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PubMed1999

Evidence that dopaminergic axons provide a dense innervation of specific neuronal subpopulations in the rat basolateral amygdala.

Dopaminergic inputs from the ventral tegmental area and substantia nigra are involved in numerous emotional and behavioral functions mediated by the amygdala. Previous studies have shown that some dopaminergic axons selectively innervate subpopulations of neurons in the rat basolateral amygdala by forming dense pericellular arrays (baskets) that envelope the perikarya of these neurons. Because of the obvious functional significance of this innervation, a sequential two-color immunoperoxidase technique was used in the present study to determine which neuronal subpopulations are targeted. Pericellular baskets were seen in sections stained for tyrosine hydroxylase, but not for dopamine-beta-hydroxylase, suggesting that these axonal arrays are dopaminergic. Most baskets enveloped small ovoid or piriform perikarya, although a few in the anteroventral part of the basolateral nucleus were associated with larger pyramidal cells. Double-labeling immunohistochemistry revealed that all of the smaller baskets enveloped a subpopulation of parvalbumin-immunoreactive nonpyramidal neurons, but not nonpyramidal neurons containing vasoactive intestinal polypeptide or neuropeptide Y. Since these parvalbumin containing neurons are known to be GABAergic interneurons, the results of this study suggest that the actions of dopamine in the basolateral amygdala are mediated, in part, by a subpopulation of inhibitory interneurons.

Amygdala↗
PubMed2002

GABAergic innervation of alpha type II calcium/calmodulin-dependent protein kinase immunoreactive pyramidal neurons in the rat basolateral amygdala.

Although calcium/calmodulin-dependent protein kinase II (CaMK) has been shown to play a critical role in long-term potentiation (LTP) and emotional learning mediated by the basolateral amygdala, little is known about its cellular localization in this region. We have utilized immunohistochemical methods to study the neuronal localization of CaMK, and its relationship to gamma-aminobutyric acid (GABA)-ergic structures, in the rat basolateral amygdala (ABL). Light microscopic observations revealed dense CaMK staining in the ABL. Although the cell bodies and proximal dendrites of virtually every pyramidal cell appeared to be CaMK(+), the cell bodies of small nonpyramidal neurons were always unstained. Dual localization of CaMK and GABA immunoreactivity with confocal immunofluorescence microscopy revealed that CaMK and GABA were found in different neuronal populations in the ABL. CaMK was contained only in pyramidal neurons; GABA was contained only in nonpyramidal cells. At the ultrastructural level, it was found that CaMK was localized to pyramidal cell bodies, thick proximal dendrites, thin distal dendrites, most dendritic spines, axon initial segments, and axon terminals forming asymmetrical synapses. These findings suggest that all portions of labeled pyramidal cells, with the exception of some dendritic spines, can exhibit CaMK immunoreactivity. By using a dual immunoperoxidase/immunogold-silver procedure at the ultrastructural level, GABA(+) axon terminals were seen to innervate all CaMK(+) postsynaptic domains, including cell bodies (22%), thick (>1 microm) dendrites (34%), thin (<1 microm) dendrites (22%), dendritic spines (17%), and axon initial segments (5%). These findings indicate that CaMK is a useful marker for pyramidal neurons in ultrastructural studies of ABL synaptology and that the activity of pyramidal neurons in the ABL is tightly controlled by a high density of GABAergic terminals that target all postsynaptic domains of pyramidal neurons.

Amygdala↗
PubMed2001

Dopamine attenuates prefrontal cortical suppression of sensory inputs to the basolateral amygdala of rats.

