Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices

Liu, Xianling; Lónárt, György; Sanford, Larry D.

doi:10.1016/j.brainres.2007.01.038

Cited by 6 publications

(5 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, the capacity of ovarian nerve terminals to release NE from vesicular stores in response to K ϩ -induced depolarization appears to fully develop only after the third week of postnatal life. It is possible that the sensitivity of the method we used is not sufficient to detect small changes in NE outflow, despite its demonstrated sensitivity in both the central and peripheral nervous systems (7,34,35). A more parsimonious explanation is that the innervation of neonatal-infantile ovaries has the capacity to synthesize and incorporate NE but has not yet developed the capacity to release the catecholamine on neuronal depolarization.…”

Section: Discussionmentioning

confidence: 99%

“…Total incorporation of 3 H-NE into ovarian tissue increased moderately during the neonatal-infantile period (d [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] and then abruptly during the second half of juvenile development (d 26 -30), remaining elevated at puberty (d [31][32][33][34][35], and after the first ovulation (d 40) (Fig. 1A).…”

Section: Incorporation Of 3 H-ne During Postnatal Ovarian Developmentmentioning

confidence: 99%

See 1 more Smart Citation

Functional Development of the Ovarian Noradrenergic Innervation

et al. 2007

View full text Add to dashboard Cite

A substantial fraction of the noradrenergic innervation targeting the mammalian ovary is provided by neurons of the celiac ganglion. Although studies in the rat have shown that noradrenergic nerves reach the ovary near the time of birth, it is unknown how the functional capacity of this innervation unfolds during postnatal ovarian development. To address this issue, we assessed the ability of the developing ovary to incorporate and release (3)H-norepinephrine. Incorporation of (3)H-norepinephrine was low during the first 3 wk of postnatal life, but pharmacological inhibition of norepinephrine (NE) neuronal uptake with cocaine showed that an intact transport mechanism for NE into nerve terminals is already in place by the first week after birth. Consistent with this functional assessment, the mRNA encoding the NE transporter was also expressed in the celiac ganglion at this time. During neonatal-infantile development [postnatal (PN) d 5-20], the spontaneous, vesicle-independent outflow of recently taken up NE was high, but the NE output in response to K(+)-induced depolarization was low. After PN d 20, spontaneous outflow decreased and the response to K(+) increased markedly, reaching maximal values by the time of puberty. Tyramine-mediated displacement of NE stored in vesicles, which displace vesicular NE, showed that vesicle-dependent NE storage becomes functional by PN d 12 and that vesicular release increases during the juvenile-peripubertal phases of sexual development. These results indicate that vesicular release of NE from ovarian noradrenergic nerves begins to operate by the third week of postnatal life, becoming fully functional near the time of puberty.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Incorporation Of 3 H-ne During Postnatal Ovarian Developmentmentioning

confidence: 99%

Functional Development of the Ovarian Noradrenergic Innervation

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Several studies reveal that LC-NE plays an essential role in the acquisition of cued fear conditioning and this may be dependent upon projections to the BLA (Oei and King, 1980 ; Goldstein et al, 1996 ; Pitman and Delahanty, 2005 ; Liu et al, 2007 ; Tully et al, 2007 ; Rodrigues et al, 2009 ; Tully and Bolshakov, 2010 ; Johnson et al, 2011 ; Krugers et al, 2011 ; Pitman et al, 2012 ; Uematsu et al, 2017 ). This is likely due to stress-induced LC activation in response to the footshock US.…”

Section: Ne and Fear Conditioningmentioning

confidence: 99%

Noradrenergic Modulation of Fear Conditioning and Extinction

Giustino

Maren

2018

Front. Behav. Neurosci.

167

147

View full text Add to dashboard Cite

The locus coeruleus norepinephrine (LC-NE) system plays a broad role in learning and memory. Here we begin with an overview of the LC-NE system. We then consider how both direct and indirect manipulations of the LC-NE system affect cued and contextual aversive learning and memory. We propose that NE dynamically modulates Pavlovian conditioning and extinction, either promoting or impairing learning aversive processes under different levels of behavioral arousal. We suggest that under high levels of stress (e.g., during/soon after fear conditioning) the locus coeruleus (LC) promotes cued fear learning by enhancing amygdala function while simultaneously blunting prefrontal function. Under low levels of arousal, the LC promotes PFC function to promote downstream inhibition of the amygdala and foster the extinction of cued fear. Thus, LC-NE action on the medial prefrontal cortex (mPFC) might be described by an inverted-U function such that it can either enhance or hinder learning depending on arousal states. In addition, LC-NE seems to be particularly important for the acquisition, consolidation and extinction of contextual fear memories. This may be due to dense adrenoceptor expression in the hippocampus (HPC) which encodes contextual information, and the ability of NE to regulate long-term potentiation (LTP). Moreover, recent work reveals that the diversity of LC-NE functions in aversive learning and memory are mediated by functionally heterogeneous populations of LC neurons that are defined by their projection targets. Hence, LC-NE function in learning and memory is determined by projection-specific neuromodulation that accompanies various states of behavioral arousal.

show abstract

“…What's more, fear conditioning increases depolarization-evoked NE release (Liu et al 2007). Moreover, ARs seem particularly pivotal for a late phase of LTP in the LA, which persists for at least three hours and requires the synthesis of new mRNA and protein (Huang et al 2000).…”

Section: Electrophysiological Properties Of Neurons In Fear Circuitrymentioning

confidence: 99%

The Influence of Stress Hormones on Fear Circuitry

Rodrigues

LeDoux

Sapolsky

2009

Annu. Rev. Neurosci.

492

320

View full text Add to dashboard Cite

Fear arousal, initiated by an environmental threat, leads to activation of the stress response, a state of alarm that promotes an array of autonomic and endocrine changes designed to aid self-preservation. The stress response includes the release of glucocorticoids from the adrenal cortex and catecholamines from the adrenal medulla and sympathetic nerves. These stress hormones, in turn, provide feedback to the brain and influence neural structures that control emotion and cognition. To illustrate this influence, we focus on how it impacts fear conditioning, a behavioral paradigm widely used to study the neural mechanisms underlying the acquisition, expression, consolidation, reconsolidation, and extinction of emotional memories. We also discuss how stress and the endocrine mediators of the stress response influence the morphological and electrophysiological properties of neurons in brain areas that are crucial for fear-conditioning processes, including the amygdala, hippocampus, and prefrontal cortex. The information in this review illuminates the behavioral and cellular events that underlie the feedforward and feedback networks that mediate states of fear and stress and their interaction in the brain.

show abstract

Transient fear-induced alterations in evoked release of norepinephrine and GABA in amygdala slices

Cited by 6 publications

References 49 publications

Functional Development of the Ovarian Noradrenergic Innervation

Functional Development of the Ovarian Noradrenergic Innervation

Noradrenergic Modulation of Fear Conditioning and Extinction

The Influence of Stress Hormones on Fear Circuitry

Contact Info

Product

Resources

About