Biomedical subjects

E W Kairiss

Publications and source records attributed to E W Kairiss.

11 recordsLinked to original sources

PubMed1998

Cortical memory dynamics.

Biological memories have a number of unique features, including (1) hierarchical, reciprocally interacting layers, (2) lateral inhibitory interactions within layers, and (3) Hebbian synaptic modifications. We incorporate these key features into a mathematical and computational model in which we derive and study Hebbian learning dynamics and recall dynamics. Introducing the construct of a feasible memory (a memory that formally responds correctly to a specified collection of noisy cues that are known in advance), we study stability and convergence of the two kinds of dynamics by both analytical and computational methods. A conservation law for memory feasibility under Hebbian dynamics is derived. An infomax net is one where the synaptic weights resolve the most uncertainty about a neural input based on knowledge of the output. The infomax notion is described and is used to grade memories and memory performance. We characterize the recall dynamics of the most favorable solutions from an infomax perspective. This characterization includes the dynamical behavior when the net is presented with external stimuli (noisy cues) and a description of the accuracy of recall. The observed richness of dynamical behavior, such as its initial state sensitivity, provides some hints for possible biological parallels to this model.

Animals↗

PubMed1994

Electrophysiology and morphology of neurons in rat perirhinal cortex.

The intrinsic membrane properties of perirhinal cortical neurons were studied by intracellular recording in in vitro rat brain slices. Gross morphology was also examined through injection of the fluorescent dye carboxyfluorescein. The cells encountered displayed a diversity of electrophysiological properties, and were similar to cells reported in other neocortical areas with regard to spiking patterns, afterpotentials, and morphology. However, very few (4%) intrinsically bursting neurons were encountered. Two pyramidal cells with thick apical dendrites were filled, and both fired doublets of action potentials for their first suprathreshold events. Of the filled pyramidal cells with thin apical dendrites, most (9/11) fired single action potentials for their first suprathreshold events. A variety of classification schemes were used to group the data, and several schemes were found to be equally successful. According to one of the schemes, cells recorded with carboxyfluorescein filled electrodes had significantly greater action potential widths at half-amplitude and more depolarized resting potentials than cells recorded without this dye.

Action Potentials↗

PubMed1994

Quantal mechanism of long-term potentiation in hippocampal mossy-fiber synapses.

1. The quantal mechanism underlying the expression of long-term potentiation (LTP) was studied in the mossy-fiber (mf) synapses of the rat hippocampus. Whole-cell recordings were used to measure the excitatory postsynaptic currents (EPSCs) before and after LTP induction in brain slices maintained at 31 +/- 1 degrees C. 2. Evoked EPSCs were recorded from 473 CA3 pyramidal neurons. The mf synapses were stimulated using paired pulses (40-ms interpulse interval) repeated every 2-10 s. At least 400 pairs of mf responses were obtained before and during the expression of LTP, which was produced by high-frequency (100 Hz) mf stimulation. Sufficiently stationary data were obtained from five neurons that exhibited LTP and that also satisfied strict criteria and procedures that are necessary for eliciting and identifying unitary mf responses. 3. Three independent lines of evidence implicated a presynaptic component to the mechanism underlying mf LTP. The first was based on a graphical version of the classical method of variance. The graphical variance (GV) method was evaluated by clamping the cell at two different holding potentials during paired-pulse facilitation (PPF). The results indicated that the GV method can distinguish changes in mean quantal content m and mean quantal size q in rat mf synapses. The same analysis, when applied to PPF before and after LTP induction, indicated that both result from an increase in m. 4. The second line of evidence was based on the classical method of failures. Consistent with the inference that mf LTP is due to an increase in m, there was a statistically significant reduction in the number of quantal release failures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Long-term synaptic potentiation in the amygdala.

