understood because their analysis is demanding technically. In this review of the TINS Microcircuits Special Feature, we attempt to shed light on the problem by comparing the operation of four types of microcircuit, to identify common molecular and cellular components. Central pattern generator (CPG) networks underlying rhythmic movements and hippocampal microcircuits that generate gamma and theta rhythms are compared with the neocortical microcircuits used in cognitive tasks and a cerebellar network. The long-term goal is to identify the components of a molecular and synaptic tool kit for the design of different microcircuits.

Animals↗

Can't shake that feeling: event-related fMRI assessment of sustained amygdala activity in response to emotional information in depressed individuals.

BACKGROUND: Previous research suggests that depressed individuals engage in prolonged elaborative processing of emotional information. A computational neural network model of emotional information processing suggests this process involves sustained amygdala activity in response to processing negative features of information. This study examined whether brain activity in response to emotional stimuli was sustained in depressed individuals, even following subsequent distracting stimuli. METHODS: Seven depressed and 10 never-depressed individuals were studied using event-related functional magnetic resonance imaging during alternating 15-sec emotional processing (valence identification) and non-emotional processing (Sternberg memory) trials. Amygdala regions were traced on high-resolution structural scans and co-registered to the functional data. The time course of activity in these areas during emotional and non-emotional processing trials was examined. RESULTS: During emotional processing trials, never-depressed individuals displayed amygdalar responses to all stimuli, which decayed within 10 sec. In contrast, depressed individuals displayed sustained amygdala responses to negative words that lasted throughout the following non-emotional processing trials (25 sec later). The difference in sustained amygdala activity to negative and positive words was moderately related to self-reported rumination. CONCLUSIONS: Results suggest that depression is associated with sustained activity in brain areas responsible for coding emotional features.

Adult↗

Parkinson's disease and the control of size and speed in handwriting.

This experiment investigated whether Parkinson's disease (PD) patients experience problems in producing stroke size, stroke duration or both, in a handwriting task. Thirteen PD patients and 15 elderly controls wrote four patterns of varying complexity on a digitizer tablet. The participants were instructed to execute the writing movements: at a normal size and speed; as fast as possible; two times larger than normal; and two times larger and as fast as possible. PD patients had no difficulty increasing speed while maintaining size and had no difficulty increasing size while maintaining speed. However, they showed significantly smaller size increases in the two times larger condition as compared to the elderly controls. The conditions were also simulated by a neural network model of normal and PD movement control that produced a stroke pattern that approximated the experimental data. For the instructions used, the results suggest that when patients scale speed, they have no difficulty controlling force amplitude, but when they scale stroke size, they have a problem controlling force amplitude. Thus, PD patients may have reduced capability to maintain a given force level for the stroke time periods tested with the instructions.

Aged↗

Artificial neural networks estimate the contribution of taste neurons to coding.

Taste qualities are believed to be coded in the activity of populations of taste neurons. However, it is not clear whether all neurons are equally responsible for coding. To clarify the point the relative contribution of each taste neuron to coding was assessed by constructing simple three-layer neural networks with input neurons that represent cortical taste neurons of the rat. The networks were trained by the back-propagation learning algorithm to classify the neural response patterns to the basic taste stimuli (sucrose, HCl, quinine-hydrochloride, and NaCl). The networks had four output neurons representing the basic taste qualities, the values of which provide a measure for similarity of test stimuli to the basic taste stimuli. We estimated relative contributions of input neurons to the taste discrimination of the network by examining their significance S(j), which is defined as the sum of the absolute values of the connection weights from the jth input neuron to the hidden layer. When the input neurons with a smaller S(j) (e.g., 15 out of 39 input units) were "pruned" from the trained network, the ability of the network to discriminate the basic taste qualities was not greatly affected. On the other hand, the taste discrimination of the network progressively deteriorated much more rapidly with pruning of input neurons with a larger S(j). These results suggest that cortical taste neurons differentially contribute to the coding of taste qualities. Input neurons with a larger S(j) tended to be with a larger variation of neural discharge rates to the basic taste stimuli. The variation of neural discharges may be important in the coding of taste qualities.

Algorithms↗

Neural recoding in human pattern vision: model and mechanisms.

We describe a model of neural recoding in spatial vision that specifies how the outputs of selected units akin to VI cells are normalized and combined to signal information about particular stimulus attributes. The recoding portion of the model is linked to psychophysical behavior via a two-stage signal-detection decision module that specifies how the outputs of the combining mechanisms are used in making fine spatial discriminations. We describe how masking and cue summation experiments isolate each of the processing stages, how earlier results from such studies guided development of the model, and we demonstrate how these procedures permit empirical estimates of model parameters as well as tests of alternative formulations. An important part of our work describes the characteristics of two complementary types of higher-level mechanisms isolated from previously published discrimination data. One sums normalized primary-level responses over disparate frequencies to signal precise information about the orientation of a stimulus; the other sums over all orientations to signal the spatial grain of texture-like patterns. We demonstrate how the model accounts for a large body of previously published discrimination data, and present the results of a new quantitative test of model predictions.

