Drorit Saar
University of Haifa
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Featured researches published by Drorit Saar.
European Journal of Neuroscience | 1998
Drorit Saar; Yoram Grossman; Edi Barkai
Learning‐related cellular modifications were studied in the rat piriform cortex. Water‐deprived rats were divided to three groups: ‘trained’ rats were trained in a four‐arm maze to discriminate positive cues in pairs of odours, ‘control’ rats were ‘pseudo‐trained’ by random water rewarding, and ‘naive’ rats were water‐deprived only. In one experimental paradigm, the trained group was exposed to extensive training with rats learning to discriminate between 35 and 50 pairs of odours. Piriform cortex pyramidal neurons from ‘trained’, ‘control’ and ‘naive’ rats did not differ in their passive membrane properties and single spike characteristics. However, the after‐hyperpolarizations (AHPs) that follow six‐spike trains were reduced after ‘extensive training’ by 43% and 36% compared with ‘control’ and ‘naive’, respectively. This effect was not observed in the piriform cortex of another group of rats, in which hyperexcitability was induced by chemical kindling. In another experimental paradigm rats were trained only until they demonstrated ‘rule learning’, usually after discriminating between one and two pairs of odours (‘mild training’). In this experiment, a smaller, yet significant, reduction (20%) in AHPs was observed. AHP reduction was apparent in most of the sampled neurons. AHP remained reduced up to 3 days after the last training session. 5 days or more after the last training session, AHP amplitude recovered to pre‐training value and did not differ between ‘trained’ rats and the others. Accordingly, training suspension for 5 days or more resulted in slower learning of novel odours. We suggest that increased neuronal excitability, manifested as reduced AHP, is related to the ability of the cortical network to enter a ‘learning mode’ which creates favourable conditions for enhanced learning capability.
The Journal of Neuroscience | 2001
Drorit Saar; Yoram Grossman; Edi Barkai
We studied the role of acetylcholine (ACh) in creating learning-related long-lasting modifications in the rat cortex. Rats were trained to discriminate positive and negative cues in pairs of odors, until they demonstrated rule learning and entered a mode of high capability for learning of additional odors. We have previously reported that pyramidal neurons in olfactory (piriform) cortex from trained rats had reduced spike afterhyperpolarization (AHP) for 3 d after rule learning. In the present study we examined the mechanism underlying this long-lasting modification. The cholinergic agonist carbachol reduced both slow AHP and firing adaptation in neurons from pseudotrained rats, but had no effect on neurons from trained rats, suggesting pre-existing cholinergic effect. Intracellular application of the calcium chelator BAPTA abolished the difference in slow AHP and in adaptation between groups, suggesting that the difference resulted from reduction in the ACh-sensitive, Ca2+-dependent potassium current, IAHP. At the behavioral level, application of the muscarinic blocker scopolamine before each training session delayed rule learning but had no effect on further acquisition of odor memory. We suggest that intense ACh activity during rule learning enhances neuronal excitability in the piriform cortex by reducing IAHP and that the effect outlasts the stage of rule learning, so that ACh activity is not crucial for further odor learning.
Reviews in The Neurosciences | 2001
Edi Barkai; Drorit Saar
This review describes research that combines cellular physiology with behavioral neuroscience, to study the cellular mechanisms underlying learning and memory in the mammalian brain. Rats were trained with an olfactory conditioning paradigm, in which they had to memorize odors in order to be rewarded with drinking water. Such training results in rule learning, which enables enhanced acquisition of odor memory. Training results in the following learning-related physiological modifications in intrinsic and synaptic properties in olfactory (piriform) cortex pyramidal neurons: 1. increased neuronal excitability, indicated by reduced afterhyperpolarization, and 2. increased synaptic transmission, indicated by reduced paired-pulse facilitation. These modifications are correlated to enhanced learning capability rather than to storage of memory for specific odors. In addition, using a different paradigm of odor-training, it is shown that NMDA and betra-adrenergic receptors are involved at different stages of long-term memory consolidation.
Journal of Neurophysiology | 2012
Drorit Saar; Iris Reuveni; Edi Barkai
Training rats to perform rapidly and efficiently in an olfactory discrimination task results in robust enhancement of excitatory and inhibitory synaptic connectivity in the rat piriform cortex, which is maintained for days after training. To explore the mechanisms by which such synaptic enhancement occurs, we recorded spontaneous miniature excitatory and inhibitory synaptic events in identified piriform cortex neurons from odor-trained, pseudo-trained, and naive rats. We show that olfactory discrimination learning induces profound enhancement in the averaged amplitude of AMPA receptor-mediated miniature synaptic events in piriform cortex pyramidal neurons. Such physiological modifications are apparent at least 4 days after learning completion and outlast learning-induced modifications in the number of spines on these neurons. Also, the averaged amplitude of GABA(A) receptor-mediated miniature inhibitory synaptic events was significantly enhanced following odor discrimination training. For both excitatory and inhibitory transmission, an increase in miniature postsynaptic current amplitude was evident in most of the recorded neurons; however, some neurons showed an exceptionally great increase in the amplitude of miniature events. For both excitatory and inhibitory transmission, the frequency of spontaneous synaptic events was not modified after learning. These results suggest that olfactory discrimination learning-induced enhancement of synaptic transmission in cortical neurons is mediated by postsynaptic modulation of AMPA receptor-dependent currents and balanced by long-lasting modulation of postsynaptic GABA(A) receptor-mediated currents.
