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At least 109 records · Page 6Linked to original sources
PubMed2000

Muscarinic agonist carbachol depresses excitatory synaptic transmission in the rat basolateral amygdala in vitro.

Intracellular recordings in slice preparations of the basolateral amygdala were used to test which excitatory amino acid receptors mediate the excitatory postsynaptic potentials due to stimulation of the external capsule. These recordings were also used to examine the action of muscarinic agonists on the evoked excitatory potentials. Intracellular recordings from amygdaloid pyramidal neurons revealed that carbachol (2-20 microM) suppressed, in a dose-dependent manner, excitatory postsynaptic responses evoked by stimulation of the external capsule (EC). This effect was blocked by atropine. The estimated effective concentration to produce half-maximal response (EC(50)) was 6.2 microM. Synaptic suppression was observed with no changes in the input resistance of the recorded cells, suggesting a presynaptic mechanism. In addition, the results obtained using the paired-pulse protocol provided additional support for a presynaptic action of carbachol. To identify which subtype of cholinergic receptors were involved in the suppression of the EPSP, four partially selective muscarinic receptor antagonists were used at different concentrations: pirenzepine, a compound with a similar high affinity for muscarinic M1 and M4 receptors; gallamine, a noncompetitive antagonist for M2; methoctramine, an antagonist for M2 and M4; and 4-diphenylacetoxy-N-methylpiperidine, a compound with similar high affinity for muscarinic receptors M1 and M3. None of them independently antagonized the suppressive effect of carbachol on the evoked EPSP completely, suggesting that more than one muscarinic receptor subtype is involved in the effect. These experiments provide evidence that in the amygdala muscarinic agonists block the excitatory synaptic response, mediated by glutamic acid, by acting on several types of presynaptic receptors.

Amygdala↗
PubMed2002

Basolateral amygdala lesions block the memory-enhancing effect of 8-Br-cAMP infused into the entorhinal cortex of rats after training.

There is extensive evidence suggesting that the basolateral nucleus of the amygdala plays a critical role in modulating memory consolidation processes in other brain regions. The present experiments examined interactions between the basolateral amygdala and the entorhinal cortex in modulating memory consolidation for inhibitory avoidance training. Several studies have reported that activation of the second messenger system adenosine 3',5'-cyclic monophosphate (cAMP) in several brain regions enhances memory and induces long-term plasticity. In the present experiments, a unilateral infusion of the cAMP analogue, 8-Br-cAMP (0.25 or 1.25 microg in 0.5 microL), administered into the entorhinal cortex of male Sprague-Dawley rats immediately after training, enhanced 48-h retention. An N-methyl-d-aspartate-induced lesion of the ipsilateral basolateral amygdala did not impair retention, but blocked the memory-enhancing effect of 8-Br-cAMP (infused into the entorhinal cortex) post-training. A lesion of the contralateral basolateral amygdala did not block the 8-Br-cAMP-induced retention enhancement. These findings indicate that an intact basolateral amygdala is essential for modulation of memory consolidation involving the entorhinal cortex, and are consistent with evidence that the basolateral amygdala regulates memory consolidation mediated by other brain regions.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2004

Glutamic acid and histamine-sensitive neurons in the ventral hippocampus and the basolateral amygdala of the rat: functional interaction on memory and learning processes.

The possibility of a functional interaction between the amygdala and the ventral hippocampus during learning of a conditioned avoidance response when both brain structures are chemically stimulated with glutamic acid and/or histamine receptor antagonists (pyrilamine, H1-histamine antagonist and ranitidine, H2-histamine receptor antagonist) was studied in rats. Adult male rats were stereotaxically implanted with guide cannulae into the basolateral amygdala (A) and the ventral hippocampus (H). Seventy-two hours after the implant, rats were microinjected with 1 microl of saline solution, 10 nmol glutamic acid or 45 nmol of histamine receptor antagonists in several brain structures combinations. These combinations were: HsalAsal; HmsgAmsg; HmsgAsal; HsalAmsg; HpyrAmsg; HmsgApyr; HranAmsg and HmsgAran. Five minutes after the injection, rats were subjected to a learning task which consisted to avoid an electric shock applied to the animal's feet when an ultrasonic tone of 40 kHz is on for 30 s. Results showed that the simultaneous application of glutamic acid into hippocampus and amygdala interfered with the latency to escape and memory consolidation process. Stimulation with glutamic acid alone into the hippocampus or into the amygdala (HsalAmsg and HmsgAsal groups) interfered slightly with latency but impaired the consolidation process. Blocking the H1-histamine receptors of the amygdala affected slightly latency and efficiency of learning, meanwhile the blocking of H2-histamine receptors interfered with both parameters. Blocking H1- and H2-histamine receptors of the hippocampus significantly impaired latency and efficiency of learning of rats stimulated with glutamic acid into the amygdala. In conclusion, the experimental evidence suggests that hippocampal glutamic acid-neurons functionally interact with histamine-neurons in the basolateral amygdala to modulate memory and learning process.

