Electrophysiological effects of sustained delivery of CRF and its receptor agonists in hippocampal slices

Rebaudo, Renata; Melani, Raffaella; Balestrino, Maurizio; Izvarina, N. L.

doi:10.1016/s0006-8993(01)03160-2

Cited by 31 publications

(15 citation statements)

References 18 publications

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“…It has been described that CRH (125–250 nM) increases neuronal excitability (Aldenhoff et al, 1983; Hollrigel et al, 1998; Wang et al, 1998; Sillaber et al, 2002) and enhances activity propagation through the hippocampal formation (von Wolff et al, 2011). In contrast, the application of either lower or higher CRH concentrations resulted in a depression of neuronal activity (Rebaudo et al, 2001). In our experiments we exclusively delivered a CRH concentration of 125 nM and observed enhanced neuronal excitability, in accordance with other studies (Smith and Dudek, 1994; Hollrigel et al, 1998; Blank et al, 2002; Eckart et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Activation of CRH receptor type 1 expressed on glutamatergic neurons increases excitability of CA1 pyramidal neurons by the modulation of voltage-gated ion channels

Kratzer¹,

Mattusch²,

Metzger³

et al. 2013

Front. Cell. Neurosci.

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Corticotropin-releasing hormone (CRH) plays an important role in a substantial number of patients with stress-related mental disorders, such as anxiety disorders and depression. CRH has been shown to increase neuronal excitability in the hippocampus, but the underlying mechanisms are poorly understood. The effects of CRH on neuronal excitability were investigated in acute hippocampal brain slices. Population spikes (PS) and field excitatory postsynaptic potentials (fEPSP) were evoked by stimulating Schaffer-collaterals and recorded simultaneously from the somatic and dendritic region of CA1 pyramidal neurons. CRH was found to increase PS amplitudes (mean ± Standard error of the mean; 231.8 ± 31.2% of control; n = 10) while neither affecting fEPSPs (104.3 ± 4.2%; n = 10) nor long-term potentiation (LTP). However, when Schaffer-collaterals were excited via action potentials (APs) generated by stimulation of CA3 pyramidal neurons, CRH increased fEPSP amplitudes (119.8 ± 3.6%; n = 8) and the magnitude of LTP in the CA1 region. Experiments in slices from transgenic mice revealed that the effect on PS amplitude is mediated exclusively by CRH receptor 1 (CRHR1) expressed on glutamatergic neurons. The effects of CRH on PS were dependent on phosphatase-2B, L- and T-type calcium channels and voltage-gated potassium channels but independent on intracellular Ca2+-elevation. In patch-clamp experiments, CRH increased the frequency and decay times of APs and decreased currents through A-type and delayed-rectifier potassium channels. These results suggest that CRH does not affect synaptic transmission per se, but modulates voltage-gated ion currents important for the generation of APs and hence elevates by this route overall neuronal activity.

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Section: Discussionmentioning

confidence: 99%

Activation of CRH receptor type 1 expressed on glutamatergic neurons increases excitability of CA1 pyramidal neurons by the modulation of voltage-gated ion channels

Kratzer¹,

Mattusch²,

Metzger³

et al. 2013

Front. Cell. Neurosci.

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“…In the hippocampus, it has been proposed that stress associated with a novel environment may impair learning and memory retrieval by saturating the mechanisms that generate glutamate receptor-mediated long-term potentiation (LTP) such that they are limited in their ability to subsequently respond to other stimuli that would normally promote learning (for review, Diamond et al, 2005;Kim et al, 2006;Howland and Wang, 2008;Collingridge et al, 2010). Consistent with this model, CRF has been shown to prevent LTP in the hippocampus (Rebaudo et al, 2001). It is provocative to consider a mirror mechanism by which AAS-dependent increases in CRF at the synapse may 'de-saturate' transmission between the CeA and dlBnST by enhancing GABAergic inhibition, extending the response range in this critical circuit in the extended amygdala and thus allowing the more pronounced expression of sustained fear/anxiety to stressful stimuli that was observed in these animals.…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Factor Modulation of Forebrain GABAergic Transmission has a Pivotal Role in the Expression of Anabolic Steroid-Induced Anxiety in the Female Mouse