The basolateral complex of the amygdala (BLA) plays a significant role in affective behavior that is likely regulated by afferents from the medial prefrontal cortex (mPFC). Studies suggest that dopamine (DA) is a necessary component for production of appropriate affective responses. In this study, prefrontal cortical and sensory cortical [temporal area 3 (Te3)] inputs to the BLA and their modulation by DA receptor activation was examined using in vivo single-unit extracellular recordings. We found that Te3 inputs are more capable of driving BLA projection neuron firing, whereas mPFC inputs potently elicited firing from BLA interneurons. Moreover, mPFC stimulation before Te3 stimulation attenuated the probability of Te3-evoked spikes in BLA projection neurons, possibly via activation of inhibitory interneurons. DA receptor activation by apomorphine attenuated mPFC inputs, while augmenting Te3 inputs. Additionally, DA receptor activation suppressed mPFC-induced inhibition of Te3-evoked spikes. Thus, the mPFC may attenuate sensory-driven amygdala-mediated affective responses via recruitment of BLA inhibitory interneurons that suppress sensory cortical inputs. In situations of enhanced DA levels in the BLA, such as during stress and after amphetamine administration, mPFC regulation of BLA will be dampened, leading to a disinhibition of sensory-driven affective responses.

Action Potentials↗
PubMed1989

Coexistence of GABA and peptide immunoreactivity in non-pyramidal neurons of the basolateral amygdala.

Colocalization of gamma-aminobutyric acid (GABA) immunoreactivity with somatostatin (SOM), neuropeptide Y (NPY), cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP) immunoreactivity was demonstrated in non-pyramidal neurons of the basolateral amygdala using a two-color immunoperoxidase procedure. Approximately 80-90% of SOM- and NPY-positive neurons in the basolateral amygdala were also immunoreactive for GABA. Virtually all large CCK-positive neurons also exhibited GABA-like immunoreactivity. About one-half of VIP-positive neurons and small CCK-positive cells were also immunoreactive for GABA.

Amygdala↗
PubMed1996

Roles of the basolateral amygdala and hippocampus in social recognition in rats.

Lesions of the amygdala or hippocampus have a large impact on social behavior of rats. In this study we investigated whether a social recognition test was also affected by those lesions. An NMDA-induced lesion of the basolateral amygdala did not impair the ability to distinguish a familiar from an unfamiliar juvenile rat. It was argued that the cortico-medial amygdala may be more important for social recognition than the basolateral amygdala. Fimbria-transected rats could no longer distinguish a familiar from an unfamiliar juvenile. Moreover, during all encounters they spent less time investigating the juvenile. The precise nature of this deficit, especially the reason for the overall reduced social investigation time, could not be specified with the classical procedure of the social recognition test.

Amygdala↗
PubMed1983

Neuronal configurations in lateral and basolateral amygdala.

The lateral and basolateral nuclei of the rat amygdala have been studied with the rapid Golgi method. Both nuclei have similar cell types, which closely resemble cells in the cerebral cortex. Therefore, we suggest that what is known about cortical circuitry can be used as a guide for studying synaptic circuitry in the lateral and basolateral nuclei. The most abundant neurons that are impregnated in both nuclei are pyramidal cells. They have conical cell bodies and easily recognizable apical and basilar dendrites. The ones in the center of each nucleus have long axes that roughly parallel the long axis of the nucleus. Towards the periphery, pyramidal cells have apical dendrites that either stick directly across the nucleus or follow along a nuclear border. The peripheral dendrites tend to enclose the nuclei. There is considerable overlap among the dendritic trees and the dendrites of one nucleus extend into the territory of the other. Pyramidal cells have extensive axonal systems. The principal axon of basolateral cells usually projects rostrally but long collaterals leave the nucleus in other directions. The axons of lateral nucleus pyramidal cells are also widely distributed. The major thrust of their axons is caudal and lateral. Stellate cells are the most common variety of the non-pyramidal cells. They occur in both nuclei and have round cell bodies, 10-15 micron diameter, and spherical dendritic trees that are confined to a limited region of the nucleus. Their axons form dense terminal fields that remain within the vicinity of the parent cell's dendritic tree. Another type of non-pyramidal cell is the cone cell, whose non-spiny, varicose dendrites describe cones. These neurons are found mainly in the apex of the lateral nucleus. The most rare non-pyramidal cells are the extended neurons, which have long, straight dendrites that reach beyond the nucleus into surrounding neuropil. They are mostly in the rostral part of the basolateral nucleus but also occur in the lateral nucleus, near the ventricular border. The axons of cone cells and the extended neurons have been only partially impregnated. We also have examined stellate cells in the guinea-pig lateral and basolateral nuclei. They have many of the same features as those in the rat brain, except that their dendritic trees and axonal systems are more complicated. There are two large groups of afferents: one consists of longitudinally running axons and the other of transversely coursing fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed2003

Individual nucleus accumbens-projection neurons receive both basolateral amygdala and ventral subicular afferents in rats.