Amygdala↗
PubMed2006

Protein synthesis inhibition in the basolateral amygdala following retrieval does not impair expression of morphine-associated conditioned place preference.

Conditioned place preference is an animal model used to evaluate the affective properties of natural rewards and drugs of abuse. This animal model is a kind of classical conditioning that depends on learning and memory. The basolateral amygdala (BLA) plays an important role in the consolidation and extinction of memory for this task. However, there is a lack of evidence demonstrating protein synthesis dependent reconsolidation following retrieval in conditioned animals. In other words, is it possible to observe morphine-associated place preference if recall of this preference is disrupted? Accordingly, we investigated this hypothesis by BLA infusion of protein synthesis inhibitor, anisomycin, immediately after retrieval (test) in conditioned place preference paradigm. In the first experiment, the conditioned animals were exposed to the two sides of the apparatus for 15 min in a drug-free state during retrieval. In the second experiment, the animals received an injection of morphine (7.5 mg/kg, i.p.) and immediately after, they were exposed to the two sides of the apparatus for 15 min. Finally in the third experiment, after habituation and training in the conditioned place preference task, the animals received an injection of the unconditioned stimulus (morphine, i.p.; 7.5 mg/kg) followed by confinement for 10 min in the morphine-paired compartment (conditioned stimulus) during memory retrieval. For the three experiments the animals were subsequently exposed in a free-drug state to the two sides of the apparatus for the retest. Our results show that the protein synthesis inhibition in all of these experimental designs had no effect on conditioned place preference memory under conditions that would initiate reconsolidation, suggesting that if reconsolidation of a conditioned place preference task exists it is not mediated by protein synthesis in basolateral amygdala. The effect of anisomycin on consolidation of contextual fear conditioning was also investigated as a positive control to assure that the negative results were not due to methodological problems. Using the same dose of anisomycin (62.5 microg/1 microl) in morphine-associated place preference procedures, we have found that this anisomycin dose blocks the consolidation of contextual fear memory, ruling out the possibility that these negative results can be attributed to methodological problem of some sort.

Amygdala↗
PubMed1986

Effects of basolateral amygdala lesions on taste aversions produced by lactose and lithium chloride in the rat.

In Experiment 1, intact rats were given either lactose or sucrose solutions. Although on first exposure they readily consumed lactose, its ingestion produced a conditioned taste avoidance which was partly extinguished by repeated sucrose exposure after lactose conditioning. In Experiment 2, rats with large bilateral electrolytic lesions of the basolateral amygdala and those with either sham or no operations were given two pairings of saline with LiCl injections (upper gastrointestinal tract discomfort) and in a separate condition access to high levels of lactose (lower gastrointestinal tract discomfort). Conditioned taste avoidances were measured both by two-bottle tests and by video recordings of the rats' orofacial and somatic responses. The lesions attenuated LiCl-induced taste aversion but not lactose-induced taste avoidance, results demonstrating that taste avoidance can occur without the basolateral amygdala. The results suggested that aversions based on distaste can be distinguished from avoidances based on danger, not only in terms of orofacial responses but also in terms of their neuroanatomical substrate.

Amygdala↗
PubMed2000

Prolonged c-Jun expression in the basolateral amygdala following bulbectomy: possible implications for antidepressant activity and time of onset.

Olfactory bulbectomy is a well established animal model of depression. Neurochemical and behavioral alterations observed following olfactory bulbectomy, are due, in part, to the neurodegeneration of specific brain structures. Amygdaloid dysfunction in particular, is known to play a substantial role in the syndrome of the olfactory bulbectomized rat. The present study examined both short- and long-term alterations in immediate early gene expression, tyrosine hydroxylase and serotonin immunoreactivity, and classical silver staining, following olfactory bulbectomy in the basolateral amygdala. The results indicated no consistent change in Fos expression observed over the experimental period. Following bulbectomy, long term (up to 64 days post-lesion) Jun expression, not coincident with silver staining, was observed in the basolateral nucleus. The basolateral nucleus was also intensely immunoreactive for serotonin at this timepoint post-bulbectomy. Thus, following bulbectomy long term alterations in Jun expression occurs in the serotonin rich basolateral amygdala. As a site of action for antidepressant compounds, alterations at the immediate early gene level in this region may have implications both for the model, and antidepressant drug action therein.

