Neurons of the lateral and basolateral amygdaloid nuclei: A golgi study in the rat

McDonald, Alexander J.

doi:10.1002/cne.902120307

Cited by 344 publications

(355 citation statements)

References 55 publications

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“…The pipette tips were broken back to the desired diameter under visual observation and the pipettes filled with a drug solution of known concentration prepared in ACSF. Drugs used in this study were: acetylcholine chloride, carbamyl chloride (carbachol), oxotremorine, methacholine, atropine sulphate, pirenzepine, dimethylpiperidinium chloride (DMPP), hexamethonium chloride, tetraethylammonium (TEA), Lucifer Yellow CH (dilithium salt) (all obtained from Sigma Chemical Co.) and muscarine and oxotremorine-M (each from Research Biochemicals Inc. (McDonald, 1982(McDonald, , 1984Millhouse & DeOlmos, 1983). In keeping with this, greater than 93 % of all the impalements that were obtained in this study were made from neurons which displayed a uniform profile of passive and active electrophysiological properties (see below).…”

Section: Methodsmentioning

confidence: 99%

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

Washburn

Moises

1992

The Journal of Physiology

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SUMMARY1. Intracellular recordings were obtained from pyramidal-type neurons in the basolateral amygdaloid nucleus (BLA) in slices of rat ventral forebrain and used to compare the actions of exogenously applied cholinomimetics to the effects produced by electrical stimulation of amygdalopetal cholinergic afferents from basal forebrain.2. Bath application of carbachol depolarized pyramidal cells with an associated increase in input resistance (Ri), reduced the slow after-hyperpolarization (AHP)that followed a series of current-evoked action potentials and blocked spike frequency accommodation. All of these effects were reversed by the muscarinic antagonist atropine but not by the nicotinic antagonist hexamethonium. 3. Electrical stimulation of amygdaloid afferents within the external capsule evoked a series of synaptic potentials consisting of a non-cholinergic fast excitatory postsynaptic potential (EPSP), followed by early and late inhibitory postsynaptic potentials (IPSPs). Each of these synaptic potentials was reduced by carbachol in an atropine-sensitive manner.4. Local application of carbachol to pyramidal cells produced a short-latency hyperpolarization followed by a prolonged depolarization. The hyperpolarization and depolarization to carbachol were blocked by atropine but not hexamethonium.5. The carbachol-induced hyperpolarization was associated with a decrease in Ri and had a reversal potential nearly identical to that of the early IPSP. The inhibitory response was blocked by perfusion of medium containing tetrodotoxin (TTX), bicuculline or picrotoxin, while the subsequent depolarization was unaffected. On the basis of these data, it is concluded that the muscarinic hyperpolarization is mediated through the rapid excitation of presynaptic GABAergic interneurons in the slice.6. The findings that the carbachol-induced depolarization was associated with an increase in Ri, often had a reversal potential below -80 mV, was sensitive to changes in extracellular potassium concentration and was blocked by intracellular ionophoresis of the potassium channel blocker caesium suggest that it resulted from a muscarinic blockade of one or more potassium conductances. M. S. WASHBURN AND H. C MOISES evoked a series of fast EPSPs followed by IPSPs. These non-cholinergic potentials were followed by a slow EPSP that lasted from 10 s-4 min. The slow EPSP was enhanced by eserine and blocked by atropine. It was also blocked by TTX or cadmium, indicating that it was dependent on spike propagation and calciumdependent release of acetylcholine (ACh).8. Stimulation of cholinergic afferents in the slice mimicked other effects produced by carbachol including blockade of the slow AHP and accommodation of action potential discharge and these actions were potentiated by eserine and blocked by atropine.9. The present results provide the first demonstration of muscarinic cholinergic actions in an area of the amygdala known to receive cholinergic innervation. These effects appear to involve both direct and indirect mechanisms.

