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N A Schmajuk

Publications and source records attributed to N A Schmajuk.

At least 19 recordsLinked to original sources
PubMed2006

Startle and prepulse inhibition as a function of background noise: a computational and experimental analysis.

Schmajuk and Larrauri [Schmajuk NA, Larrauri JA. Neural network model of prepulse inhibition. Behav Neurosci 2005;119:1546-62.] introduced a real-time model of acoustic startle, prepulse inhibition (PPI) and facilitation (PPF) in animals and humans. The model assumes that (1) positive values of changes in noise level activate an excitatory and a facilitatory pathway, and (2) absolute values of changes in noise level activate an inhibitory pathway. The model describes many known properties of the phenomena and the effect of brain lesions on startle, PPI, and PPF. The purpose of the present study is to (a) establish the magnitude of startle and PPI as a function of pulse, prepulse, and background intensity, and (b) test the model predictions regarding an inverted-U function that relates startle to the intensity of the background noise.

Acoustic Stimulation↗
PubMed2004

A pre-clinical study showing how dopaminergic drugs administered during pre-exposure can impair or facilitate latent inhibition.

RATIONALE: It has been suggested that, in classical conditioning, dopamine (DA) codes for (a) attention to the conditioned stimulus (CS) or (b) the intensity of the unconditioned stimulus. OBJECTIVES: To clarify the role of DA in pre-clinical classical conditioning studies. METHODS: An existing model of classical conditioning presented by Schmajuk, Lam, and Gray (J Exp Psychol Anim Behav Process 22:321-349, 1996) suggests that DA cells in the ventral midbrain area code for the attentionally modulated internal representation of the CS. It is assumed that this representation is increased by dopaminergic agonists and decreased by dopaminergic antagonists. Computer simulations with the model describe the effect of nicotine and haloperidol on latent inhibition. RESULTS: Simulations replicate experimental results demonstrating that both nicotine and haloperidol affect latent inhibition when administered during the pre-exposure phase. In addition, the model reproduces data showing that administration of nicotine or haloperidol results in the impairment or facilitation of latent inhibition depending on the duration of CS or the number of CSs. CONCLUSIONS: The model demonstrates that pre-clinical experimental results, including cell activity and pharmacological data, are consistent with an attentional role for DA in classical conditioning.

Computer Simulation↗
PubMed2001

Nucleus accumbens, entorhinal cortex and latent inhibition: a neural network model.

A neural network model of classical conditioning (Schmajuk, Lam, and Gray, J. Exp. Psychol.: Anim. Behav. Process, 22, 1996, 321-349) is applied to the description of the neural substrates of latent inhibition. Experimental data suggest that latent inhibition might be controlled by a circuit that involves the hippocampus, the entorhinal cortex, the nucleus accumbens, and the mesolimbic dopaminergic projection from the ventral tegmental area to the accumbens. By mapping different nodes and connections in the model onto this brain circuit, computer simulations demonstrate that, in most cases, the model provides a good quantitative description of: (1) the impairment of latent inhibition by lesions of the shell of the nucleus accumbens; (2) the restoration of latent inhibition by haloperidol following lesions of the shell; (3) the preservation of latent inhibition by lesions of the core of the nucleus accumbens; (4) the facilitation of latent inhibition by combined shell core lesions and by core lesions with extended conditioning; (5) the impairment of latent inhibition following lesions of the entorhinal cortex or the hippocampus; and (6) the restoration of latent inhibition by haloperidol following lesions of the entorhinal cortex and ventral subiculum. In addition, the model is able to describe neural activity in the nucleus accumbens.

Animals↗
PubMed2001

Hippocampal dysfunction in schizophrenia.

Although not necessarily primary to the disease, hippocampal dysfunction in schizophrenia is suggested by morphological changes in the hippocampal formation reported in schizophrenic patients. This notion receives additional support from studies showing that 1) similar behavioral deficits are exhibited by both schizophrenics and animals with hippocampal lesions, and 2) some of these behavioral deficits are reversed by neuroleptics in both schizophrenics and lesioned animals. A brain-mapped neural network model is used to explain how some impairments in attention can be caused by hippocampal dysfunction and ameliorated by dopaminergic blockers.

Animals↗
PubMed2000

Haloperidol reinstates latent inhibition impaired by hippocampal lesions: data and theory.

