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2. 17β‐Estradiol reduces inhibitory synaptic currents in entorhinal cortex neurons through G protein‐coupled estrogen receptor‐1 activation of extracellular signal‐regulated kinase.

Author

Batallán Burrowes, Ariel A., Moisan, Élyse, Garrone, Aurelie, Buynack, Lauren M., and Chapman, C. Andrew

Subjects
NEURAL transmission, PROTEIN kinases, NEURONS, HIPPOCAMPUS (Brain), ELECTROPHYSIOLOGY, ENTORHINAL cortex
Abstract

Estrogens are believed to modulate cognitive functions in part through the modulation of synaptic transmission in the cortex and hippocampus. Administration of 17β‐estradiol (E2) can rapidly enhance excitatory synaptic transmission in the hippocampus and facilitate excitatory synaptic transmission in rat lateral entorhinal cortex via activation of the G protein‐coupled estrogen receptor‐1 (GPER1). To assess the mechanisms through which GPER1 activation facilitates synaptic transmission, we assessed the effects of acute 10 nM E2 administration on pharmacologically isolated evoked excitatory and inhibitory synaptic currents in layer II/III entorhinal neurons. Female Long‐Evans rats were ovariectomized between postnatal day (PD) 63 and 74 and implanted with a subdermal E2 capsule to maintain continuous low levels of E2. Electrophysiological recordings were obtained between 7 and 20 days after ovariectomy. Application of E2 for 20 min did not significantly affect AMPA or NMDA receptor‐mediated excitatory synaptic currents. However, GABA receptor‐mediated inhibitory synaptic currents (IPSCs) were markedly reduced by E2 and returned towards baseline levels during the 20‐min washout period. The inhibition of GABA‐mediated IPSCs was blocked in the presence of the GPER1 receptor antagonist G15. GPER1 can modulate protein kinase A (PKA), but blocking PKA with intracellular KT5720 did not prevent the E2‐induced reduction in IPSCs. GPER1 can also stimulate extracellular signal‐regulated kinase (ERK), a negative modulator of GABAA receptors, and blocking activation of ERK with PD90859 prevented the E2‐induced reduction of IPSCs. E2 can therefore result in a rapid GPER1 and ERK signaling‐mediated reduction in GABA‐mediated IPSCs. This provides a novel mechanism through which E2 can rapidly modulate synaptic excitability in entorhinal layer II/III neurons and may also contribute to E2 and ERK‐dependent alterations in synaptic transmission in other brain areas. [ABSTRACT FROM AUTHOR]

Published
2024
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8. DCC Expression by Neurons Regulates Synaptic Plasticity in the Adult Brain

Author

Horn, Katherine E., Glasgow, Stephen D., Gobert, Delphine, Bull, Sarah-Jane, Luk, Tamarah, Girgis, Jacklyn, Tremblay, Marie-Eve, McEachern, Danielle, Bouchard, Jean-François, Haber, Michael, Hamel, Edith, Krimpenfort, Paul, Murai, Keith K., Berns, Anton, Doucet, Guy, Chapman, C. Andrew, Ruthazer, Edward S., and Kennedy, Timothy E.

Published
2013
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23. Dopaminergic suppression of synaptic transmission in the lateral entorhinal cortex

Author

Caruana, Douglas A., Chapman, C. Andrew, Caruana, Douglas A., and Chapman, C. Andrew

Abstract

Dopaminergic projections to the superficial layers of the lateral entorhinal cortex can modulate the strength of olfactory inputs to the region. We have found that low concentrations of dopamine facilitate field EPSPs in the entorhinal cortex, and that higher concentrations of dopamine suppress synaptic responses. Here, we have used whole-cell current clamp recordings from layer II neurons to determine the mechanisms of the suppression. Dopamine (10 to 50 μM) hyperpolarized membrane potential and reversibly suppressed the amplitude of EPSPs evoked by layer I stimulation. Both AMPA- and NMDA-mediated components were suppressed, and paired-pulse facilitation was also enhanced indicating that the suppression is mediated largely by reduced glutamate release. Blockade of D2-like receptors greatly reduced the suppression of EPSPs. Dopamine also lowered input resistance, and reduced the number of action potentials evoked by depolarizing current steps. The drop in input resistance was mediated by activation of D1-like receptors, and was prevented by blocking K+ channels with TEA. The dopaminergic suppression of synaptic transmission is therefore mediated by a D2 receptor-dependent reduction in transmitter release, and a D1 receptor-dependent increase in a K+ conductance. This suppression of EPSPs may dampen the strength of sensory inputs during periods of elevated mesocortical dopamine activity.