Oberlander

Henderson

2012

Neuropsychopharmacol

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Increased anxiety is commonly observed in individuals who illicitly administer anabolic androgenic steroids (AAS). Behavioral effects of steroid abuse have become an increasing concern in adults and adolescents of both sexes. The dorsolateral bed nucleus of the stria terminalis (dlBnST) has a critical role in the expression of diffuse anxiety and is a key site of action for the anxiogenic neuromodulator, corticotropin releasing factor (CRF). Here we demonstrate that chronic, but not acute, exposure of female mice during adolescence to AAS augments anxiety-like behaviors; effects that were blocked by central infusion of the CRF receptor type 1 antagonist, antalarmin. AAS treatment selectively increased action potential (AP) firing in neurons of the central amygdala (CeA) that project to the dlBnST, increased the frequency of GABA(A) receptor-mediated spontaneous inhibitory postsynaptic currents (sIPSCs) in dlBnST target neurons, and decreased both c-FOS immunoreactivity (IR) and AP frequency in these postsynaptic cells. Acute application of antalarmin abrogated the enhancement of GABAergic inhibition induced by chronic AAS exposure whereas application of CRF to brain slices of naïve mice mimicked the actions of this treatment. These results, in concert with previous data demonstrating that chronic AAS treatment results in enhanced levels of CRF mRNA in the CeA and increased CRF-IR in the dlBnST neuropil, are consistent with a mechanism in which the enhanced anxiety elicited by chronic AAS exposure involves augmented inhibitory activity of CeA afferents to the dlBnST and CRF-dependent enhancement of GABAergic inhibition in this brain region.

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“…Interestingly, this enhancement of potentiation of NMDAR EPSCs exhibited a novel pharmacology in cocaine-treated mice, with a requirement for both CRFR1 and CRFR2 and for both PKA and PKC. Many physiological actions of CRF exhibit antagonistic interactions of CRFR1 and CRFR2 (Hillhouse and Grammatopoulos, 2006); however, CRFR1 and CRFR2 can also exhibit additive or more complex interactions (Rebaudo et al, 2001; Hauger et al, 2006; Gao et al, 2008). In the amygdala, CRFR2/PKC mediates a potentiation of glutamate receptor currents, with an additional enhancement after cocaine through the CRFR1/PKA pathway recruited (Pollandt et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Chronic Cocaine Enhances Corticotropin-Releasing Factor-Dependent Potentiation of Excitatory Transmission in Ventral Tegmental Area Dopamine Neurons

Hahn¹,

Hopf²,

Bonci³

2009

J. Neurosci.

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Current concepts suggest that stress-induced release of neuromodulators such as corticotropin-releasing factor (CRF) can drive drugdependent behaviors. Although previous drug exposure can enhance behavioral and neurochemical responses to stress, it is unclear how such drug exposure alters the CRF modulation of excitatory synapses onto ventral tegmental area (VTA) dopamine neurons, a key locus of drug-and stress-induced neuroadaptation. Here, we demonstrate that, after repeated cocaine exposure, the magnitude and duration of the CRF-induced potentiation of NMDA receptor (NMDAR)-mediated neurotransmission was significantly increased compared with naive and saline-treated mice. Furthermore, CRF enhanced AMPA receptor (AMPAR)-mediated transmission only in mice that were exposed to cocaine. Increased frequency of AMPAR-mediated spontaneous miniature EPSCs and the intracellular blockade of CRF potentiation of AMPAR-mediated transmission suggest both presynaptic and postsynaptic effects of CRF. Importantly, pharmacological experiments revealed that CRF receptor 1 and protein kinase A pathways were newly recruited after repeated cocaine for the enhancement of CRF-induced NMDAR potentiation and the appearance of AMPAR potentiation. Thus, enhanced CRF-induced potentiation of excitatory synaptic transmission onto VTA dopamine neurons after cocaine preexposure is likely to produce an abnormal increase in dopamine release during stressful events and could augment activation of addictive behaviors in response to stress.

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Electrophysiological effects of sustained delivery of CRF and its receptor agonists in hippocampal slices

Cited by 31 publications

References 18 publications

Activation of CRH receptor type 1 expressed on glutamatergic neurons increases excitability of CA1 pyramidal neurons by the modulation of voltage-gated ion channels

Activation of CRH receptor type 1 expressed on glutamatergic neurons increases excitability of CA1 pyramidal neurons by the modulation of voltage-gated ion channels

Corticotropin-Releasing Factor Modulation of Forebrain GABAergic Transmission has a Pivotal Role in the Expression of Anabolic Steroid-Induced Anxiety in the Female Mouse

Chronic Cocaine Enhances Corticotropin-Releasing Factor-Dependent Potentiation of Excitatory Transmission in Ventral Tegmental Area Dopamine Neurons

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