Cholinergic responses of morphologically and electrophysiologically characterized neurons of the basolateral complex in rat amygdala slices

Yajeya, Javier; Fuente, Antonio de la; Merchán, Miguel Á.; Riolobos, Adelaida Sánchez; Heredia, Margarita; Criado, Julio J.

doi:10.1016/s0306-4522(96)00614-8

Cited by 33 publications

(40 citation statements)

References 34 publications

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“…Second, and importantly, all cells incorporated in the present analysis showed an input resistance well below 400 M⍀ and spike frequency accommodation, similar to properties reported earlier for pyramidal neurons and incompatible with interneurons. These morphological and electrophysiological characteristics are largely in line with earlier studies (Paré et al 1995;Rainnie et al 1993;Washburn and Moises 1992;Yajeya et al 1997).…”

Section: Effects Of Corticosterone On Membrane Properties Of Ca1 and supporting

confidence: 90%

“…Slices were mounted on glass slides under a coverslip, with Vectashield (Vector Laboratories). Immunofluorescent cells in fixed sections were evaluated using a Zeiss LSM 510 (Carl Zeiss, Jena, Germany) confocal laser-scanning device equipped with a dry Plan-Neofluar ϫ20/0.75 lens or a fluorescent microscope (Zeiss Axiophot; Carl Zeiss, Oberkochen, Germany Neurons in the BLA were selected for recording if they displayed a pyramidal-shaped cell body, in agreement with the morphology of principal neurons in the BLA of various species (Paré et al 1995;Rainnie et al 1993;Washburn and Moises 1992;Yajeya et al 1997). Interneurons, which are usually smaller and display multipolar, spineless dendrites, were avoided.…”

Section: Recordingmentioning

confidence: 99%

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Differential Effects of Corticosterone on the Slow Afterhyperpolarization in the Basolateral Amygdala and CA1 Region: Possible Role of Calcium Channel Subunits

Liebmann¹,

Karst²,

Sidiropoulou³

et al. 2008

Journal of Neurophysiology

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Liebmann L, Karst H, Sidiropoulou K, van Gemert N, Meijer OC, Poirazi P, Joëls M. Differential effects of corticosterone on the slow afterhyperpolarization in the basolateral amygdala and CA1 region: possible role of calcium channel subunits. J Neurophysiol 99: 958-968, 2008. First published December 12, 2007 doi:10.1152/jn.01137.2007. The stress hormone corticosterone increases the amplitude of the slow afterhyperpolarization (sAHP) in CA1 pyramidal neurons, without affecting resting membrane potential, input resistance, or action potential characteristics. We here examined how corticosterone affects these properties in the basolateral amygdala (BLA). In the amygdala, corticosterone does not change the AHP amplitude, nor any of the passive and active membrane properties studied. The lack of effect on the AHP is surprising since in both areas corticosterone increases highvoltage-activated sustained calcium currents, which supposedly regulate the sAHP. We wondered whether corticosterone targets different calcium channel subunits in the two areas because currents through only one of the subunits (Cav1.3) are thought to alter the AHP amplitude. In situ hybridization studies revealed that CA1 cells express Cav1.2 and Cav1.3 subunits; corticosterone does not transcriptionally regulate Cav1.2 but increases Cav1.3 expression compared with vehicle treatment. In the BLA, Cav1.3 expression was not detectable, both after control and corticosterone treatment. Cav1.2 is moderately expressed. In a modeling study, we examined putative consequences of changes in specific calcium channel subunit expression and calcium extrusion by corticosterone for the AHP in CA1 and amygdala neurons. A differential distribution and transcriptional regulation of Cav1.2 and Cav1.3 in the CA1 area versus BLA partly explain the observed differences in AHP amplitude. The functional implication of these findings could be that stress-induced arousal of activity in the BLA is more prolonged than that in the CA1 hippocampal area, so that information with an emotional component is more effectively encoded.

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Section: Effects Of Corticosterone On Membrane Properties Of Ca1 and supporting

confidence: 90%

Section: Recordingmentioning

confidence: 99%

Differential Effects of Corticosterone on the Slow Afterhyperpolarization in the Basolateral Amygdala and CA1 Region: Possible Role of Calcium Channel Subunits

Liebmann¹,

Karst²,

Sidiropoulou³

et al. 2008

Journal of Neurophysiology

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Section: Discussionmentioning

confidence: 99%

“…Amygdalar neurons via muscarinic mediation have been associated with bursting phenomena (Yajeya et al, 1997), postsynaptically (Washburn and Moises, 1992) and presynaptically (Sugita et al, 1991). Bursting activity was further tied to a complement of presynaptic muscarinic receptors that were estimated to be comprised of 50% M 3 , 30% M 2 , and 20% or less M 1 , but most likely not due to the well characterized M-current (Yajeya et al, 1997). Moreover, similar neuronal depolarization responses due to cholinergic mechanisms have been implicated in other paralimbic structures such as hippocampus, entorhinal, and piriform cortices and anterior cingulate (Benson et al, 1988;Colino and Halliwell, 1993;Hasselmo and Bower, 1992;Klink and Alonso, 1997;McCormick and Prince, 1986), as well as septum, basal forebrain, striatum, thalamus, and neocortical structures (Hasuo et al, 1988;Hsu et al, 1995;McCormick and Prince, 1987;Szerb et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

