scholarly journals A role for the anterior piriform cortex in early odor preference learning: evidence for multiple olfactory learning structures in the rat pup

2013 ◽  
Vol 110 (1) ◽  
pp. 141-152 ◽  
Author(s):  
Gillian L. Morrison ◽  
Christine J. Fontaine ◽  
Carolyn W. Harley ◽  
Qi Yuan
Keyword(s):  
Nmda Receptors ◽  
Ex Vivo ◽  
Glutamate Release ◽  
Piriform Cortex ◽  
Long Term Potentiation ◽  
Preference Learning ◽  
Excitatory Postsynaptic Potential ◽  
Adrenergic Blockade ◽  
Odor Preference ◽  
Anterior Piriform Cortex

cFos activation in the anterior piriform cortex (aPC) occurs in early odor preference learning in rat pups ( Roth and Sullivan 2005 ). Here we provide evidence that the pairing of odor as a conditioned stimulus and β-adrenergic activation in the aPC as an unconditioned stimulus generates early odor preference learning. β-Adrenergic blockade in the aPC prevents normal preference learning. Enhancement of aPC cAMP response element-binding protein (CREB) phosphorylation in trained hemispheres is consistent with a role for this cascade in early odor preference learning in the aPC. In vitro experiments suggested theta-burst-mediated long-term potentiation (LTP) at the lateral olfactory tract (LOT) to aPC synapse depends on N-methyl-d-aspartate (NMDA) receptors and can be significantly enhanced by β-adrenoceptor activation, which causes increased glutamate release from LOT synapses during LTP induction. NMDA receptors in aPC are also shown to be critical for the acquisition, but not expression, of odor preference learning, as would be predicted if they mediate initial β-adrenoceptor-promoted aPC plasticity. Ex vivo experiments 3 and 24 h after odor preference training reveal an enhanced LOT-aPC field excitatory postsynaptic potential (EPSP). At 3 h both presynaptic and postsynaptic potentiations support EPSP enhancement while at 24 h only postsynaptic potentiation is seen. LOT-LTP in aPC is excluded by odor preference training. Taken together with earlier work on the role of the olfactory bulb in early odor preference learning, these outcomes suggest early odor preference learning is normally supported by and requires multiple plastic changes at least at two levels of olfactory circuitry.

Duration of NMDA-Dependent Synaptic Potentiation in Piriform Cortex In Vivo Is Increased After Epileptiform Bursting

1998 ◽  
Vol 80 (4) ◽  
pp. 1623-1629 ◽  
Author(s):  
A. Kapur ◽  
L. B. Haberly
Keyword(s):  
Seizure Activity ◽  
Piriform Cortex ◽  
Long Term Potentiation ◽  
Excitatory Postsynaptic Potential ◽  
Synaptic Potentiation ◽  
Lateral Olfactory Tract ◽  
Afferent Fibers ◽  
Stimulation Of

Kapur, A. and L. B. Haberly. Duration of NMDA-dependent synaptic potentiation in piriform cortex in vivo is increased after epileptiform bursting. J. Neurophysiol. 80: 1623–1629, 1998. Stimulation of afferent fibers with current pulse trains has been reported to induce long-term potentiation (LTP) in piriform cortex in vitro but not in vivo. LTP has been observed in vivo only when trains are paired with behavioral reinforcement and as a consequence of kindled epileptogenesis. This study was undertaken in the urethan-anesthetized rat to determine if the reported failures to observe pulse-train evoked LTP in vivo may be related to a lesser persistence rather than lack of occurrence, if disinhibition might facilitate induction, and to examine the nature of the relationship between seizure activity and LTP. Stimulation of afferent fibers in the lateral olfactory tract with θ-burst trains under control conditions potentiated the monosynaptic field excitatory postsynaptic potential (EPSP) by approximately the same extent (20.3 ± 2%; n = 12) as reported for the slice. However, in contrast to the slice, potentiation in vivo decayed to a low level within 1–2 h after induction (70% loss in 1.5 h, on average). The N-methyl-d-aspartate (NMDA)-receptor antagonists d-APV and MK-801 blocked the induction of this decremental potentiation. Pharmacological reduction of γ-aminobutyric acid–mediated inhibition at the recording site did not increase the duration of potentiation. In contrast, θ-burst stimulation applied after recovery from a period of epileptiform bursting induced stable NMDA-dependent potentiation. Mean increase in the population EPSP was approximately the same as under control conditions (21 ± 2%; n = 6), but in five of six experiments there was little or no decay in potentiation for the duration of the monitoring period (≤6 h). It is concluded that seizure activity has an enabling action on the induction of persistent synaptic potentiation by stimulus trains that bypasses the need for behavioral reinforcement.