Humans↗

Parallel neural networks for learning sequential procedures.

Recent studies have shown that multiple brain areas contribute to different stages and aspects of procedural learning. On the basis of a series of studies using a sequence-learning task with trial-and-error, we propose a hypothetical scheme in which a sequential procedure is acquired independently by two cortical systems, one using spatial coordinates and the other using motor coordinates. They are active preferentially in the early and late stages of learning, respectively. Both of the two systems are supported by loop circuits formed with the basal ganglia and the cerebellum, the former for reward-based evaluation and the latter for processing of timing. The proposed neural architecture would operate in a flexible manner to acquire and execute multiple sequential procedures.

Animals↗

The impact of corticothalamic feedback on the output dynamics of a thalamocortical neurone model: the role of synapse location and metabotropic glutamate receptors.

The spatio-temporal integration of cortical excitatory postsynaptic potentials was investigated in a multi-compartment model of a thalamocortical neurone. Consistent with experimental data, cortical excitatory postsynaptic potentials contained a metabotropic glutamate receptor-mediated component and were generated by synapses located on distal dendrites. Within this framework, three synaptic distributions (each with equal maximal synaptic conductances) were compared: symmetric, with synapses distributed equally between all dendritic trees, single-dendrite, where synapses were allocated on all distal segments of one dendrite, and single-segment, which comprised one synapse on a single dendritic compartment. We addressed three main issues: (1) the propagation of cortical excitatory postsynaptic potentials to the soma, (2) the interaction of cortical excitatory postsynaptic potentials with proximally generated retinal excitatory postsynaptic potentials, and (3) the effectiveness of cortical excitatory postsynaptic potentials in entraining and perturbing the delta oscillation. The somatic and dendritic amplitudes of the cortical excitatory postsynaptic potentials depended on the distribution of the synapses, being largest and smallest, respectively, for the symmetric distribution, and smallest and largest, respectively, for the single-segment distribution. When a retinal excitatory postsynaptic potential followed a subthreshold cortical excitatory postsynaptic potential with a short (2-200 ms) delay, its ability to evoke action potentials was increased, with single-segment cortical excitatory postsynaptic potentials having the longest-lasting facilitatory effect. When a retinal excitatory postsynaptic potential arrived with a longer delay (210-400 ms), the effect of the cortical excitatory postsynaptic potential was to decrease the number of retinally evoked action potentials. These facilitatory and depressant effects of the cortical excitatory postsynaptic potentials were dependent on the presence of their metabotropic glutamate receptor, and were enhanced by increasing the strength of this glutamate receptor component. Axial resistivity and distal dendritic A-type current had little qualitative effect on these modulatory actions of the cortical excitatory postsynaptic potential. Cortical excitatory postsynaptic potentials were more effective than retinal excitatory postsynaptic potentials in perturbing the phase of the delta oscillation, indicating that they are ideally suited to entraining this form of rhythmic activity. Again, this effect was closely dependent on the presence of metabotropic glutamate receptor but was largely independent of synapse distribution. These results indicate that the distribution of activated synapses and the presence of metabotropic glutamate receptor are crucial factors in determining the effect of cortical feedback excitation on thalamocortical neurons. Moreover, the distinct postsynaptic receptor composition of cortical inputs renders them ideally suited to synchronising low-frequency oscillatory activity in thalamocortical neurons.

Cerebral Cortex↗

A neural network approach to the acoustic startle reflex and prepulse inhibition.

Prepulse inhibition (PPI) is the normal suppression of the startle reflex when an intense stimulus is preceded by a weak non-startling prestimulus. PPI is widely used as a model for sensorimotor gating processes and has been shown to be impaired in various neuropsychiatric disorders, including schizophrenia. We have reproduced startle-like behavior and basic PPI modifications with a neural network. The network design was constrained by the attempt (1) to use as few connections as possible and (2) to relate neuroanatomical structures to the simulated network. Performance of the network was evaluated by the behavior of the simulated motor neurons in response to prepulse and pulse stimuli presented with various lead intervals and prepulse intensities. A delayed inhibitory pathway via the pedunculopontine nucleus (PPTg) to the caudal pontine reticular nucleus was found to be a necessary but insufficient requirement to reproduce basic PPI output patterns. Additional requirements included (a) a low threshold at or below the caudal pontine reticular formation, (b) signal amplification in the inhibitory pathway and (c) prolongation of activity in the inhibitory pathway. On the grounds of the most appropriate output patterns of the simulations, we propose a mechanism of sustained activation in the PPTg due to recursive connections. Relations between stimuli, behavior (motor output) and the underlying architecture are discussed. Potentially, this modeling technique can be extended to investigate the impact of drugs and higher brain regions on PPI.

Animals↗