The effect of haloperidol administration on the impairment of latent inhibition produced by aspirative lesions of the hippocampus was examined in the rat eyeblink response preparation. During the preexposure phase, rats with hippocampal or control lesions were either exposed to a tone or allowed to sit in the training apparatus. During the conditioning phase, the tone was paired with an airpuff to the eye after the rats were injected with either saline or haloperidol. Although saline-injected rats with hippocampal lesions did not show latent inhibition, the phenomenon was reinstated in rats that received haloperidol injections. A possible locus of the interaction between hippocampal lesions and haloperidol is the nucleus accumbens. The reported data are well described by a neural network model of classical conditioning. This study contributes to the understanding of the neurophysiology of latent inhibition as well as the neuropsychological bases of schizophrenia.

Animals↗
PubMed1998

Perplexing effects of hippocampal lesions on latent inhibition: a neural network solution.

Experimental data indicate that hippocampal lesions might impair, spare, or even facilitate latent inhibition (LI). Furthermore, when LI is impaired by the lesions, it might be reinstated by haloperidol administration. The present article applies a neural network model of classical conditioning (N. A. Schmajuk, Y. W. Lam, & J. A. Gray, 1996) to investigate the possible causes of these puzzling results. According to the model, LI is manifested because preexposure of the conditioned stimulus (CS) reduces Novelty, defined as proportional to the sum of the mismatches between predicted and observed events, thereby reducing attention to the CS and retarding conditioning. It is assumed that hippocampal lesions affect the prediction of events. Computer simulations reveal that, depending on the behavioral protocol (i.e., procedure and total time of CS preexposure), Novelty in hippocampal lesioned animals might be larger, equal, or smaller (corresponding to smaller, equal, or larger LI) than in normal controls. Reinstatement of LI by haloperidol administration is explained by assuming that dopaminergic antagonists decrease the value of Novelty, when Novelty increases following hippocampal lesions.

Animals↗
PubMed1998

Occasion setting: a neural network approach.

Classical conditioning data show that a conditioned stimulus (CS) can act either as a simple CS--eliciting conditioned responses (CRs) by signaling the occurrence of an unconditioned stimulus (US)--or as an occasion setter--controlling the responses generated by another CS. In this article, the authors apply a simple extension of a network model of conditioning, originally presented by N. A. Schmajuk and J. J. DiCarlo (S-D; 1992), to the description of these 2 different CS functions. In the model, CS inputs are connected to the CR output both directly and indirectly through a hidden unit layer that codes configural stimuli. In this framework, a CS acts as (a) a simple stimulus through its direct connections with the output units and as (b) an occasion setter through its indirect configural connections via the hidden units. Computer simulations demonstrate that the network accounts for a large part of the data on occasion setting.

Animals↗
PubMed1998

Psychopharmacology of latent inhibition: a neural network approach.

A neural network model of classical conditioning is applied to the description of some aspects of the psychopharmacology of latent inhibition (LI). According to the model, LI is manifested because preexposure of the conditioned stimulus (CS) reduces Novelty, defined as proportional to the sum of the mismatches between predicted and observed events, thereby reducing attention to the CS and retarding conditioning. In the framework of the model, it is assumed that indirect dopaminergic (DA) agonists (e.g. amphetamine and nicotine) increase, and DA receptor antagonists (e.g. haloperidol and alpha-flupenthixol) decrease, the effect of Novelty on attention. Computer simulations demonstrate that, under these assumptions, the model correctly describes: (1) the impairment of LI by amphetamine when a strong unconditioned stimulus (US) is used, (2) the impairment of LI by amphetamine when a nonsalient CS is used, (3) the impairment of LI by amphetamine administration when a short CS is used, (4) the facilitation of LI by alpha-flupenthixol when a weak US is used, (5) the facilitation of LI by haloperidol when a nonsalient CS is used, (6) the facilitation of LI by haloperidol with a strong US, and (7) the facilitation of LI by haloperidol with extended conditioning.

Amphetamine↗
PubMed1997

Stimulus configuration, occasion setting, and the hippocampus.