scholarly journals CB1 Receptors in the Anterior Piriform Cortex Control Odor Preference Memory

2019 ◽  
Vol 29 (15) ◽  
pp. 2455-2464.e5 ◽  
Author(s):  
Geoffrey Terral ◽  
Arnau Busquets-Garcia ◽  
Marjorie Varilh ◽  
Svein Achicallende ◽  
Astrid Cannich ◽  
...  
Keyword(s):  
Piriform Cortex ◽  
Cb1 Receptors ◽  
Odor Preference ◽  
Anterior Piriform Cortex

scholarly journals Selective Abolition of the NMDA Component of Long-Term Potentiation in Mice Lacking mGluR5

1998 ◽  
Vol 5 (4) ◽  
pp. 331-343
Author(s):  
Zhengping Jia ◽  
YouMing Lu ◽  
Jeff Henderson ◽  
Franco Taverna ◽  
Carmelo Romano ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Long Term Potentiation ◽  
Mutant Mice ◽  
Excitatory Postsynaptic Potential ◽  
Metabotropic Glutamate ◽  
Term Potentiation

The mechanisms underlying the differential expression of long-term potentiation (LTP) by AMPA and NMDA receptors, are unknown, but could involve G-protein-linked metabotropic glutamate receptors. To investigate this hypothesis we created mutant mice that expressed no metabotropic glutamate receptor 5 (mGluR5), but showed normal development. In an earlier study of these mice we analyzed field-excitatory postsynaptic potential (fEPSPs) in CA1 region of the hippocampus and found a small decrease; possibly arising from changes in the NMDAR-mediated component of synaptic transmission. In the present study we used whole-cell patch clamp recordings of evoked excitatory postsynaptic currents (EPSCs) in CA1 pyramidal neurons to identify the AMPAR- and NMDAR-mediated components of LTP. Recordings from control mice following tetanus, or agonist application (IS, 3R-1-amino-cyclopentane 1,3-dicarboxylic acid) (ACPD), revealed equal enhancement of the AMPA and NMDA receptor-mediated components. In contrast, CA1 neurons from mGluR5-deficient mice showed a complete loss of the NMDA-receptor-mediated component of LTP (LTPNMDA), but normal LTP of the AMPA-receptor-mediated component (LTPAMPA). This selective loss of LTPNMDA was seen in three different genotypic backgrounds and was apparent at all holding potentials (−70 mV to +20 mV). Furthermore, the LTPNMDA deficit in mGluR5 mutant mice could be rescued by stimulating protein kinase C (PKC) with 4β-phorbol-12,13-dibutyrate (PDBu). These results suggest that PKC may couple the postsynaptic mGluR5 to the NMDA-receptor potentiation during LTP, and that this signaling mechanism is distinct from LTPAMPA. Differential enhancement of AMPAR and NMDA receptors by mGluR5 also supports a postsynaptic locus for LTP.

Kindling-induced epileptiform potentials in piriform cortex slices originate in the underlying endopiriform nucleus

1996 ◽  
Vol 76 (3) ◽  
pp. 1430-1438 ◽  
Author(s):  
W. H. Hoffman ◽  
L. B. Haberly
Keyword(s):  
Nmda Receptors ◽  
Feedback Inhibition ◽  
Epileptiform Activity ◽  
Piriform Cortex ◽  
Local Application ◽  
Excitatory Postsynaptic Potential ◽  
Generation Process ◽  
Population Activity ◽  
Epileptiform Events

