Sparing from the attentional blink is not spared from structural limitations.

When a series of three successive to-be-reported items (targets) is displayed in a rapid serial visual presentation (RSVP) stream of distractors, it has been shown that no attentional blink--a marked impairment in the report of the second of two targets, typically observed when the targets appear within 200-600 ms of one another--occurs in target accuracy. The present study examines three recently introduced computational models that provide different explanations of this protracted sparing effect. Using a standard RSVP design and these models, we provide empirical data and simulations that illustrate that structural limitations affect the processing of successive targets. In addition, we compare the candidate mechanisms that might underlie these limitations.

A reciprocal relationship between bottom-up trace strength and the attentional blink bottleneck: relating the LC-NE and ST(2) models.

There is considerable current interest in neural modeling of the attentional blink phenomenon. Two prominent models of this task are the Simultaneous Type Serial Token (ST(2)) model and the Locus Coeruleus-Norepinephrine (LC-NE) model. The former of these generates a broad spectrum of behavioral data, while the latter provides a neurophysiologically detailed account. This paper explores the relationship between these two approaches. Specifically, we consider the spectrum of empirical phenomena that the two models generate, particularly emphasizing the need to generate a reciprocal relationship between bottom-up trace strength and the blink bottleneck. Then we discuss the implications of using ST(2) token mechanisms in the LC-NE setting.

Size of CA1-evoked synaptic potentials is related to theta rhythm phase in rat hippocampus.

Cholinergic and GABAergic neurons projecting to the hippocampus fire with specific phase relations to theta rhythm oscillations in the electroencephalogram (EEG). To determine if this phasic input has an impact on synaptic transmission within the hippocampus, we recorded evoked population excitatory postsynaptic potential (EPSPs) during different phases of theta rhythm by using techniques similar to those described in Rudell and Fox. Synaptic potentials elicited by stimulation of region CA3 of the contralateral hippocampus were recorded in region CA1 and CA3. In these experiments, the initial slope of evoked potentials showed a change in magnitude during different phases of the theta rhythm recorded in the dentate fissure, with individual trials showing an average of 9.5% change in slope of potentials, and the average across all experiments showing a change of 7.8%. Evoked potentials were maximal 18 degrees after the positive peak of the dentate fissure theta EEG. These potentials were also smaller by 18.2% during theta as opposed to non-theta states. Phasic changes in modulation of synaptic transmission could contribute to phase precession of hippocampal place cells and could enhance storage of new sequences of activity as demonstrated by computational models.

Electrical stimulation of the horizontal limb of the diagonal band of broca modulates population EPSPs in piriform cortex.

Electrical stimulation of the horizontal limb of the diagonal band of Broca (HDB) was coupled with recording of evoked potentials in the piriform cortex. Stimulation of the HDB caused an enhancement of the late, disynaptic component of the evoked potential elicited by stimulation of the lateral olfactory tract but caused a suppression of the synaptic potential elicited by stimulation of the posterior piriform cortex. The muscarinic antagonist scopolamine blocked both effects of HDB stimulation. The enhancement of disynaptic potentials could be due to cholinergic depolarization of pyramidal cells, whereas the suppression of potentials evoked by posterior piriform stimulation could be due to presynaptic inhibition of intrinsic fiber synaptic transmission by acetylcholine.

Free recall and recognition in a network model of the hippocampus: simulating effects of scopolamine on human memory function.

Free recall and recognition are simulated in a network model of the hippocampal formation, incorporating simplified simulations of neurons, synaptic connections, and the effects of acetylcholine. Simulations focus on modeling the effects of the acetylcholine receptor blocker scopolamine on human memory. Systemic administration of scopolamine is modeled by blockade of the cellular effects of acetylcholine in the model, resulting in memory impairments replicating data from studies on human subjects. This blockade of cholinergic effects impairs the encoding of new input patterns (as measured by delayed free recall), but does not impair the delayed free recall of input patterns learned before the blockade. The impairment is selective to the free recall but not the recognition of items encoded under the influence of scopolamine. In the model, scopolamine blocks strengthening of recurrent connections in region CA3 to form attractor states for new items (encoding impaired) but allows recurrent excitation to drive the network into previously stored attractor states (retrieval spared). Neuron populations representing items (individual words) have weaker recurrent connections than neuron populations representing experimental context. When scopolamine further weakens the strength of recurrent connections it selectively prevents the subsequent reactivation of item attractor states by context input (impaired free recall) without impairing the subsequent reactivation of context attractor states by item input (spared recognition). This asymmetry in the strength of attractor states also allows simulation of the list-strength effect for free recall but not recognition. Simulation of a paired associate learning paradigm predicts that scopolamine should greatly enhance proactive interference due to retrieval of previously encoded associations during storage of new associations.

Encoding and retrieval of episodic memories: role of cholinergic and GABAergic modulation in the hippocampus.

This research focuses on linking episodic memory function to the cellular physiology of hippocampal neurons, with a particular emphasis on modulatory effects at cholinergic and gamma-aminobutyric acid B receptors. Drugs which block acetylcholine receptors (e.g., scopolamine) have been shown to impair encoding of new information in humans, nonhuman primates, and rodents. Extensive data have been gathered about the cellular effects of acetylcholine in the hippocampus. In this research, models of individual hippocampal subregions have been utilized to understand the significance of particular features of modulation, and these hippocampal subregions have been combined in a network simulation which can replicate the selective encoding impairment produced by scopolamine in human subjects.