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Section: Methodsmentioning

confidence: 99%

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

Washburn

Moises

1992

The Journal of Physiology

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“…Amplified outputs were filtered at 1 kHz and digitized (10 kHz, ITC-18; HEKA), and then transmitted to and stored on an Apple Computer (MacPro; Apple) running the AxoGraph X software (Axograph Scientific). Neurons were classified as LAT projection neurons and used for analysis if they (1) were histologically confirmed to lie within the LAT, (2) had a morphology consistent with projection neurons (McDonald, 1982;McDonald, 1992), and (3) had a resting membrane potential at least − 60 mV.…”

Section: In Vitro Whole-cell Recordingsmentioning

confidence: 99%

Effects of Repeated Stress on Age-Dependent GABAergic Regulation of the Lateral Nucleus of the Amygdala

Zhang

Rosenkranz

2016

Neuropsychopharmacol

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The adolescent age is associated with lability of mood and emotion. The onset of depression and anxiety disorders peaks during adolescence and there are differences in symptomology during adolescence. This points to differences in the adolescent neural circuitry that underlies mood and emotion, such as the amygdala. The human adolescent amygdala is more responsive to evocative stimuli, hinting to less local inhibitory regulation of the amygdala, but this has not been explored in adolescents. The amygdala, including the lateral nucleus (LAT) of the basolateral amygdala complex, is sensitive to stress. The amygdala undergoes maturational processes during adolescence, and therefore may be more vulnerable to harmful effects of stress during this time period. However, little is known about the effects of stress on the LAT during adolescence. GABAergic inhibition is a key regulator of LAT activity. Therefore, the purpose of this study was to test whether there are differences in the local GABAergic regulation of the rat adolescent LAT, and differences in its sensitivity to repeated stress. We found that LAT projection neurons are subjected to weaker GABAergic inhibition during adolescence. Repeated stress reduced in vivo endogenous and exogenous GABAergic inhibition of LAT projection neurons in adolescent rats. Furthermore, repeated stress decreased measures of presynaptic GABA function and interneuron activity in adolescent rats. In contrast, repeated stress enhanced glutamatergic drive of LAT projection neurons in adult rats. These results demonstrate age differences in GABAergic regulation of the LAT, and age differences in the mechanism for the effects of repeated stress on LAT neuron activity. These findings provide a substrate for increased mood lability in adolescents, and provide a substrate by which adolescent repeated stress can induce distinct behavioral outcomes and psychiatric symptoms.

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“…Whole cell recordings were obtained at 30 ± 1°C with EPC-10 amplifier and Pulse v8.76 software (HEKA Elektronik, Lambreht/Pfaltz, Germany). Putative glutamatergic neurons in BLA were identified by their pyramidal morphology (McDonald, 1982) under Dodt gradient contrast optics (cusom made) at 850 nm LED illumination (Thorlabs, Newton, NJ) and were recorded using 2-4 MΩ pipette filled with Cs-methanesulfonate 120 mM, NaCl 5 mM, MgCl 2 1 mM, HEPES 10 mM and EGTA 0.2 mM, ATP-Mg 2 mM, GTP-Na 0.1 mM, and QX314 10 mM, pH 7.3, osmolarity 285 osM. Membrane potentials were corrected by the junction potential of 12 mV.…”

Section: Electrophysiologymentioning

confidence: 99%

Observation of Distressed Conspecific as a Model of Emotional Trauma Generates Silent Synapses in the Prefrontal-Amygdala Pathway and Enhances Fear Learning, but Ketamine Abolishes those Effects

Ito

Erişir

Morozov

2015

Neuropsychopharmacol

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Witnessing pain and distress in others can cause psychological trauma and increase odds of developing PTSD in the future, on exposure to another stressful event. However, the underlying synaptic process remains unknown. Here we report that mice exposed to a conspecific receiving electrical footshocks exhibited enhanced passive avoidance (PA) learning when trained 24 h after the exposure. The exposure activated neurons in the dorsomedial prefrontal cortex (dmPFC) and basolateral amygdala (BLA) and altered synaptic transmission from dmPFC to BLA. It increased amplitude, slowed decay of NMDA receptor-mediated currents, and generated silent synapses. Administration of sub-anesthetic ketamine immediately after the exposure prevented the enhancement of PA learning and silent synapse formation. These findings suggest that ketamine can prevent pathophysiological consequences of psychological trauma.

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Neurons of the lateral and basolateral amygdaloid nuclei: A golgi study in the rat

Cited by 344 publications

References 55 publications

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

Muscarinic responses of rat basolateral amygdaloid neurons recorded in vitro.

Effects of Repeated Stress on Age-Dependent GABAergic Regulation of the Lateral Nucleus of the Amygdala

Observation of Distressed Conspecific as a Model of Emotional Trauma Generates Silent Synapses in the Prefrontal-Amygdala Pathway and Enhances Fear Learning, but Ketamine Abolishes those Effects

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