Amygdala↗
PubMedDate not supplied

Complex effects of NMDA receptor antagonist APV in the basolateral amygdala on acquisition of two-way avoidance reaction and long-term fear memory.

Although much has been learned about the role of the amygdala in Pavlovian fear conditioning, relatively little is known about an involvement of this structure in more complex aversive learning, such as acquisition of an active avoidance reaction. In the present study, rats with a pretraining injection of the N-methyl-D-aspartate (NMDA) receptor antagonist, 2-amino-5-phosphonopentanoic acid (APV), into the basolateral amygdala (BLA) were found to be impaired in two-way active avoidance learning. During multitrial training in a shuttle box, the APV-injected rats were not different from the controls in sensitivity to shock or in acquisition of freezing to contextual cues. However, APV injection led to impaired retention of contextual fear when tested 48 h later, along with an attenuation of c-Fos expression in the amygdala. These results are consistent with the role of NMDA receptors of the BLA in long-term memory of fear, previously documented in Pavlovian conditioning paradigms. The APV-induced impairment in the active avoidance learning coincided with deficits in directionality of the escape reaction and in attention to conditioned stimuli. These data indicate that normal functioning of NMDA receptors in the basolateral amygdala is required during acquisition of adaptive instrumental responses in a shuttle box but is not necessary for acquisition of short-term contextual fear in this situation.

2-Amino-5-phosphonovalerate↗
PubMed1996

Excitotoxic lesions of the basolateral amygdala impair the acquisition of cocaine-seeking behaviour under a second-order schedule of reinforcement.

In these experiments we sought to establish the intravenous (i.v.) self-administration of cocaine under a second-order schedule of reinforcement in order: (i) to obtain reliable, drug-free levels of responding with cocaine as a reinforcer, and (ii) to enable investigation of the neural mechanisms by which arbitrary cues gain motivational salience and, as conditioned reinforcers, control over drug-seeking behaviour. Initially, each infusion of cocaine was made contingent upon a response on one of two identical levers and was paired with a 20-s light conditioned stimulus (CS). Responses on the second lever were recorded, but had no programmed consequence. When rats acquired stable rates of self-administration, a second-order schedule of the type FRx(FRy:S) was introduced, with values of "x" being increased progressively to 10 and then "y" from 2 through 8. Priming (i.e. non-contingent) infusions of cocaine were never given. Once the first infusion was obtained under the second-order schedule, further infusions were made contingent on each response (to a maximum of ten infusions/day). Each stage was repeated daily until the first infusion of each session was achieved within a 5-min criterion. Rats with bilateral, excitotoxic lesions of the basolateral amygdala readily acquired the i.v. self-administration of cocaine under a continuous reinforcement schedule, initially administering more infusions and maintaining a slightly elevated level of self-administration than controls. Despite increased numbers of CS/drug pairings, basolateral amygdala-lesioned rats were severely impaired in the acquisition of the second-order schedule of i.v. cocaine reinforcement. Lesioned rats showed a cocaine dose-response function that was shifted upwards relative to control subjects. There was no significant difference between drug-naive amygdala-lesioned and control animals in the locomotor response to intraperitoneal injections of cocaine. These experiments indicate the feasibility and utility of second-order schedules in studying the neurobehavioural basis of cocaine-seeking behaviour. They suggest a dissociation in the neural mechanisms underlying cocaine-taking and cocaine seeking behaviour, and demonstrate the potential importance of the basolateral amygdala in the processes by which previously neutral stimuli gain control over drug-seeking behaviour.

Amygdala↗
PubMed2003

Subtypes of substance P receptor immunoreactive interneurons in the rat basolateral amygdala.

