Biomedical subjects

Joe Guillaume Pelletier

Publications and source records attributed to Joe Guillaume Pelletier.

10 recordsLinked to original sources

PubMed2006

Emotional enhancement of memory via amygdala-driven facilitation of rhinal interactions.

Emotions generally facilitate memory, an effect mediated by the basolateral amygdala (BLA). To study the underlying mechanisms, we recorded BLA, perirhinal and entorhinal neurons during an appetitive trace-conditioning task. We focused on the rhinal cortices because they constitute the interface between the hippocampus, a mediator of memory consolidation, and the neocortex, the storage site of declarative memories. We found that, after unexpected rewards, BLA activity increased impulse transmission from perirhinal to entorhinal neurons and that this effect decayed as the association between conditioned stimuli and rewards was learned. At this late phase of learning, the BLA effect occurred when the animals were anticipating the reward. By enhancing the processing of sensory cues, the BLA-mediated facilitation of rhinal interactions may explain how the amygdala promotes memory formation in emotional conditions.

Action Potentials↗

PubMed2006

Identification of basolateral amygdala projection cells and interneurons using extracellular recordings.

This study tested whether firing rate and spike shape could be used to distinguish projection cells from interneurons in extracellular recordings of basolateral amygdala (BLA) neurons. To this end, we recorded BLA neurons in isoflurane-anesthetized animals with tungsten microelectrodes. Projection cells were identified by antidromic activation from cortical projection sites of the BLA. Although most projection cells fired spontaneously at low rates (<1 Hz), an important subset fired at higher rates (up to 6.8 Hz). In fact, the distribution of firing rates in projection cells and unidentified BLA neurons overlapped extensively, even though the latter cell group presumably contains a higher proportion of interneurons. The only difference between the two distributions was a small subset (5.1%) of unidentified neurons with unusually high firing rates (9-16 Hz). Similarly, distributions of spike durations in both cell groups were indistinguishable, although most of the fast-firing neurons had spike durations at the low end of the distribution. However, we observed that spike durations depended on the exact position of the electrode with respect to the recorded cell, varying by as much as 0.7 ms. Thus neither firing rate nor spike waveform allowed for unequivocal separation of projection cells from interneurons. Nevertheless, we propose the use of two firing rate cutoffs to obtain relatively pure samples of projection cells and interneurons: < or =1 Hz for projection cells and > or =7 Hz for fast-spiking interneurons. Supplemented with spike-duration cutoffs of > or =0.7 ms for projection cells and < or =0.5 ms for interneurons, this approach should keep instances of misclassifications to a minimum.

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PubMed2005

Prefrontal control of the amygdala.

Accumulating evidence indicates that phobic and posttraumatic anxiety disorders likely result from a failure to extinguish fear memories. Extinction normally depends on a new learning that competes with the original fear memory and is driven by medial prefrontal cortex (mPFC) projections to the amygdala. Although mPFC stimulation was reported to inhibit the central medial (CEm) amygdala neurons that mediate fear responses via their brainstem and hypothalamic projections, it is unclear how this inhibition is generated. Because the mPFC has very sparse projections to CEm output neurons, the mPFC-evoked inhibition of the CEm is likely indirect. Thus, this study tested whether it resulted from a feedforward inhibition of basolateral amygdala (BLA) neurons that normally relay sensory inputs to the CEm. However, our results indicate that mPFC inputs excite rather than inhibit BLA neurons, implying that the inhibition of CEm cells is mediated by an active gating mechanism downstream of the BLA.

Amygdala↗

PubMed2005

Characterization of synaptic conductances and integrative properties during electrically induced EEG-activated states in neocortical neurons in vivo.