The nucleus accumbens is regarded as the limbic-motor interface, in view of its limbic afferent and somatomotor and autonomic efferent connections. Within the accumbens, there appear to be specific areas in which limbic afferent fibres, derived from the hippocampus and the amygdala, overlap. These afferent inputs have been suggested to converge monosynaptically on cells within the accumbens and are hypothesized to play a role in paradigms such as conditioned place preference. Convergence between inputs from basolateral amygdala and hippocampus can be demonstrated with electrophysiological recording methods, but these do not conclusively preclude polysynaptic mechanisms. We examined the synaptic input to the projection neurons of the accumbens, the medium-sized densely spiny neurons. We labelled the projection neurons with a small injection of biotinylated dextran amine into the accumbens, and the afferents from the basolateral amygdala and ventral subiculum of the hippocampus with injections of biotinylated dextran amine and Phaseolus vulgaris-leucoagglutinin respectively, and revealed the anterogradely labelled fibres with different chromogens. The labelled accumbens-projection neurons were studied with correlated light and electron microscopy for identified monosynaptic inputs. With this technique we have demonstrated anatomically that monosynaptic convergence between the ventral subicular region of the hippocampus and the basolateral region of the amygdala occurs at the level of the proximal as well as distal dendrites. Finally, we suggest that these anatomical arrangements may represent the framework for the integrative role that has been assigned to the accumbens.

Amygdala↗
PubMed1993

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

The excitability level of pyramidal neurons in the basolateral amygdala (BLA) is greatly increased following muscarinic receptor activation, an effect associated with an increased rate of action potential firing and reduction of the afterhyperpolarization (AHP). We impaled BLA pyramidal neurons in slices of rat ventral forebrain with a single microelectrode to examine the currents underlying the AHP and spike frequency accommodation and determine their sensitivities to muscarinic modulation. In voltage-clamp, depolarizing steps were followed by biphasic outward tail currents, consisting of rapidly decaying (IFast) and slowly decaying (ISlow) current components. These corresponded temporally with the medium and slow portions of the AHP, respectively. The reversal potential for the IFast component of the AHP tail current shifted in the depolarizing direction with increases in the extracellular K+ concentration. The amplitude of IFast was reduced during perfusion of 0-Ca2+ medium or by superfusion of TEA (1-5 mM) or carbachol (10-40 microM). It is suggested that IFast was produced by the rapidly decaying Ca(2+)-activated K+ current (IC) and the muscarinic-sensitive M-current (IM). The ISlow tail current component reversed at the estimated values for EK in medium containing either normal or elevated K+ levels. This component was eliminated by perfusion of 0-Ca2+ medium or inclusion of cyclic-AMP in the recording electrode. It was not blocked by TEA (5 mM) or apamin (50-500 nM), but was reduced by carbachol in a dose-dependent manner (IC50 = 0.5 microM). Electrical stimulation of cholinergic afferent pathways to the BLA produced inhibition of ISlow, an effect which was enhanced by eserine and prevented by atropine. Loss of the ISlow component was always accompanied by similar reductions in accommodation and the slow AHP. It was concluded that this tail current component resulted from the slowly decaying Ca(2+)-activated K+ current, IAHP. Thus, the muscarinic inhibition of IAHP contributes to the enhanced excitability exhibited by BLA pyramidal neurons following cholinergic stimulation.

Amygdala↗
PubMed2004

Regulation of chronic stress-induced changes in hypothalamic-pituitary-adrenal activity by the basolateral amygdala.