Published
2008

24. Postsynaptic signals mediating induction of long-term synaptic depression in the entorhinal cortex

Author

Kourrich, Saïd, Glasgow, Stephen D., Caruana, Douglas A., Chapman, C. Andrew, Kourrich, Saïd, Glasgow, Stephen D., Caruana, Douglas A., and Chapman, C. Andrew

Abstract

The entorhinal cortex receives a large projection from the piriform cortex, and synaptic plasticity in this pathway may affect olfactory processing. In vitro whole cell recordings have been used here to investigate postsynaptic signalling mechanisms that mediate the induction of long-term synaptic depression (LTD) in layer II entorhinal cortex cells. To induce LTD, pairs of pulses, using a 30-millisecond interval, were delivered at 1Hz for 15minutes. Induction of LTD was blocked by the NMDA receptor antagonist APV and by the calcium chelator BAPTA, consistent with a requirement for calcium influx via NMDA receptors. Induction of LTD was blocked when the FK506 was included in the intracellular solution to block the phosphatase calcineurin. Okadaic acid, which blocks activation of protein phosphatases 1 and 2a, also prevented LTD. Activation of protein phosphatases following calcium influx therefore contributes to induction of LTD in layer II of the entorhinal cortex.

Published
2008

26. Inhibiting dopamine reuptake blocks the induction of long-term potentiation and depression in the lateral entorhinal cortex of awake rats

Author

Caruana, Douglas A., Reed, Sean J., Sliz, Diane J., Chapman, C. Andrew, Caruana, Douglas A., Reed, Sean J., Sliz, Diane J., and Chapman, C. Andrew

Abstract

Synaptic plasticity in olfactory inputs to the lateral entorhinal cortex may result in lasting changes in the processing of olfactory stimuli. Changes in dopaminergic tone can have strong effects on basal evoked synaptic responses in the superficial layers of the entorhinal cortex, and the current study investigated whether dopamine may modulate the induction of long-term potentiation (LTP) and depression (LTD) in piriform cortex inputs to layer II of the lateral entorhinal cortex in awake rats. Groups of animals were pretreated with either saline or the selective dopamine reuptake inhibitor GBR12909 prior to low or high frequency stimulation to induce LTD or LTP. In saline-treated groups, synaptic responses were potentiated to 122.4 ± 6.4% of baseline levels following LTP induction, and were reduced to 84.5 ± 4.9% following induction of LTD. Changes in synaptic responses were maintained for up to 60 min and returned to baseline levels within 24 h. In contrast, induction of both LTP and LTD was blocked in rats pretreated with GBR12909. Dopaminergic suppression of synaptic plasticity in the entorhinal cortex may serve to restrain activity-dependent plasticity during reward-relevant behavioral states or during processing of novel stimuli.

Published
2007

27. Receptor protein tyrosine phosphatase sigma regulates synapse structure, function and plasticity

Author

Horn, Katherine E., primary, Xu, Bin, additional, Gobert, Delphine, additional, Hamam, Bassam N., additional, Thompson, Katherine M., additional, Wu, Chia-Lun, additional, Bouchard, Jean-François, additional, Uetani, Noriko, additional, Racine, Ronald J., additional, Tremblay, Michel L., additional, Ruthazer, Edward S., additional, Chapman, C. Andrew, additional, and Kennedy, Timothy E., additional

Published
2012
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48. The role of the paraventricular nucleus of the thalamus in the augmentation of heroin seeking induced by chronic food restriction.

Author

Chisholm, Alexandra, Iannuzzi, Jessica, Rizzo, Damaris, Gonzalez, Natasha, Fortin, Émilie, Bumbu, Alexandra, Batallán Burrowes, Ariel A., Chapman, C. Andrew, and Shalev, Uri

Subjects
PARAVENTRICULAR nucleus, HEROIN, THALAMUS, DRUG abstinence, DRUG addiction, FOOD, SUBSTANCE abuse & psychology, ANIMAL behavior, BIOLOGICAL models, RESEARCH, SUBSTANCE abuse, MOTIVATION (Psychology), ANIMAL experimentation, RESEARCH methodology, EVALUATION research, MEDICAL cooperation, RATS, COMPARATIVE studies, HYPOTHALAMUS, RESEARCH funding, PHARMACODYNAMICS
Abstract

Drug addiction is a chronic disorder that is characterized by compulsive drug seeking and involves cycling between periods of compulsive drug use, abstinence, and relapse. In both human addicts and animal models of addiction, chronic food restriction has been shown to increase rates of relapse. Previously, our laboratory has demonstrated a robust increase in drug seeking following a period of withdrawal in chronically food-restricted rats compared with sated rats. To date, the neural mechanisms that mediate the effect of chronic food restriction on drug seeking have not been elucidated. However, the paraventricular nucleus of the thalamus (PVT) appears to be a promising target to investigate. The objective of the current study was to examine the role of the PVT in the augmentation of heroin seeking induced by chronic food restriction. Male Long-Evans rats were trained to self-administer heroin for 10 days. Rats were then removed from the training chambers and experienced a 14-day withdrawal period with either unrestricted (sated) or mildly restricted (FDR) access to food. On day 14, rats underwent a 1-hour heroin-seeking test under extinction conditions, during which neural activity in the PVT was either inhibited or increased using pharmacological or chemogenetic approaches. Unexpectedly, inhibition of the PVT did not alter heroin seeking in food-restricted or sated rats, while enhancing neural activity in the PVT-attenuated heroin seeking in food-restricted rats. These results indicate that PVT activity can modulate heroin seeking induced by chronic food restriction. [ABSTRACT FROM AUTHOR]