1. Previous studies in vivo and in vitro have shown that kindling from several locations in the limbic system induces the onset of epileptiform activity in the piriform (olfactory) cortex in the rat. In the present study we tested the hypothesis that kindled epileptiform events in piriform cortex are initiated in the underlying endopiriform nucleus. The experiments were performed in slices taken from rats that were previously kindled by conventional means. 2. Both stimulus-evoked and spontaneous interictal-like epileptiform events were observed in most slices from the anterior piriform cortex, but in few slices from the posterior piriform cortex. These events resembled those described in unanesthetized and urethan-anesthetized rats in previous studies. 3. Findings in support of the hypothesis were as follows. Epileptiform events in the endopiriform nucleus preceded those in the piriform cortex. Epileptiform events could occur in endopiriform nucleus alone, but were only observed in the piriform cortex following occurrence in the endopiriform nucleus. A buildup in population activity preceded the onset of all-or-none epileptiform events in the endopiriform nucleus. Epileptiform events could be triggered by local application of glutamate in the endopiriform nucleus and adjacent claustrum, but not from the piriform cortex. Finally, local application of Co2+ in the endopiriform nucleus, but not in the piriform cortex or elsewhere in the slices, blocked the occurrence of epileptiform events. 4. Additional experiments were performed to further characterize the generation process. 6,7-Dinitroquinoxaline-2,3-dione (DNQX) blocked epileptiform events and the preceding accelerating buildup in multiunit activity at a concentration below that required to block the monosynaptic excitatory postsynaptic potential (EPSP). This suggests that EPSPs mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors underlie epileptiform events in slices of piriform cortex, and that multisynaptic interactions within the endopiriform nucleus are required for generation of these epileptiform EPSPs. By contrast, block of N-methyl-D-aspartate (NMDA) receptors decreased the amplitude of epileptiform EPSPs but did not block their occurrence, indicating that NMDA receptors contribute to generation but are not required. When membrane potential was depolarized to increase driving force, fast inhibitory postsynaptic potentials were found to consistently accompany the buildup process and epileptiform EPSPs. This indicates that if initiation of epileptiform activity in the endopiriform nucleus results from a compromise in feedback inhibition, this compromise is partial rather than complete. 5. Epileptiform EPSPs in slices of piriform cortex from kindled rats displayed similarities in properties, locus of origin, and mechanism of generation to those previously studied in slices from normal rats in which epileptiform activity was induced by a brief period of bursting activity. These similarities suggest that study of bursting-induced epileptiform EPSPs may provide insight into certain aspects of kindling-induced epileptogenesis.

NT-3 Evokes an LTP-Like Facilitation of AMPA/Kainate Receptor–Mediated Synaptic Transmission in the Neonatal Rat Spinal Cord

2000 ◽  
Vol 84 (2) ◽  
pp. 752-758 ◽  
Author(s):  
Viktor L. Arvanov ◽  
Bradley S. Seebach ◽  
Lorne M. Mendell
Keyword(s):  
Spinal Cord ◽  
Synaptic Transmission ◽  
Nmda Receptors ◽  
Kinase Inhibitor ◽  
Long Term Potentiation ◽  
Neonatal Rat ◽  
Kainate Receptor ◽  
Excitatory Postsynaptic Potential ◽  
Rat Spinal Cord ◽  
Monosynaptic Epsp

Neurotrophin-3 (NT-3) is a neurotrophic factor required for survival of muscle spindle afferents during prenatal development. It also acts postsynaptically to enhance the monosynaptic excitatory postsynaptic potential (EPSP) produced by these fibers in motoneurons when applied over a period of weeks to the axotomized muscle nerve in adult cats. Similar increases in the amplitude of the monosynaptic EPSP in motoneurons are observed after periodic systemic treatment of neonatal rats with NT-3. Here we show an acute action of NT-3 in enhancing the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA/kainate) receptor–mediated fast monosynaptic EPSP elicited in motoneurons by dorsal root (DR) stimulation in the in vitro hemisected neonatal rat spinal cord. The receptor tyrosine kinase inhibitor K252a blocks this action of NT-3 as does the calcium chelator bis-( o-aminophenoxy)- N, N, N′, N′-tetraacetic acid (BAPTA) injected into the motoneuron. The effect of NT-3 resembles long-term potentiation (LTP) in that transient bath application of NT-3 to the isolated spinal cord produces a long-lasting increase in the amplitude of the monosynaptic EPSP. An additional similarity is that activation of N-methyl-d-aspartate (NMDA) receptors is required to initiate this increase but not to maintain it. The NMDA receptor blocker MK-801, introduced into the motoneuron through the recording microelectrode, blocks the effect of NT-3, indicating that NMDA receptors in the motoneuron membrane are crucial. The effect of NT-3 on motoneuron NMDA receptors is demonstrated by its enhancement of the depolarizing response of the motoneuron to bath-applied NMDA in the presence of tetrodotoxin (TTX). The potentiating effects of NT-3 do not persist beyond the first postnatal week. In addition, EPSPs with similar properties evoked in the same motoneurons by stimulation of descending fibers in the ventrolateral funiculus (VLF) are not modifiable by NT-3 even in the initial postnatal week. Thus, NT-3 produces synapse-specific and age-dependent LTP-like enhancement of AMPA/kainate receptor–mediated synaptic transmission in the spinal cord, and this action requires the availability of functional NMDA receptors in the motoneuron.