Little is known about the role of the basolateral amygdala (BLA) in regulating hypothalamic-pituitary-adrenal (HPA) activity, particularly chronic stress-induced HPA activity. In the current studies, we examined the effects of manipulations of the BLA on HPA responses to the eighth restraint, to novel restraint after repeated cold, or to acute novel restraint alone. Excitotoxic lesions of the BLA, in general, inhibited HPA activity in both acute and chronically stressed animals. To examine the role of the BLA in chronic stress without affecting the response to the first stress, we injected the GABA agonist muscimol to temporarily inactivate the BLA prior to restraint in the same three groups of animals. In contrast to the lesion data, muscimol enhanced the HPA response to acute restraint and to novel restraint after repeated cold, but it did not affect responses to the eighth restraint. These data suggest that the BLA inhibits HPA responses to novel stress but is not important in animals repeatedly exposed to the same stressor. Future studies will focus on the neuro-anatomical substrates of BLA's effects on HPA activity including whether inputs from the pPVTh are important.

Adrenocorticotropic Hormone↗
PubMed2001

Reinforcement of early long-term potentiation (early-LTP) in dentate gyrus by stimulation of the basolateral amygdala: heterosynaptic induction mechanisms of late-LTP.

The basolateral amygdala (BLA) can influence distinct learning and memory formation. Hippocampal long-term potentiation (LTP), the most prominent cellular model of memory formation, can be modulated by stimulation of the BLA in its induction and early maintenance. However, it is not known how the late maintenance of LTP beyond its initial phases might be affected. Behavioral stimuli have been shown to result in a reinforcement of a transient early-LTP into a lasting potentiation. Here we show that BLA stimulation mimics the behavioral effects on early-LTP in freely moving rats when the BLA is activated within a time window of 30 min before or after tetanization of the perforant path. The reinforcement of LTP was blocked by inhibitors of muscarinergic and beta-adrenergic but not dopaminergic receptors and was dependent on translation. Through these heterosynaptic associative interactions, hippocampal sensory information can be stabilized by amygdaloidal influences.

Adrenergic beta-Antagonists↗
PubMed1998

Bidirectional synaptic plasticity in the rat basolateral amygdala: characterization of an activity-dependent switch sensitive to the presynaptic metabotropic glutamate receptor antagonist 2S-alpha-ethylglutamic acid.

This study examines forms of activity-dependent synaptic plasticity in the basolateral amygdala in vitro and demonstrates that a brief high frequency stimulus (HFS) train can induce a switch in the direction of the enduring change in synaptic strength induced by subsequent low-frequency stimulation (LFS). LFS (1 Hz, 15 min) of the external capsule (EC) induced a persistent 1.7-fold enhancement in the amplitude of synaptic potentials recorded intracellularly in basolateral amygdala neurons. The enhancement occurred gradually during the stimulation and was maintained for >30 min after termination of the stimulus train. LFS-induced enduring synaptic facilitation was not affected by the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoate (APV; 100 microM). Brief high-frequency EC stimulation (HFS; 100 Hz, 1 sec) induced APV-sensitive short-term potentiation (2.5-fold) that generally decayed within 10 min. When LFS was applied after recovery from the short-term potentiating effect of HFS (HFS/LFS), there was an initial transient (<10 min) enhancement of the synaptic response followed by persistent synaptic depression (synaptic potential amplitude reduced by 22% at 30 min). This represents the first demonstration of stimulus-dependent long-lasting synaptic depression in the amygdala. Application of the presynaptic (group II) metabotropic glutamate receptor antagonist 2S-alpha-ethylglutamic acid (EGLU; 50 microM) prevented the HFS-dependent switch from synaptic facilitation to depression. Thus, LFS in the in vitro amygdala slice can induce either enduring synaptic potentiation or depression, depending on whether a priming HFS train has been applied. This experience-dependent switch, a novel form of metaplasticity, is not dependent on NMDA receptors but may require group II metabotropic glutamate receptors. In the amygdala, experiential modification of activity-dependent long-term synaptic plasticity adds flexibility to the ways in which synaptic strength can be modified and could play a role in diverse amygdala-dependent processes, including the formation, storage, and extinction of emotional memory and the regulation of epileptogenesis.

Amygdala↗
PubMed2001

Lesions of the basolateral amygdala disrupt selective aspects of reinforcer representation in rats.