The activation of the electroencephalogram (EEG) is paralleled with an increase in the firing rate of cortical neurons, but little is known concerning the conductance state of their membrane and its impact on their integrative properties. Here, we combined in vivo intracellular recordings with computational models to investigate EEG-activated states induced by stimulation of the brain stem ascending arousal system. Electrical stimulation of the pedonculopontine tegmental (PPT) nucleus produced long-lasting (approximately 20 s) periods of desynchronized EEG activity similar to the EEG of awake animals. Intracellularly, PPT stimulation locked the membrane into a depolarized state, similar to the up-states seen during deep anesthesia. During these EEG-activated states, however, the input resistance was higher than that during up-states. Conductance measurements were performed using different methods, which all indicate that EEG-activated states were associated with a synaptic activity dominated by inhibitory conductances. These results were confirmed by computational models of reconstructed pyramidal neurons constrained by the corresponding intracellular recordings. These models indicate that, during EEG-activated states, neocortical neurons are in a high-conductance state consistent with a stochastic integrative mode. The amplitude and timing of somatic excitatory postsynaptic potentials were nearly independent of the position of the synapses in dendrites, suggesting that EEG-activated states are compatible with coding paradigms involving the precise timing of synaptic events.

Animals↗

PubMed2005

Interaction between amygdala and neocortical inputs in the perirhinal cortex.

The rhinal cortices play a critical role in high-order perceptual/mnemonic functions and constitute the main route for impulse traffic to and from the hippocampus. However, previous work has revealed that neocortical stimuli that activate a large proportion of perirhinal neurons are unable to discharge entorhinal cells. In search of mechanisms that might facilitate impulse transfer from the neocortex to the entorhinal cortex, we have examined changes in excitability produced by activation of the lateral amygdala (LA) in isoflurane-anesthetized animals. LA stimulation activated a large proportion of peri- and entorhinal neurons. However, conditioning LA stimuli did not increase the ability of neocortical inputs to activate entorhinal cells even though such pairing produced marked increases in neocortically evoked field potentials and orthodromic firing in the perirhinal cortex. Moreover, increased neocortically evoked perirhinal field potentials and unit responses persisted when the conditioning LA shock was replaced by another neocortical stimulus at the same or at a different site as the testing shock. This perirhinal paired-pulse facilitation (PPF) was maximal with interstimulus intervals of approximately 100 ms. Intracellular recordings of perirhinal neurons revealed that the PPF was generally associated with a rapid shift in the balance between inhibition and excitation, leading to an overall increase in perirhinal responsiveness. The significance of these findings for the role of the perirhinal cortex is discussed.

Action Potentials↗

PubMed2004

Role of amygdala oscillations in the consolidation of emotional memories.

Much evidence indicates that emotional arousal generally improves memory and that the amygdala is responsible for this effect. The available data suggest that stress hormones and neuromodulators released in emotionally arousing conditions alter the activity of basolateral amygdala (BLA) neurons in the hours after the learning episode. In turn, these changes would facilitate synaptic plasticity elsewhere in the brain; however, the biological mechanisms underlying the facilitation of memory consolidation by the BLA remain unknown. This article focuses on data suggesting that synchronized oscillatory BLA activity promotes synaptic plasticity by facilitating interactions between neocortical and temporal lobe areas involved in declarative memory.

Adrenal Cortex Hormones↗

PubMed2004

Low-probability transmission of neocortical and entorhinal impulses through the perirhinal cortex.