Published
2020
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49. Effects of GABAAinhibition on the expression of long‐term potentiation in CA1 pyramidal cells are dependent on tetanization parameters

Author

Chapman, C. Andrew, Perez, Yaël, and Lacaille, Jean‐Claude

Abstract

Long‐term potentiation (LTP) of excitatory synaptic responses of principal neurons in the hippocampus is accompanied by changes in GABAergic inhibition mediated by interneurons. The impact of inhibition on LTP of excitatory postsynaptic responses in CA1 pyramidal cells was assessed by monitoring changes in field potentials evoked by Schaffer collateral stimulation in hippocampal slices in vitro.First, to determine the effect of inhibition on population EPSPs, slices were exposed to the GABAAreceptor antagonist bicuculline (10 μM). Both the slope and amplitude of field EPSPs (fEPSPs) were significantly enhanced by bicuculline indicating that inhibition modulates excitatory postsynaptic responses of pyramidal cells. To assess if stimulation‐dependent changes in inhibition influence LTP of excitatory responses of pyramidal cells, LTP was examined in the presence and absence of bicuculline (20 μM) following either 100 Hz tetanization, or theta‐patterned stimulation (short bursts delivered at 5 Hz). In normal medium, 100 Hz stimulation produced marked short‐term potentiation that decayed 5–10 min post‐tetanus and both stimulation paradigms produced similar LTP at 30 min post‐tetanus. In comparison, LTP of the fEPSP slope and amplitude was significantly enhanced after theta‐patterned stimulation, but not after 100 Hz stimulation, in bicuculline. The greater potentiation of field responses following theta‐patterned stimulation in the presence of bicuculline indicates that a larger potentiation of excitatory responses was unmasked during suppression of inhibitory inputs. These results suggest that a long‐lasting enhancement of inhibition in pyramidal cells was also induced following theta‐patterned stimulation in normal ACSF. Since suppression of inhibition did not uncover a significantly larger potentiation following 100 Hz tetanization, the influence of inhibition on LTP of excitatory responses appears to be stimulation‐dependent. In conclusion, theta‐patterned stimulation appears to be more effective at inducing plasticity within inhibitory circuits, and this plasticity may partially offset concurrent increases in the excitability of the CA1 network. Hippocampus 1998;8:289–298.© 1998 Wiley‐Liss, Inc.

Published
1998
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50. Effects of GABA<INF>A</INF> inhibition on the expression of long-term potentiation in CA1 pyramidal cells are dependent on tetanization parameters

Author

Chapman, C. Andrew, Perez, Yaël, and Lacaille, Jean-Claude

Abstract

Long-term potentiation (LTP) of excitatory synaptic responses of principal neurons in the hippocampus is accompanied by changes in GABAergic inhibition mediated by interneurons. The impact of inhibition on LTP of excitatory postsynaptic responses in CA1 pyramidal cells was assessed by monitoring changes in field potentials evoked by Schaffer collateral stimulation in hippocampal slices in vitro. First, to determine the effect of inhibition on population EPSPs, slices were exposed to the GABAA receptor antagonist bicuculline (10 μM). Both the slope and amplitude of field EPSPs (fEPSPs) were significantly enhanced by bicuculline indicating that inhibition modulates excitatory postsynaptic responses of pyramidal cells. To assess if stimulation-dependent changes in inhibition influence LTP of excitatory responses of pyramidal cells, LTP was examined in the presence and absence of bicuculline (20 μM) following either 100 Hz tetanization, or theta-patterned stimulation (short bursts delivered at 5 Hz). In normal medium, 100 Hz stimulation produced marked short-term potentiation that decayed 5–10 min post-tetanus and both stimulation paradigms produced similar LTP at 30 min post-tetanus. In comparison, LTP of the fEPSP slope and amplitude was significantly enhanced after theta-patterned stimulation, but not after 100 Hz stimulation, in bicuculline. The greater potentiation of field responses following theta-patterned stimulation in the presence of bicuculline indicates that a larger potentiation of excitatory responses was unmasked during suppression of inhibitory inputs. These results suggest that a long-lasting enhancement of inhibition in pyramidal cells was also induced following theta-patterned stimulation in normal ACSF. Since suppression of inhibition did not uncover a significantly larger potentiation following 100 Hz tetanization, the influence of inhibition on LTP of excitatory responses appears to be stimulation-dependent. In conclusion, theta-patterned stimulation appears to be more effective at inducing plasticity within inhibitory circuits, and this plasticity may partially offset concurrent increases in the excitability of the CA1 network. Hippocampus 1998;8:289–298. © 1998 Wiley-Liss, Inc.

Published
1998
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