The amygdala is known to play a role in learning about motivationally significant events. We investigated this role further by examining the effects of excitotoxic lesions of the basolateral amygdala on the ability of rats to use instrumental outcomes to direct responding (the differential outcomes effect) and on the ability of Pavlovian cues to modulate instrumental performance based on shared outcomes (reinforcer-selective Pavlovian-to-instrumental transfer). We found that basolateral amygdala (BLA) lesions did not affect the ability of rats to learn a basic instrumental conditional discrimination, but did disrupt the ability of differential outcomes to facilitate acquisition. In Pavlovian-to-instrumental transfer, BLA lesions did not disrupt the basic enhancement of instrumental performance but did abolish the reinforcer specificity of that enhancement. These results suggest that the BLA is involved in the representation of the sensory aspects of motivationally significant events.

Amygdala↗
PubMedDate not supplied

Memory enhancement induced by post-training intrabasolateral amygdala infusions of beta-adrenergic or muscarinic agonists requires activation of dopamine receptors: Involvement of right, but not left, basolateral amygdala.

Previous findings indicate that the noradrenergic, dopaminergic, and cholinergic innervations of the basolateral amygdala (BLA) modulate memory consolidation. The current study investigated whether memory enhancement induced by post-training intra-BLA infusions of a beta-adrenergic or muscarinic cholinergic agonist requires concurrent activation of dopamine (DA) receptors in the BLA. Rats with implanted BLA cannulae were trained on an inhibitory avoidance (IA) task and, 48 h later, tested for retention. Infusions of the beta-adrenergic agonist clenbuterol into the right BLA, but not the left, enhanced retention, and concurrent infusions of the nonspecific DA receptor antagonist cis-Flupenthixol (Flu) blocked the enhancement. Post-training infusions of the muscarinic agonist oxotremorine into the right BLA also enhanced retention, and concurrent infusions of Flu blocked this effect. Additional experiments investigated whether memory modulation was lateralized to the right BLA. Post-training DA infusions into the right BLA, but not the left, enhanced retention. Post-training infusions of lidocaine or muscimol, which impair retention when infused bilaterally, had no effect when infused unilaterally into either the right or left BLA. These findings, together with earlier work, suggest that the dopaminergic system in the BLA is critically involved in memory modulation induced by noradrenergic and cholinergic influences. Additionally, these findings indicate that the enhancement, but not impairment, of memory consolidation is lateralized to the right BLA.

Adrenergic beta-Agonists↗
PubMed1984

Evidence that efferents from the basolateral amygdala innervate the dorsolateral neostriatum in rats.

The dorsolateral precommissural caudate-putamen complex has been characterized recently as a 'non-limbic' region of the neostriatum. In the present study, however, it was found that numerous neurons in the basolateral amygdala were labeled retrogradely following infusions of Evans Blue into that neostriatal region. Control infusions demonstrated that such labeling could not be attributed to the spread of the red fluorescent tracer into surrounding neocortical areas. On the basis of these data, it is proposed that: (1) the amygdalo-neostriatal pathway may be more extensive than previously believed, and (2) the basolateral amygdala may serve as an important link between the limbic and extrapyramidal motor systems.

Acetylcholinesterase↗
PubMed1996

Localization of AMPA glutamate receptor subunits in subpopulations of non-pyramidal neurons in the rat basolateral amygdala.

A two-color immunoperoxidase technique was used to investigate the localization of GluR1 and GluR2/3 alpha-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA) glutamate receptor subunits in subpopulations of non-pyramidal neurons in the rat basolateral amygdala. Antibodies to neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), and calcium binding proteins were used to mark three distinct subsets of non-pyramidal cells. Only non-pyramidal neurons containing the calcium binding proteins parvalbumin (PV) and calbindin D-28k (CB) exhibited robust GluR1-like immunoreactivity (GluR1-ir). Light GluR1-ir was observed in some neurons with NPY-ir and VIP-ir, as well as in some pyramidal cells. Only pyramidal cells exhibited robust GluR2/3-ir. No significant amount of GluR2/3-ir was seen in any of the three main classes of non-pyramidal cells. These findings indicate that in the rat basolateral amygdala GluR2/3-ir is found primarily in pyramidal neurons whereas GluR1-ir is found mainly in non-pyramidal neurons that contain PV or CB.

