A transcriptomic analysis of type I–III neurons in the bed nucleus of the stria terminalis

Hazra, Rimi; Guo, Ji-Ming; Ryan, Steven J.; Jasnow, Aaron M.; Dabrowska, Joanna; Rainnie, Donald G.

doi:10.1016/j.mcn.2011.01.011

Cited by 43 publications

(67 citation statements)

References 89 publications

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“…Such features include the input resistance, membrane time constants, depolarizing voltage sag, afterdepolarization, and others that characterize the voltage responses of BNST neurons under current step stimulation. Previous studies identified three main types of BNST neurons (Hammack et al 2007;Hazra et al 2011). Specifically, type I neurons are characterized by the presence of a depolarizing voltage sag indicative of their intrinsic hyperpolarization-activated cation current (I h ).…”

Section: Resultsmentioning

confidence: 99%

Differential effects of static and dynamic inputs on neuronal excitability

Szűcs

Huerta

2015

Journal of Neurophysiology

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Szücs A, Huerta R. Differential effects of static and dynamic inputs on neuronal excitability. J Neurophysiol 113: [232][233][234][235][236][237][238][239][240][241][242][243] 2015. First published October 1, 2014; doi:10.1152/jn.00226.2014.-The intrinsic excitability of neurons is known to be dynamically regulated by activity-dependent plasticity and homeostatic mechanisms. Such processes are commonly analyzed in the context of input-output functions that describe how neurons fire in response to constant levels of current. However, it is not well understood how changes of excitability as observed under static inputs translate to the function of the same neurons in their natural synaptic environment. Here we performed a computational study and hybrid experiments on rat bed nucleus of stria terminalis neurons to compare the two scenarios. The inward rectifying K ir current (I Kir ) and the hyperpolarization-activated cation current (I h ) were found to be considerably more effective in regulating the firing under synaptic inputs than under static stimuli. This prediction was experimentally confirmed by dynamic-clamp insertion of a synthetic inwardly rectifying K ir current into the biological neurons. At the same time, ionic currents that activate with depolarization were more effective regulating the firing under static inputs. When two intrinsic currents are concurrently altered such as those under homeostatic regulation, the effects in firing responses under static vs. dynamic inputs can be even more contrasting. Our results show that plastic or homeostatic changes of intrinsic membrane currents can shape the current step responses of neurons and their firing under synaptic inputs in a differential manner. intrinsic excitability; firing; integration; physiological properties; computational model; dynamic clamp INTRINSIC EXCITABILITY, AS one of the most distinctive properties of neurons, refers to their propensity to generate action potentials in response to depolarizing current or excitatory synaptic inputs. This behavior reflects the concerted action of voltagedependent ionic channels in the membrane of the neuron. Beyond the classic spike-generating conductances, i.e., the transient Na and the delayed rectifier type K channels, neurons express a variety of additional voltage-gated channels that regulate the rate and structure of their firing. Neuronal output is therefore produced by a complex interplay between the synaptic inputs and the voltage-dependent membrane conductances. An increasing number of studies demonstrate that intrinsic cellular properties of neurons are subject to activitydependent plastic changes and homeostatic regulation similarly to those of synaptic properties (Hyun et al. 2013;Jung and Hoffman 2009;O'Leary et al. 2010;van Welie et al. 2004). In this respect, learning, memory, and various other forms of activity-dependent plasticity are also strongly linked to intrinsic excitability and the operation of the voltage-gated channels (Desai et al. 1999;Schulz 2006;Turrigiano 2011).Experimen...

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Section: Resultsmentioning

confidence: 99%

Differential effects of static and dynamic inputs on neuronal excitability

Szűcs

Huerta

2015

Journal of Neurophysiology

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“…Only those cell samples positive for 18S rRNA were subjected to amplification with primers. The procedure used to determine mRNA transcript expression in single cells has been described in detail previously (Hazra et al 2011). The sequences for the oligonucleotide primers are detailed in Table 1.…”

Section: Methodsmentioning

confidence: 99%

“…RT-PCR was also performed on whole BLA of P7 rats, from tissue isolated by microdissection from 300-m-thick slices. The slices were made with the protocol for electrophysiological recording described above, and RNA isolation and RT-PCR were performed as described previously (Hazra et al 2011).…”