The manner in which the circuitry of the amygdala computes its suspected mnemonic functions has been a mystery, partly because the cytoarchitectual complexity of this nuclear group has impeded the necessary cellular analysis. Here we report in vitro methods and results that may help elucidate cellular learning mechanisms in amygdala neurons. The amygdala brain slice preparation was combined with the single-electrode clamp (SEC) technique for intracellular analysis of membrane properties and synaptic responses. With respect to the active and passive membrane properties, we found considerable diversity among the population of cells that were sampled in the lateral and basolateral nuclei (n = 85). Synaptic inputs to these neurons were studied by stimulating the external capsule (EC), which was shown to produce a complex response that typically consisted of an excitatory followed by an inhibitory component. Based on several criteria, the excitatory component appeared to reflect a monosynaptic connection from the EC. One immediate goal was to discover whether the excitatory component displays the phenomenon of long-term potentiation (LTP)--a persistent increase in synaptic strength that can be induced by brief periods of the appropriate synaptic stimulation. Indeed, we found that high-frequency (100 Hz) stimulation of the EC induced LTP in 80% of the cells from which suitable recordings were obtained (n = 20). This finding of LTP in the amygdala is significant in regard to current efforts to explore linkages between this use-dependent form of synaptic plasticity and rapid kinds of associative learning.

Amygdala↗

PubMed1990

Hebbian synapses: biophysical mechanisms and algorithms.

We have examined the evolution of the concept of a Hebbian synaptic modification and have suggested a contemporary definition. The biophysical mechanism demonstrated in vitro to control the induction of one type of hippocampal LTP has been shown to satisfy our definition of a Hebbian synaptic modification. Whether this biophysical mechanism is involved in the organization of behavior in the manner that Hebb originally envisioned remains to be seen. We have also summarized several modification algorithms that have been explored in theoretical studies of learning in adaptive networks. These algorithms also satisfied our definition of a Hebbian modification, but their relationships to known neurobiology require further exploration. By reviewing the biophysical mechanisms and formal algorithms together, we have exposed obvious similarities and differences. Such comparisons may help bridge the gap between computational theory and knowledge of the neurobiology of use-dependent synaptic change. Current models of LTP reveal that the activity-modification relationships are extremely sensitive to the biophysical/molecular details. The activity-modification relationships obviously can have a major influence on adaptive neurodynamics at the network level. As more accurate representations of the biological complexity and diversity are introduced into adaptive network simulations, we expect to gain new insights into the classes of computation that particular networks are capable of performing.

Algorithms↗

PubMed1988

Long-term synaptic potentiation.

Long-term synaptic potentiation (LTP) is a leading candidate for a synaptic mechanism of rapid learning in mammals. LTP is a persistent increase in synaptic efficacy that can be quickly induced. The biophysical process that controls one type of LTP is formally similar to a synaptic memory mechanism postulated decades ago by the psychologist Donald Hebb. A key aspect of the modification process involves the N-methyl-D-aspartate (NMDA) receptor-ionophore complex. This ionophore allows calcium influx only if the endogenous ligand glutamate binds to the NMDA receptor and if the voltage across the associated channel is also sufficiently depolarized to relieve a magnesium block. According to one popular hypothesis, the resulting increase in the intracellular calcium concentration activates protein kinases that enhance the postsynaptic conductance. Further biophysical and molecular understanding of the modification process should facilitate detailed explorations of the mnemonic functions of LTP.

Animals↗

PubMed1988

The role of the pyriform cortex in the generation of interictal spikes in the kindled preparation.

The development of interictal spikes (IIS) was monitored during amygdala or pyriform cortex kindling in a series of 4 experiments. It was found that (1) spike-like transients were often present in the pyriform cortex EEG before kindling had begun; (2) these transients developed progressively into large amplitude and complex IIS as kindling proceeded; (3) the pyriform cortex IIS continued to show the greatest proportion of earliest onset spikes in most animals after kindling was completed; (4) other sites (including the ventral, but not the dorsal hippocampus) gradually developed the capacity to generate IIS as kindling progressed; (5) although specific sites within the pyriform cortex may serve as a generator, their location along the longitudinal axis of the pyriform lobe varied from animal to animal (and did not appear to depend upon the location of the kindling electrode); (6) although there often appeared to be 2 spike types, based on the polarity of the first component, there were also transitional waveforms, raising the possibility that they were variations on a single spike type, and (7) the IIS were often preceded, usually in the pyriform cortex, by reliable pre-spike events (smaller spikes or a 'ripple' on the EEG).