Caffeine-Mediated Presynaptic Long-Term Potentiation in Hippocampal CA1 Pyramidal Neurons

2003 ◽  
Vol 89 (6) ◽  
pp. 3029-3038 ◽  
Author(s):  
Eduardo D. Martín ◽  
Washington Buño
Keyword(s):  
Nmda Receptors ◽  
Glutamate Release ◽  
Ryanodine Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Cellular Mechanisms ◽  
Pipette Solution ◽  
Term Potentiation

We report a new form of long-term potentiation (LTP) in Schaffer collateral (SC)-CA1 pyramidal neuron synapses that originates presynaptically and does not require N-methyl-d-aspartate (NMDA) receptor activation nor increases in postsynaptic-free Ca2+. Using rat hippocampal slices, application of a brief “pulse” of caffeine in the bath evoked a nondecremental LTP (CAFLTP) of SC excitatory postsynaptic currents. An increased probability of transmitter release paralleled the CAFLTP, suggesting that it originated presynaptically. The P1 adenosine receptor antagonist 8-cyclopentyltheophylline and the P2 purinoreceptor antagonists suramin and piridoxal-5′-phosphate-azophenyl 2′,4′-disulphonate blocked the CAFLTP. Inhibition of Ca2+ release from caffeine/ryanodine stores by bath-applied ryanodine inhibited the CAFLTP, but ryanodine in the pipette solution was ineffective, suggesting a presynaptic effect of ryanodine. Previous induction of the “classical” LTP did not prevent the CAFLTP, suggesting that the LTP and the CAFLTP have different underlying cellular mechanisms. The CAFLTP is insensitive to the block of NMDA receptors by 2-amino-5-phosphonopentanoic acid and to Ca2+ chelation with intracellular 1,2-bis (2-aminophenoxy) ethane- N,N,N′ ,N′-tetraacetic acid, indicating that neither postsynaptic NMDA receptors nor increases in cytosolic-free Ca2+ participate in the CAFLTP. We conclude that the CAFLTP requires the interaction of caffeine with presynaptic P1, P2 purinoreceptors, and ryanodine receptors and is caused by an increased probability of glutamate release at SC terminals.

scholarly journals Optical Imaging of Odor Preference Memory in the Rat Olfactory Bulb

2002 ◽  
Vol 87 (6) ◽  
pp. 3156-3159 ◽  
Author(s):  
Qi Yuan ◽  
Carolyn W. Harley ◽  
John H. McLean ◽  
Thomas Knöpfel
Keyword(s):  
Olfactory Bulb ◽  
Optical Imaging ◽  
Imaging Techniques ◽  
Training Session ◽  
Preference Learning ◽  
Excitatory Postsynaptic Potential ◽  
Odor Preference ◽  
Optical Signals ◽  
Olfactory Preference ◽  
Rat Pups

Early olfactory preference learning in rat pups occurs when novel odors are paired with reinforcing tactile stimulation that activate the noradrenergic locus coeruleus. Pairing of odor and a noradrenergic agonist in the olfactory bulb is both necessary and sufficient for odor preference learning. This suggests the memory change occurs in the olfactory bulb. Previous electrophysiological experiments demonstrated that odor preference training induces an increase in the field excitatory postsynaptic potential to olfactory nerve input and an alteration, after training, in glomerular [14C]2- deoxyglucose uptake and in single-unit responses of principal cells. We investigate here whether, 24 h after olfactory preference training, there is an alteration in intrinsic optical signals at the glomerular level. Six-day-old rat pups were trained, as previously, for a peppermint odor preference. Trained pups and control littermates were subjected to imaging of odor-induced intrinsic optical signals 1 day after the training session. Trained pups exhibited significantly larger responses to the peppermint compared with untrained littermates previously exposed to the same odor. The response of trained pups to a control odor (amyl acetate) was, however, not significantly different from that of untrained littermates. These observations demonstrate that odor preference memory can be read-out by optical imaging techniques.

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