Section: Methodsmentioning

confidence: 99%

Postnatal maturation of GABAergic transmission in the rat basolateral amygdala

Ehrlich

Ryan

Hazra

et al. 2013

Journal of Neurophysiology

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“…The procedure used to determine mRNA transcript expression in single cells has been described in detail elsewhere (23,43). BNST slices were obtained as previously described (44).…”

Section: Methodsmentioning

confidence: 99%

Cell-type specific deletion of GABA(A)α1 in corticotropin-releasing factor-containing neurons enhances anxiety and disrupts fear extinction

Gafford

Guo

Flandreau

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Corticotropin-releasing factor (CRF) is critical for the endocrine, autonomic, and behavioral responses to stressors, and it has been shown to modulate fear and anxiety. The CRF receptor is widely expressed across a variety of cell types, impeding progress toward understanding the contribution of specific CRF-containing neurons to fear dysregulation. We used a unique CRF-Cre driver transgenic mouse line to remove floxed GABA(A)α1 subunits specifically from CRF neurons [CRF-GABA(A)α1 KO]. This process resulted in mice with decreased GABA(A)α1 expression only in CRF neurons and increased CRF mRNA within the amygdala, bed nucleus of the stria terminalis (BNST) and paraventricular nucleus of the hypothalamus. These mice show normal locomotor and pain responses and no difference in depressive-like behavior or Pavlovian fear conditioning. However, CRF-GABA(A)α1 KO increased anxiety-like behavior and impaired extinction of conditioned fear, coincident with an increase in plasma corticosterone concentration. These behavioral impairments were rescued with systemic or BNST infusion of the CRF antagonist R121919. Infusion of Zolpidem, a GABA(A)α1-preferring benzodiazepine-site agonist, into the BNST of the CRF-GABA(A)α1 KO was ineffective at decreasing anxiety. Electrophysiological findings suggest a disruption in inhibitory current may play a role in these changes. These data indicate that disturbance of CRF containing GABA(A)α1 neurons causes increased anxiety and impaired fear extinction, both of which are symptoms diagnostic for anxiety disorders, such as posttraumatic stress disorder.central amygdala | plasticity | HPA axis | short term synaptic depression | knockout T he neuropeptide corticotrophin-releasing factor (CRF) is involved in initiation of the endocrine, autonomic, and behavioral responses to stressors and its dysfunction is implicated in a variety of mood and anxiety disorders (1). Large populations of CRF-containing neurons are located within brain areas crucial for fear and anxiety, including the central amygdala (CeA), bed nucleus of the stria terminalis (BNST), and paraventricular nucleus of the hypothalamus (PVN). Although site-specific and conditional knockout approaches are increasingly being used (2, 3), the broad expression of CRF receptors and the varied cell types in which the CRF peptide is produced (4, 5) make it challenging to identify region and cell-type specific influences of CRF. One way to manipulate specific subpopulations of CRF neurons is to use mice with the Cre recombinase gene driven by the CRF promoter to allow different subgroups of CRFergic cells to be manipulated.The interaction between CRF and GABA activity in brain structures important for fear and anxiety has been identified as a potential mechanism underlying anxiety disorders (6). CRF administration increases GABA release within the amygdala (7, 8) and causes deficits in GABA(A) receptor-mediated inhibitory transmission (9). Lifelong CRF overexpression leads to changes in GABA receptor subtype expression and sensitivity (1...

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A transcriptomic analysis of type I–III neurons in the bed nucleus of the stria terminalis

Abstract: The activity of neurons in the anterolateral cell group of the bed nucleus of the stria terminalis (BNST ALG ) plays a critical role in anxiety-and stress-related behaviors.

Cited by 43 publications

References 89 publications

Differential effects of static and dynamic inputs on neuronal excitability

Differential effects of static and dynamic inputs on neuronal excitability

Postnatal maturation of GABAergic transmission in the rat basolateral amygdala

Cell-type specific deletion of GABA(A)α1 in corticotropin-releasing factor-containing neurons enhances anxiety and disrupts fear extinction

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