Local injections of the neurotoxin SP-saporin into the basolateral amygdala (BLA) are reported to specifically lesion substance P receptor immunoreactive (SPR-IR) interneurons, and to reduce anxiety related behavior. Hence, this technique might provide a means to study how defined interneuron populations regulate neuronal activity in the BLA. However, what interneuron subgroups in the BLA might be targeted by SP-saporin lesions has not been established. This study has used dual-labeling immunofluorescence in the rat BLA to examine SPR-IR neurons for their colocalization with the calcium-binding proteins; calbindin-D28k (CB), parvalbumin (PV), and calretinin (CR); and the neuropeptides somatostatin (SOM) and neuropeptide Y (NPY). We found that all NPY-IR neurons and 45% of SOM-IR interneurons expressed SPR-IR, and that 50% and 51% of the SPR-IR interneuron population expressed NPY- and SOM-IR, respectively. Previous studies have reported that approximately a third of SOM-IR interneurons also express NPY, which suggests a large degree of overlap between the NPY, SOM and SPR expressing neurons in the BLA. We also found that the majority of SPR-IR cells were CB-IR (62%), but that these interneurons represented only 2.8% of the total CB-IR population. Moreover, SPR-IR interneurons did not express either PV-or CR- IR. Hence, SP-saporin lesions would ablate all interneurons in the BLA that contain NPY, but leave the majority of the CB-IR cells intact, and have no effect on the CR- and PV-IR populations. Consequently, these results support the use of SP-saporin lesions as a useful technique to study the role of NPY-IR interneurons in the BLA.

Amygdala↗
PubMed2002

Activation of histaminergic H3 receptors in the rat basolateral amygdala improves expression of fear memory and enhances acetylcholine release.

The basolateral amygdala (BLA) is involved in learning that certain environmental cues predict threatening events. Several studies have shown that manipulation of neurotransmission within the BLA affects the expression of memory after fear conditioning. We previously demonstrated that blockade of histaminergic H3 receptors decreased spontaneous release of acetylcholine (ACh) from the BLA of freely moving rats, and impaired retention of fear memory. In the present study, we examined the effect of activating H3 receptors within the BLA on both ACh release and expression of fear memory. Using the microdialysis technique in freely moving rats, we found that the histaminergic H3 agonists R-alpha-methylhistamine (RAMH) and immepip, directly administered into the BLA, augmented spontaneous release of ACh in a similar manner. Levels of ACh returned to baseline on perfusion with control medium. Rats receiving intra-BLA, bilateral injections of the H3 agonists at doses similar to those enhancing ACh spontaneous release, immediately after contextual fear conditioning, showed stronger memory for the context-footshock association, as demonstrated by longer freezing assessed at retention testing performed 72 h later. Post-training, bilateral injections of 15 ng oxotremorine also had a similar effect on memory retention, supporting the involvement of the cholinergic system. Thus, our results further support a physiological role for synaptically released histamine, that in addition to affecting cholinergic transmission in the amygdala, modulates consolidation of fear memories

Acetylcholine↗
PubMed2003

Different roles for orbitofrontal cortex and basolateral amygdala in a reinforcer devaluation task.

The orbitofrontal cortex (OFC) and basolateral amygdala (BLA) are critical for using learned representations of outcomes to guide behavior. Neurophysiological findings suggest complementary roles in which the BLA acquires associations between cues and outcomes and the OFC subsequently uses them to guide behavior. Here, we have used a reinforcer devaluation paradigm to test this hypothesis. In this paradigm, rats are first trained to associate a light conditioned stimulus (CS) with a food outcome, and then the food is devalued by pairing it with illness. After this devaluation procedure, responding to the CS is assessed in a single probe session. Previously, we have shown that BLA and OFC lesions made before training do not affect the acquisition of conditioned responding but do impair the sensitivity of that responding to reinforcer devaluation. Rats with such lesions fail to exhibit the spontaneous decrease in conditioned responding to the light cue observed in controls in the probe test. Here, we have extended those findings by showing that performance in the probe test is impaired by OFC lesions made after light-food conditioning but not by BLA lesions made after that training. These findings indicate that the OFC and BLA play different roles in mediating normal goal-directed performance in this, and likely other, settings. The BLA seems critical to forming representations linking cues to the incentive properties of outcomes but not for maintaining these representations in memory, updating them with new information, or for expressing them in behavior. In contrast, the OFC seems essential for one or more of these latter processes.

Amygdala↗
PubMedDate not supplied

[Interneuronal relationships in the basolateral amygdala of cats trained for choice in the quality of food reinforcement].

The alimentary instrumental conditioned bar-pressing reflex was elaborated in cats by the method of "active choice" of either short-delayed reinforcement with bread-meat mixture of delayed more valuable reinforcement with meat. The animals differed in behavior strategy: some animals preferred bar-pressing with the long delay (the so-called "self-control" group), other animals pressed the bar with short delay (the so-called "impulsive" group). The multiunit activity in the basolateral amygdala was recorded with chronically implanted nichrome microelectrodes. The interactions between the spike trains of the neighbouring neurons selected from the multiunit activity were evaluated by means of statistical crosscorrelation analysis. It was shown that the number of correlations between the discharges of neurons was significantly higher in the "impulsive" cats. In both groups the number of cross-correlations was maximal in cases of a difficult choice, i.e., during the omission of the conditioned bar-pressing response. In "impulsive" cats the number of interneuronal correlations was highest with the latencies in the range of 0-30 msec. We suggest that the basolateral amygdala is involved in the system of structures which determine the individual-typological characteristics of animals.