A Potential Cholinergic Mechanism of Procaine's Limbic Activation

Benson

Carson

Kiesewetter

et al. 2004

Neuropsychopharmacol

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The local anesthetic procaine, when administered to humans intravenously (i.v.), yields brief intense emotional and sensory experiences, and concomitant increases in anterior paralimbic cerebral blood flow, as measured by positron emission tomography (PET). Procaine's high muscarinic affinity, together with the distribution of muscarinic receptors that overlaps with brain regions activated by procaine, suggests a muscarinic contribution to procaine's emotional and sensory effects. This study evaluates the effects of procaine on cerebral muscarinic cholinergic receptors in the anesthetized rhesus monkey. Whole brain and regional muscarinic receptor binding was measured before and after procaine administration on the same day in three anesthetized rhesus monkeys with PET and the radiotracer 3-(3-(3[ 18 F]fluoropropylthio)-1,2,5-thiadiazol-4-yl)-1,2,5,6-tetrahydro-1-methylpyridine ([ 18 F]FP-TZTP), a cholinergic ligand that has preferential binding to muscarinic (M 2 ) receptors. On separate days each animal received six different doses of i.v. procaine in a randomized fashion. Procaine blocked up to B90% of [ 18 F]FP-TZTP specific binding globally in a dose-related manner. There were no regional differences in procaine's inhibitory concentration for 50% blockade (IC 50 ) for [ 18 F]FP-TZTP. Tracer delivery, which was highly correlated to cerebral blood flow in previous monkey studies, was significantly increased at all doses of procaine with the greatest increases occurring near procaine's IC 50 for average cortex. Furthermore, anterior limbic regions showed greater increases in tracer delivery than nonlimbic regions. Procaine has high affinity to muscarinic M 2 receptors in vivo in the rhesus monkey. This, as well as a preferential increase of tracer delivery to paralimbic regions, suggests that action at these receptors could contribute to i.v. procaine's emotional and sensory effects in man. These findings are consistent with other evidence of cholinergic modulation of mood and emotion.

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“…Although the activation of these two neurotransmitter systems in the BLA may occur under different experimental conditions (14,15) and induce slightly differential electrophysiological responses in BLA neurons (16)(17)(18), they have highly comparable effects on memory consolidation. Posttraining infusion of either a ␤-adrenoceptor or muscarinic cholinergic agonist into the amygdala enhances inhibitory avoidance retention (11,12,19,20), and inactivation of either receptor type in the BLA blocks the memoryenhancing effects of systemic glucocorticoids (ref.…”

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confidence: 99%

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

Roozendaal

Nguyen²,

Power³

et al. 1999

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

262

157

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Previously, we reported that bilateral excitotoxic lesions of the basolateral nucleus of the amygdala ( There is considerable evidence that the basolateral nucleus of the amygdala (BLA) is critically involved in regulating the consolidation of different forms of memory, including explicit͞ declarative memory. Many findings indicate that this amygdala nucleus mediates the memory-modulatory effects of adrenal stress hormones released by emotional arousal (1, 2). Findings of several recent studies from our laboratory indicate that posttraining infusions of the specific glucocorticoid receptor (GR or type II) agonist RU 28362 administered into the BLA induce dose-dependent enhancement of inhibitory avoidance retention (3) and that excitotoxic lesions of the BLA induced before training block the memory-enhancing effects of systemically administered glucocorticoids (4) as well as the memory-impairing effects induced by adrenalectomy (5, 6). BLA lesions also block the memory-enhancing effects of the GR agonist administered directly into the hippocampus (7). These findings suggest that BLA neuronal activity modulates stress-induced memory consolidation processes in, or involving, the hippocampus and are consistent with the view that the BLA is not a locus of memory storage but regulates consolidation processes in other brain regions (2).Extensive evidence indicates that noradrenergic and cholinergic systems in the amygdala participate in modulating memory consolidation (8-13). Although the activation of these two neurotransmitter systems in the BLA may occur under different experimental conditions (14, 15) and induce slightly differential electrophysiological responses in BLA neurons (16-18), they have highly comparable effects on memory consolidation. Posttraining infusion of either a ␤-adrenoceptor or muscarinic cholinergic agonist into the amygdala enhances inhibitory avoidance retention (11,12,19,20), and inactivation of either receptor type in the BLA blocks the memoryenhancing effects of systemic glucocorticoids (ref. 13; and A.E.P., B.R. and J.L.M, unpublished observation). Moreover, previous findings indicate that the BLA is a critical locus of interaction between glucocorticoids and the noradrenergic system in memory consolidation modulation (13, 21).The present experiments examined whether ␤-adrenoceptor or muscarinic cholinergic receptor activation in the BLA is critically involved in enabling facilitation of memory consolidation induced by activation of GRs in the hippocampus. In the first experiment, rats received unilateral microinfusions into the BLA of either the ␤-adrenoceptor antagonist atenolol or the muscarinic cholinergic antagonist atropine 10 min prior to training in an inhibitory avoidance task. The GR agonist RU 28362 was administered ipsilaterally into the dorsal hippocampus immediately after training, and retention was tested 48 h later. In a second experiment, we examined whether BLAhippocampus interactions in memory consolidation involve unilateral projections between these brain reg...

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Cholinergic responses of morphologically and electrophysiologically characterized neurons of the basolateral complex in rat amygdala slices

Cited by 33 publications

References 34 publications

Differential Effects of Corticosterone on the Slow Afterhyperpolarization in the Basolateral Amygdala and CA1 Region: Possible Role of Calcium Channel Subunits

Differential Effects of Corticosterone on the Slow Afterhyperpolarization in the Basolateral Amygdala and CA1 Region: Possible Role of Calcium Channel Subunits

A Potential Cholinergic Mechanism of Procaine's Limbic Activation

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

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