Amygdala↗
PubMed2006

Extinction of auditory fear conditioning requires MAPK/ERK activation in the basolateral amygdala.

Whereas the neuronal substrates underlying the acquisition of auditory fear conditioning have been widely studied, the substrates and mechanisms mediating the acquisition of fear extinction remain largely elusive. Previous reports indicate that consolidation of fear extinction depends on the mitogen-activated protein kinase/extracellular-signal regulated kinase (MAPK/ERK) signalling pathway and on protein synthesis in the medial prefrontal cortex (mPFC). Based on experiments using the fear-potentiated startle paradigm suggesting a role for neuronal plasticity in the basolateral amygdala (BLA) during fear extinction, we directly addressed whether MAPK/ERK signalling in the basolateral amygdala is necessary for the acquisition of fear extinction using conditioned freezing as a read-out. First, we investigated the regional and temporal pattern of MAPK/ERK activation in the BLA following extinction learning in C57Bl/6J mice. Our results indicate that acquisition of extinction is associated with an increase of phosphorylated MAPK/ERK in the BLA. Moreover, we found that inhibition of the MAPK/ERK signalling pathway by intrabasolateral amygdala infusion of the MEK inhibitor, U0126, completely blocks acquisition of extinction. Thus, our results indicate that the MAPK/ERK signalling pathway is required for extinction of auditory fear conditioning in the BLA, and support a role for neuronal plasticity in the BLA during the acquisition of fear extinction.

Acoustic Stimulation↗
PubMed2002

Immunohistochemical characterization of somatostatin containing interneurons in the rat basolateral amygdala.

There are discrete subpopulations of GABAergic interneurons in the basolateral amygdala (ABL) that contain particular neuropeptides or calcium-binding proteins (calbindin-D28k, parvalbumin (PV), or calretinin). The present study employed a dual-labeling immunofluorescence technique combined with confocal laser scanning microscopy to investigate the neurochemical characteristics of the interneuronal subpopulation containing somatostatin (SOM). The great majority of SOM+ neurons in the ABL exhibited GABA immunoreactivity (66-82% depending on the nucleus). These SOM+ neurons constituted 11-18% of the GABA+ population. There was also extensive colocalization of SOM with calbindin (CB) in all nuclei of the ABL, but no colocalization of SOM with parvalbumin, calretinin, or vasoactive intestinal polypeptide. In the basolateral nucleus more than 90% of SOM+ neurons also exhibited CB immunoreactivity, whereas in the lateral nucleus about two-thirds of SOM+ neurons contained significant levels of CB. These SOM/CB neurons constituted about one quarter of the CB+ population in the basolateral nucleus and about one third of the CB+ population in the lateral nucleus. These results, in conjunction with the findings of previous studies, indicate that there are at least three major subpopulations of GABAergic interneurons in the ABL: (i) SOM+ neurons (most of which also contain CB and/or neuropeptide Y); (ii) PV+ neurons (most of which also contain CB); and (iii) CR+ neurons (most of which also contain vasoactive intestinal polypeptide).

Amygdala↗
PubMed2006

Kindling of basolateral amygdala but not ventral hippocampus or perirhinal cortex disrupts sensorimotor gating in rats.

The neural mechanisms mediating prepulse inhibition (PPI) appear to have relevance to neurological and psychiatric disorders. Patients with temporal lobe epilepsy exhibit psychotic symptoms and disrupted PPI, therefore the present experiments examined the consequences of seizures induced by kindling on PPI. Rats were chronically implanted with an electrode into the basolateral amygdala, perirhinal cortex, or ventral hippocampus and stimulated twice daily until 3 fully generalized, class 5 seizures were elicited. Kindling of basolateral amygdala, but not perirhinal cortex or ventral hippocampus, disrupted PPI when testing began 2min, but not 48h, following the elicitation of the third class 5 seizure. Startle amplitudes were unaffected by kindling. These results suggest that the anatomical origin of seizures is an important factor in determining their potentially disruptive effects on PPI.

Amygdala↗