Muscarinic modulation of conductances underlying the afterhyperpolarization in neurons of the rat basolateral amygdala

Womble, Mark; Moises, Hylan C.

doi:10.1016/0006-8993(93)90301-3

Cited by 45 publications

(42 citation statements)

References 28 publications

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“…Consistent with previous reports (Womble and Moises, 1993), suppression of the sI AHP by bath application of muscarine (5-20 M) resulted in a reduction in both the AHP and spikefrequency adaptation (Fig. 1 D).…”

Section: Resultssupporting

confidence: 92%

“…In BLA projection neurons, the AHP that follows an AP train is mediated almost entirely by the apamin-insensitive sI AHP ( Fig. 1) (Womble and Moises, 1993). In this regard, neurons in the basal nucleus are similar to projection neurons in the lateral amygdala and pyramidal neurons of CA1 hippocampus (Oh et al, 2000), where blockade of SK channels has little effect on either the AHP or spike-frequency adaptation.…”

Section: Discussionmentioning

confidence: 86%

“…It was initially reported that the apamin-sensitive I AHP is not present in BLA projection neurons (Womble and Moises, 1993). However, subsequent reports have indicated that SK calcium-activated potassium channels, which mediate the I AHP , are present in projection neurons in the lateral nucleus of the BLA Chen and Lang, 2003;Faber et al, 2006).…”

Section: Resultsmentioning

confidence: 99%

“…They are also known to modulate longterm synaptic plasticity within the amygdala (Watanabe et al, 1995). Physiologically, activation of muscarinic receptors on BLA neurons suppresses several potassium currents, including the sI AHP , as well as the voltage-sensitive M-current (Washburn and Moises, 1992b;Womble and Moises, 1993). These receptors also activate a nonspecific cation conductance (Yajeya et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Competition between Calcium-Activated K⁺Channels Determines Cholinergic Action on Firing Properties of Basolateral Amygdala Projection Neurons

Power¹,

Sah²

2008

J. Neurosci.

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Acetylcholine (ACh) is an important modulator of learning, memory, and synaptic plasticity in the basolateral amygdala (BLA) and other brain regions. Activation of muscarinic acetylcholine receptors (mAChRs) suppresses a variety of potassium currents, including sI AHP , the calcium-activated potassium conductance primarily responsible for the slow afterhyperpolarization (AHP) that follows a train of action potentials. Muscarinic stimulation also produces inositol 1,4,5-trisphosphate (IP 3 ), releasing calcium from intracellular stores. Here, we show using whole-cell patch-clamp recordings and high-speed fluorescence imaging that focal application of mAChR agonists evokes large rises in cytosolic calcium in the soma and proximal dendrites in rat BLA projection neurons that are often associated with activation of an outward current that hyperpolarizes the cell. This hyperpolarization results from activation of small conductance calcium-activated potassium (SK) channels, secondary to the release of calcium from intracellular stores. Unlike bath application of cholinergic agonists, which always suppressed the AHP, focal application of ACh often evoked a paradoxical enhancement of the AHP and spike-frequency adaptation. This enhancement was correlated with amplification of the action potential-evoked calcium response and resulted from the activation of SK channels. When SK channels were blocked, cholinergic stimulation always reduced the AHP and spike-frequency adaptation. Conversely, suppression of the sI AHP by the ␤-adrenoreceptor agonist, isoprenaline, potentiated the cholinergic enhancement of the AHP. These results suggest that competition between cholinergic suppression of the sI AHP and cholinergic activation of the SK channels shapes the AHP and spike-frequency adaptation.

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Section: Resultssupporting

confidence: 92%

Section: Discussionmentioning

confidence: 86%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Competition between Calcium-Activated K⁺Channels Determines Cholinergic Action on Firing Properties of Basolateral Amygdala Projection Neurons

Power¹,

Sah²

2008

J. Neurosci.

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“…Studies have provided a variety of mechanisms by which signaling through muscarinic receptors in BLA neurons promotes neuronal excitability, such as the suppression of potassium currents and reduction of the slow afterhyperpolarization of action potentials (Washburn and Moises 1992;Womble and Moises 1993). In agreement with these data, long-term potentiation in the lateral amygdala was reduced by muscarinic receptor blockade.…”

Section: Basal Forebrain Projection To the Blamentioning

confidence: 63%

Input-specific contributions to valence processing in the amygdala

Correia

Goosens

2016

Learn. Mem.