One model of episodic memory posits that during slow-wave sleep (SWS), the synchronized discharges of hippocampal neurons in relation to sharp waves "replay" activity patterns that occurred during the waking state, facilitating synaptic plasticity in the neocortex. Although evidence of replay was found in the hippocampus in relation to sharp waves, it was never shown that this activity reached the neocortex. Instead, it was assumed that the rhinal cortices faithfully transmit information from the hippocampus to the neocortex and reciprocally. Here, we tested this idea using 3 different approaches. 1) Stimulating electrodes were inserted in the entorhinal cortex and temporal neocortex and evoked unit responses were recorded in between them, in the intervening rhinal cortices. In these conditions, impulse transfer occurred with an extremely low probability, in both directions. 2) To rule out the possibility that this unreliable transmission resulted from the artificial nature of electrical stimuli, crosscorrelation analyses of spontaneous neocortical, perirhinal, and entorhinal firing were performed in unanesthetized animals during the states of waking and SWS. Again, little evidence of propagation could be obtained in either state. 3) To test the idea that propagation occurs only when large groups of neurons are activated within a narrow time window, we computed perievent histograms of neocortical, perirhinal, and entorhinal neuronal discharges around large-amplitude sharp waves. However, these synchronized entorhinal discharges also failed to propagate across the perirhinal cortex. These findings suggest that the rhinal cortices are more than a relay between the neocortex and hippocampus, but rather a gate whose properties remain to be identified.

Animals↗

PubMed2003

Stimulation of medial prefrontal cortex decreases the responsiveness of central amygdala output neurons.

In extinction of auditory fear conditioning, rats learn that a tone no longer predicts the occurrence of a footshock. Recent lesion and unit recording studies suggest that the medial prefrontal cortex (mPFC) plays an essential role in the inhibition of conditioned fear following extinction. mPFC has robust projections to the amygdala, a structure that is known to mediate the acquisition and expression of conditioned fear. Fear conditioning potentiates the tone responses of neurons in the basolateral amygdala (BLA), which excite neurons in the central nucleus (Ce) of the amygdala. In turn, the Ce projects to the brainstem and hypothalamic areas that mediate fear responses. The present study was undertaken to test the hypothesis that the mPFC inhibits conditioned fear via feedforward inhibition of Ce output neurons. Recording extracellularly from physiologically identified brainstem-projecting Ce neurons, we tested the effect of mPFC prestimulation on Ce responsiveness to synaptic input. In support of our hypothesis, mPFC prestimulation dramatically reduced the responsiveness of Ce output neurons to inputs from the insular cortex and BLA. Thus, our findings support the idea that mPFC gates impulse transmission from the BLA to Ce, perhaps through GABAergic intercalated cells, thereby gating the expression of conditioned fear.

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PubMed2002

Amygdala oscillations and the consolidation of emotional memories.

The amygdala receives multi-modal sensory inputs and projects to virtually all levels of the central nervous system. Via these widespread projections, the amygdala facilitates consolidation of emotionally arousing memories. How the amygdala promotes synaptic plasticity elsewhere in the brain remains unknown, however. Recent work indicates that amygdala neurons show theta activity during emotional arousal, and various types of oscillations during sleep. These synchronized neuronal events could promote synaptic plasticity by facilitating interactions between neocortical storage sites and temporal lobe structures involved in declarative memory.

Journal Article↗

PubMedDate not supplied

Lasting increases in basolateral amygdala activity after emotional arousal: implications for facilitated consolidation of emotional memories.

Manipulations that reduce or enhance the activity of basolateral amygdala (BLA) neurons in the minutes to hours after training have been shown to respectively impair or facilitate retention on the inhibitory avoidance task. Although this suggests that BLA activity is altered after emotional arousal, such changes have not been directly demonstrated. To test this, we devised a feline analog of the inhibitory avoidance task and recorded BLA unit activity before and after a single inescapable footshock. Single-unit recordings revealed that the firing rate of many BLA neurons gradually increased after the footshock, peaking 30-50 min post-shock and then subsiding to baseline levels 2 h later. During this period of increased activity, the discharges of simultaneously recorded BLA cells were more synchronized than before the shock. Although it was known that pairing innocuous (conditioned stimulus, CS) and noxious stimuli modifies the responsiveness of BLA neurons to the CS, our results constitute the first demonstration that emotional arousal produces lasting increases in the spontaneous firing rates of BLA neurons. We propose that these changes in BLA activity may promote Hebbian interactions between coincident but spatially distributed activity patterns in BLA targets, facilitating the consolidation of emotional memories.

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