N. A. Schmajuk, J. Lamoureux, and P. C. Holland (in press) showed that an extension of a neural network model introduced by N. A. Schmajuk and J. J. DiCarlo (1992) characterizes many of the differences between simple conditioning and occasion setting. In the framework of this model, it is proposed that the hippocampus modulates (a) the competition among simple and complex stimuli to establish associations with the unconditioned stimulus, and (b) the configuration of simple stimuli into complex stimuli. Under the assumptions that (a) nonselective lesions of the hippocampal formation impair both configuration and competition, and (b) selective lesions of the hippocampus proper impair only stimulus configuration, the model correctly describes the effects of these lesions on paradigms in which stimuli act as occasion setters.

Animals↗
PubMed1996

Attention, configuration, and hippocampal function.

We present a neural network that characterizes a remarkably large number of classical conditioning paradigms and describes the effects of many neurophysiological manipulations. First, the network 1) describes behavior in real time 2) comprises simple and configural stimulus representations, and 3) includes attentional control of storage and retrieval. Second, mapping of the network onto the brain can be summarized by several information processing loops: 1) a hippocampal-cortical configural loop, 2) a hippocampal-cerebellar conditioned-response loop, 3) a hippocampal-accumbens-thalamic attentional loop, and 4) a hippocampal-medial raphe-medial septum error loop. Third, within this global view of brain function, it is assumed that the hippocampal formation computes 1) the aggregate prediction of environmental events and 2) the error signals for cortical learning. These assumptions are supported by rigorous computer simulations consistent with a large body of data on hippocampal and septal neural activity, induction and blockade of hippocampal long-term potentiation, administration of cholinergic agonists and antagonists, administration of haloperidol, and selective and nonselective hippocampal and cortical lesions.

Animals↗
PubMed1994

Latent inhibition of the rat eyeblink response: effect of hippocampal aspiration lesions.

The effect of hippocampal aspiration lesions on latent inhibition of eyeblink conditioning in the restrained rat preparation was examined. Rats received either sham, cortical control, or hippocampal aspiration lesions. Control animals, but not animals with hippocampal lesions, showed slower conditioning after being preexposed to the conditioned stimulus (latent inhibition). Together with previous results regarding the effect of hippocampal lesions in acquisition and extinction of delay conditioning, the present study suggests that the restrained rat preparation may serve as a reliable way of investigating hippocampal participation in different classical conditioning paradigms.

Animals↗
PubMed1993

Stimulus configuration, spatial learning, and hippocampal function.

Schmajuk and DiCarlo (Psychol. Rev., 99 (1992) 268-305) introduced a neural network, which utilizes a biologically plausible backpropagation procedure, to describe configural paradigms in classical conditioning. The model correctly describes many experimental results under the assumption that aspiration lesions of the hippocampus eliminate (a) the competition between simple and configural stimuli to gain association with the unconditioned stimulus and (b) the adjustment of initially random configural stimuli. The present study extends the network to describe place learning. Under the assumption that ibotenic acid lesions of the hippocampus only impair the adjustment of initially random configural stimuli, the model correctly shows that ibotenic acid lesions might spare a configural discrimination but impair place learning. In general, the results are taken to support a hippocampal role in the modulation of stimulus configuration.

Animals↗
PubMed1993

Maps, routes, and the hippocampus: a neural network approach.

This study describes hippocampal participation in maze navigation in terms of a real-time, biologically plausible neural network. The system is composed of (1) a goal-seeking mechanism, (2) a cognitive map system, and (3) a route system. The goal-seeking mechanism displays exploratory behavior until either the goal is found or a sufficiently strong prediction of the goal is generated. The cognitive map is a topological map that stores associations between places and views of accessible places, and between places and reward. The route system establishes associations between cues and reward. Both systems compete with each other to establish associations with the reward, with the cognitive system generally overshadowing the route system. In agreement with previous models, it is assumed that the hippocampus modulates the storage of cognitive maps in cortical areas and mediates the competition between cognitive maps and route systems. After hippocampal lesions, animals navigate through mazes making use of the route system. Computer simulations show that the network effectively describes latent learning, detour behavior, and place learning in normal and hippocampal- and cortical-lesioned animals.

Animals↗
PubMed1992

Hippocampectomy disrupts the topography of the rat eyeblink response during acquisition and extinction of classical conditioning.