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Reward and punishment are often thought of as opposing processes: rewards and the environmental cues that predict them elicit approach and consummatory behaviors, while punishments drive aversion and avoidance behaviors. This framework suggests that there may be segregated brain circuits for these valenced behaviors. The basolateral amygdala (BLA) is one brain region that contributes to both types of motivated behavior. Individual neurons in the BLA can favor positive over negative valence, or vice versa, but these neurons are intermingled, showing no anatomical segregation. The amygdala receives inputs from many brain areas and current theories posit that encoding of positive versus negative valence by BLA neurons is determined by the wiring of each neuron. Specifically, many projections from other brain areas that respond to positive and negative valence stimuli and predictive cues project strongly to the BLA and likely contribute to valence processing within the BLA. Here we review three of these areas, the basal forebrain, the dorsal raphe nucleus and the ventral tegmental area, and discuss how these may promote encoding of positive and negative valence within the BLA.The basic desire to seek reward and avoid punishment shapes virtually all of behavior, and the ability to discriminate between "good" and "bad" environmental cues is critical for guiding choices and maximizing survival. Thus, understanding the brain circuits that encode motivated behaviors is important because it contributes to our knowledge of how we learn, and it is also essential for understanding human disorders associated with abnormal processing of reward and danger (i.e., emotional disorders), such as anxiety, depression, addiction, and post-traumatic stress disorder (PTSD).The amygdala is one brain area implicated in motivated behaviors and the basolateral complex of the amygdala (BLA) receives information about diverse environmental stimuli from many brain regions. The BLA is thought to encode the association of predictive stimuli with both aversive and appetitive outcomes (Morrison and Salzman 2010;Barberini et al. 2012). Reward and punishment are reinforcers of opposite valence (positive versus negative), and these reinforcers typically lead to opposing behaviors (approach versus avoidance). Many theories have suggested that appetitive and aversive systems act in opponent fashion (Solomon and Corbit 1974;Daw et al. 2002). However, it is unclear how the BLA contributes to this. We do not yet understand the extent to which aversive and appetitive information is processed in parallel BLA circuits, or whether individual BLA neurons are involved in the regulation of both types of motivated behaviors.In this review, we propose several models by which functional segregation of valence can be achieved in the BLA. These models are based on studies describing how BLA neurons respond to reward and aversive stimuli. We then consider whether three major inputs, known to carry valenced information, support or conflict these models, and also discus...

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Cholinergic innervation of pyramidal cells and parvalbumin‐immunoreactive interneurons in the rat basolateral amygdala

Muller

Mascagni

McDonald

2011

J of Comparative Neurology

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The basolateral nucleus of the amygdala receives an extremely dense cholinergic innervation from the basal forebrain that is critical for memory consolidation. Although previous electron microscopic studies determined some of the postsynaptic targets of cholinergic afferents, the majority of postsynaptic structures were dendritic shafts whose neurons of origin were not identified. To make this determination, the present study analyzed the cholinergic innervation of the anterior subdivision of the basolateral amygdalar nucleus (BLa) of the rat using electron microscopic dual-labeling immunocytochemistry. The vesicular acetylcholine transporter (VAChT) was used as a marker for cholinergic terminals; calcium/calmodulin-dependent protein kinase II (CaMK) was used as a marker for pyramidal cells, the principal neurons of the BLa; and parvalbumin (PV) was used as a marker for the predominant interneuronal subpopulation in this nucleus. VAChT+ terminals were visualized by using diaminobenzidine as a chromogen, whereas CAMK+ or PV+ neurons were visualized with Vector very intense purple (VIP) as a chromogen. Quantitative analyses revealed that the great majority of dendritic shafts receiving cholinergic inputs were CAMK+, indicating that they were of pyramidal cell origin. In fact, 89% of the postsynaptic targets of cholinergic terminals in the BLa were pyramidal cells, including perikarya (3%), dendritic shafts (47%), and dendritic spines (39%). PV+ structures, including perikarya and dendrites, constituted 7% of the postsynaptic targets of cholinergic axon terminals. The cholinergic innervation of both pyramidal cells and PV+ interneurons may constitute an anatomical substrate for the generation of oscillatory activity involved in memory consolidation by the BLa.

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Muscarinic modulation of conductances underlying the afterhyperpolarization in neurons of the rat basolateral amygdala

Cited by 45 publications

References 28 publications

Competition between Calcium-Activated K⁺Channels Determines Cholinergic Action on Firing Properties of Basolateral Amygdala Projection Neurons

Competition between Calcium-Activated K⁺Channels Determines Cholinergic Action on Firing Properties of Basolateral Amygdala Projection Neurons

Input-specific contributions to valence processing in the amygdala

Cholinergic innervation of pyramidal cells and parvalbumin‐immunoreactive interneurons in the rat basolateral amygdala

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Muscarinic modulation of conductances underlying the afterhyperpolarization in neurons of the rat basolateral amygdala

Cited by 45 publications

References 28 publications

Competition between Calcium-Activated K+Channels Determines Cholinergic Action on Firing Properties of Basolateral Amygdala Projection Neurons

Competition between Calcium-Activated K+Channels Determines Cholinergic Action on Firing Properties of Basolateral Amygdala Projection Neurons

Input-specific contributions to valence processing in the amygdala

Cholinergic innervation of pyramidal cells and parvalbumin‐immunoreactive interneurons in the rat basolateral amygdala

Contact Info

Product

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Competition between Calcium-Activated K⁺Channels Determines Cholinergic Action on Firing Properties of Basolateral Amygdala Projection Neurons

Competition between Calcium-Activated K⁺Channels Determines Cholinergic Action on Firing Properties of Basolateral Amygdala Projection Neurons