Molecular Neurobiology | 2009
Drorit Saar; Edi Barkai
Pyramidal neurons in the piriform cortex of olfactory discrimination trained rats show enhanced intrinsic neuronal excitability that lasts for several days after learning. Such enhanced intrinsic excitability is mediated by long-term reduction in the postburst after hyperpolarization which is generated by repetitive spike firing. The molecular machinery underlying such long-lasting modulation of intrinsic excitability, as well as its exceptional durability, is yet to be fully described. In this review, we present recent advancements that reveal the identity of the current that is modulated after learning and the second messenger system by which enhanced excitability is maintained. We also discuss the significance of such long-lasting modulation to the local network’s sensitivity to noradrenaline, a major learning-relevant neuromodulator.
PLOS ONE | 2013
Iris Reuveni; Drorit Saar; Edi Barkai
Olfactory-discrimination learning was shown to induce a profound long-lasting enhancement in the strength of excitatory and inhibitory synapses of pyramidal neurons in the piriform cortex. Notably, such enhancement was mostly pronounced in a sub-group of neurons, entailing about a quarter of the cell population. Here we first show that the prominent enhancement in the subset of cells is due to a process in which all excitatory synapses doubled their strength and that this increase was mediated by a single process in which the AMPA channel conductance was doubled. Moreover, using a neuronal-network model, we show how such a multiplicative whole-cell synaptic strengthening in a sub-group of cells that form a memory pattern, sub-serves a profound selective enhancement of this memory. Network modeling further predicts that synaptic inhibition should be modified by complex learning in a manner that much resembles synaptic excitation. Indeed, in a subset of neurons all GABAA-receptors mediated inhibitory synapses also doubled their strength after learning. Like synaptic excitation, Synaptic inhibition is also enhanced by two-fold increase of the single channel conductance. These findings suggest that crucial learning induces a multiplicative increase in strength of all excitatory and inhibitory synapses in a subset of cells, and that such an increase can serve as a long-term whole-cell mechanism to profoundly enhance an existing Hebbian-type memory. This mechanism does not act as synaptic plasticity mechanism that underlies memory formation but rather enhances the response of already existing memory. This mechanism is cell-specific rather than synapse-specific; it modifies the channel conductance rather than the number of channels and thus has the potential to be readily induced and un-induced by whole-cell transduction mechanisms.
Journal of Neurophysiology | 2014
Adi Kfir; Naama Ohad-Giwnewer; Luna Jammal; Drorit Saar; David Golomb; Edi Barkai
Complex olfactory-discrimination (OD) learning results in a series of intrinsic and excitatory synaptic modifications in piriform cortex pyramidal neurons that enhance the circuit excitability. Such overexcitation must be balanced to prevent runway activity while maintaining the efficient ability to store memories. We showed previously that OD learning is accompanied by enhancement of the GABAA-mediated inhibition. Here we show that GABAB-mediated inhibition is also enhanced after learning and study the mechanism underlying such enhancement and explore its functional role. We show that presynaptic, GABAB-mediated synaptic inhibition is enhanced after learning. In contrast, the population-average postsynaptic GABAB-mediated synaptic inhibition is unchanged, but its standard deviation is enhanced. Learning-induced reduction in paired pulse facilitation in the glutamatergic synapses interconnecting pyramidal neurons was abolished by application of the GABAB antagonist CGP55845 but not by blocking G protein-gated inwardly rectifying potassium channels only, indicating enhanced suppression of excitatory synaptic release via presynaptic GABAB-receptor activation. In addition, the correlation between the strengths of the early (GABAA-mediated) and late (GABAB-mediated) synaptic inhibition was much stronger for each particular neuron after learning. Consequently, GABAB-mediated inhibition was also more efficient in controlling epileptic-like activity induced by blocking GABAA receptors. We suggest that complex OD learning is accompanied by enhancement of the GABAB-mediated inhibition that enables the cortical network to store memories, while preventing uncontrolled activity.
European Journal of Neuroscience | 2003
Drorit Saar; Edi Barkai
The Journal of Neuroscience | 1999
Drorit Saar; Yoram Grossman; Edi Barkai
Journal of Neurophysiology | 2002
Drorit Saar; Yoram Grossman; Edi Barkai