The effect of hippocampal lesions on acquisition and extinction of eyeblink conditioning in rats was examined with the procedure described by Schmajuk and Christiansen (Physiol. Behav., 48 (1990) 755-758). Male Long-Evans rats received either sham, cortical control or hippocampal lesions. Animals were trained in a delay conditioning paradigm with a 500-ms, 98-dB, white noise conditioned stimulus; a 150-ms, 5-psi air puff unconditioned stimulus; a 350-ms interstimulus interval; and a 60-s average intertrial interval. Each animal received 50 trials daily until it reached a criterion of 80% conditioned responses (CR) on a given day. After acquisition criterion was reached, extinction began the next day and continued until each animal achieved a criterion of one CR in a block of 10 consecutive trials. Although hippocampal lesions affected neither acquisition nor extinction rates, hippocampal lesioned animals showed significantly shorter CR onset latency during acquisition and extinction, and larger CR peak amplitude during acquisition. The results are discussed in terms of hippocampal modulation of cerebellar learning.

Animals↗
PubMed1992

Purposive behavior and cognitive mapping: a neural network model.

This study presents a real-time, biologically plausible neural network approach to purposive behavior and cognitive mapping. The system is composed of (a) an action system, consisting of a goal-seeking neural mechanism controlled by a motivational system; and (b) a cognitive system, involving a neural cognitive map. The goal-seeking mechanism displays exploratory behavior until either (a) the goal is found or (b) an adequate prediction of the goal is generated. The cognitive map built by the network is a topological map, i.e., it represents only the adjacency, but not distances or directions, between places. The network has recurrent and non-recurrent properties that allow the reading of the cognitive map without modifying it. Two types of predictions are introduced: fast-time and real-time predictions. Fast-time predictions are produced in advance of what occurs in real time, when the information stored in the cognitive map is used to predict the remote future. Real-time predictions are generated simultaneously with the occurrence of environmental events, when the information stored in the cognitive map is being updated. Computer simulations show that the network successfully describes latent learning and detour behavior in rats. In addition, simulations demonstrate that the network can be applied to problem-solving paradigms such as the Tower of Hanoi puzzle.

Animals↗
PubMed1992

Stimulus configuration, classical conditioning, and hippocampal function.

Hippocampal participation in classical conditioning is described in terms of a multilayer network that portrays stimulus configuration. The network (a) describes behavior in real time, (b) incorporates a layer of "hidden" units positioned between input and output units, (c) includes inputs that are connected to the output directly as well as indirectly through the hidden-unit layer, and (d) uses a biologically plausible backpropagation procedure to train the hidden-unit layer. Nodes and connections in the neural network are mapped onto regional cerebellar, cortical, and hippocampal circuits, and the effect of lesions of different brain regions is formally studied. Computer simulations of the following classical conditioning paradigms are presented: acquisition of delay and trace conditioning, extinction, acquisition-extinction series of delay conditioning, blocking, over-shadowing, discrimination acquisition, discrimination reversal, feature-positive discrimination, conditioned inhibition, negative patterning, positive patterning, and generalization. The model correctly describes the effect of hippocampal and cortical lesions in many of these paradigms, as well as neural activity in hippocampus and medial septum during classical conditioning. Some of these results might be extended to the description of anterograde amnesia in human patients.

Animals↗
PubMed1991

A neural network approach to hippocampal function in classical conditioning.

Hippocampal participation in classical conditioning in terms of Grossberg's (1975) attentional theory is described. According to the present rendition of this theory, pairing of a conditioned stimulus (CS) with an unconditioned stimulus (US) causes both an association of the sensory representation of the CS with the US (conditioned reinforcement learning) and an association of the sensory representation of the CS with the drive representation of the US (incentive motivation learning). Sensory representations compete among themselves for a limited-capacity short-term memory (STM) that is reflected in a long-term memory storage. The STM regulation hypothesis, which proposes that the hippocampus controls incentive motivation, self-excitation, and competition among sensory representations thereby regulating the contents of a limited capacity STM, is introduced. Under the STM regulation hypothesis, nodes and connections in Grossberg's neural network are mapped onto regional hippocampal-cerebellar circuits. The resulting neural model provides (a) a framework for understanding the dynamics of information processing and storage in the hippocampus and cerebellum during classical conditioning of the rabbit's nictitating membrane, (b) principles for understanding the effect of different hippocampal manipulations on classical conditioning, and (c) numerous novel and testable predictions.

Animals↗