Amygdala↗

PubMed1988

The effects of various lesions and knife-cuts on septal and amygdala kindling in the rat.

Large bilateral aspiration lesions of the hippocampus had no significant effect on septal kindling, whereas large bilateral DC lesions of the pyriform lobe resulted in a small but significant increase in the number of septal stimulations required to complete kindling. Bilateral aspiration lesions of the dorsal hippocampus or large bilateral DC lesions of the ventral hippocampus had no effect on amygdala kindling. Small DC lesions of the stria terminalis significantly facilitated amygdala kindling. Unilateral or bilateral ventral knife-cuts delivered in a coronal plane anterior to the amygdala, disrupting communication with anterior pyriform structures, produced a small but nearly significant increase in the number of stimulations required for amygdala kindling. Similar cuts placed posterior to the amygdala, disrupting communication with the hippocampus, significantly facilitated kindling. Cuts that were medially placed, to disrupt the ventral amygdala-fugal pathway, had no effect on amygdala kindling. These results show that the hippocampus is not critical for either septal or amygdala kindling. The pyriform lobe structures appear to play a facilitatory role in kindling, but none of the lesions or knife-cuts were capable of blocking or even severely retarding kindling.

Amygdala↗

PubMed1988

Effects of the NMDA antagonist 2AP5 on complex spike discharge by hippocampal pyramidal cells.

The N-methyl-D-aspartate receptor antagonist D,L-2-amino-5-phosphonopentanoate (2AP5) was administered intraventricularly to determine its effect on the complex spike firing pattern of spontaneously active hippocampal pyramidal cells recorded in urethane anaesthetized rats. Following 2AP5 delivery, complex spike firing decreased by a mean 36%, while only a 5% decrease was observed after saline injection. This effect could not be explained by changes in firing rate per se but appeared to be related to the degree of blockade of commissurally induced long-term potentiation. Thus 2AP5 not only disrupts synaptic plasticity in the hippocampus but can also alter the pattern of ongoing activity of the pyramidal cells.

2-Amino-5-phosphonovalerate↗

PubMed1987

Field potential evidence for long-term potentiation of feed-forward inhibition in the rat dentate gyrus.

Trains of high-frequency stimulation to the perforant path cause (i) long-term potentiation (LTP) of the population excitatory post-synaptic potential (EPSP), (ii) a lasting increase in the population spike, and (iii) a lasting alteration of the relationship between the EPSP and population spike (E-S relationship), consisting of a decreased x-intercept and decreased slope of the linear regression. To compare the thresholds of these changes, we applied a series of trains, increasing in duration from below LTP threshold. The EPSP potentiated with about the same low threshold as the reduction in E-S slope, whereas the reduction in E-S x-intercept required longer trains. In the second experiment, LTP of the EPSP was reduced by concurrent high-frequency stimulation of the commissural input and a lasting reduction of the population spike height was observed. In a third experiment, picrotoxin, an antagonist of gamma-aminobutyric acid (GABA)-mediated inhibition, blocked the decrease in slope of the E-S relationship which normally accompanies LTP. These results imply that perforant path/granule cell LTP is normally accompanied by long-term potentiation of a feed-forward inhibitory pathway which may involve interneurones.

Animals↗

PubMed1984

The development of the interictal spike during kindling in the rat.

An attempt was made to determine the location of the generator(s) of interictal discharge in the kindled rat preparation. Animals were kindled by stimulation of hippocampal area CA3, fornix/fimbria, perforant path, amygdala or lateral olfactory tract. The development of interictal discharge was monitored in the intact preparation, and hippocampal slices were subsequently taken from both kindled and control animals. Contrary to our initial hypothesis, the hippocampus did not appear to generate interictal discharge (as determined by onset time) even when the animal was kindled in the hippocampus or one of its input pathways. Also, hippocampal slices taken from kindled animals did not appear to be significantly more prone to either evoked or spontaneous epileptiform responses, compared to control slices, in medium containing high K+ concentrations. Among the structures from which recordings were taken, the amygdala and/or pyriform cortex appeared to show the earliest onset spikes regardless of the site of stimulation. It is proposed that the generator of interictal discharge in kindled animals may reside in the pyriform lobe.

Action Potentials↗