Amygdala↗
PubMed1999

Differential synaptic distribution of the AMPA-GluR2 subunit on GABAergic and non-GABAergic neurons in the basolateral amygdala.

The cellular and ultrastructural distribution patterns of the AMPA glutamate receptor subunit, GluR2, were determined in the rat basolateral amygdala. GluR2 immunoreactivity was widely and uniformly distributed in the basolateral nucleus, with both pyramidal and non-pyramidal neurons labelled. In fact, double label immunohistochemical analyses demonstrated that over 90% of the GABAergic interneurons were labelled for GluR2. Electron microscopic analyses further confirmed the presence of GluR2 in the soma and dendrites of GABAergic interneurons as well as in the soma, spines and dendritic shafts of pyramidal cells. As in our parallel study in the rat hippocampus, immunogold analyses revealed that GluR2 immunoreactivity was frequently preferentially located at asymmetric synapses on both pyramidal cell spines and shafts, as well as the dendritic processes and soma of GABAergic interneurons. However, the number of immunogold particles per labelled synapse on GABAergic neurons was significantly lower than at similar labelled asymmetric synapses on spines of presumed pyramidal cells. Given that the presence of GluR2 within the AMPA receptor complex decreases calcium flux, these data indicate that GABAergic local circuit neurons might possess AMPA receptors with higher calcium permeability on average than pyramidal cells, as has been suggested for hippocampus. Such cell class-specific differences in the subunit representation and resultant channel properties of AMPA receptors have implications for response properties as well as selective vulnerability of neurons within the basolateral nucleus of the amygdala.

Amygdala↗
PubMedDate not supplied

Interneuron relationships in the basolateral amygdala in cats treated to select food on the basis of quality.

Cats were initially trained to make operant conditioned food responses to light by an "active selection of reinforcement" method. Provision of low-quality (a mixture of meat and bread) or high-quality (meat) reinforcement depended on the animal pressing a pedal in response to switching on a light with a short (1 sec) or long (10 sec) delay. Some animals responded to long delays--group I, animals with "self control," while others responded with short delays--group II, "impulsive" animals. Implanted semimicroelectrodes were used in chronic experiments to record multineuron activity in the basolateral amygdala. Cross-correlation analysis was used to study interneuron interactions in the spike discharges of individual neurons, extracted from multineuron activity. The numbers of interneuron interactions were significantly higher in "impulsive" cats of group II in all behavioral situations than in animals with "self control," and were dominated in "impulsive" animals by the shortest connections, with latencies of 0-30 msec. The largest numbers of connections in both groups were seen on omission of the conditioned pedal-pressing movement response, i.e., when the reinforcement selection task was more difficult. These data indicate that the basolateral amygdala should be regarded as a structure determining the individual typological characteristics of the animals' behavior.

Amygdala↗
PubMed1995

Topographical organization in the nucleus accumbens of afferents from the basolateral amygdala and efferents to the lateral hypothalamus.

The basolateral region of the amygdala and the lateral hypothalamic area are involved in cardiovascular regulation. The aim of the present investigation was to determine if the terminal field of afferent projections from the basolateral nucleus of the amygdala to the nucleus accumbens overlap with the origin of the efferent projections from the nucleus accumbens to the lateral hypothalamic area. Neurons projecting from the nucleus accumbens to the lateral hypothalamic area were labeled by injecting the retrograde tracer Fluoro-Gold in the lateral hypothalamus of rats. In the same rats, fiber terminals from the amygdala to the nucleus accumbens were labeled by injecting the anterograde tracer Fluoro-Ruby in the basolateral region of the amygdala. Injections of Fluoro-Gold in the lateral hypothalamus labeled neurons in the posteromedial portion of the nucleus accumbens. Injections of Fluoro-Ruby in the basolateral amygdala labeled fibers and terminals in all parts of the nucleus accumbens with the highest density being found in the posteromedial part of the nucleus accumbens where Fluoro-Gold-labeled neurons were located. When regions of the posteromedial nucleus accumbens were examined under high-magnification, Fluoro-Ruby-labeled terminals appeared to make contact on Fluoro-Gold-labeled dendrites and cell bodies. This investigation demonstrates that there is a distinct overlap in the posteromedial region of the nucleus accumbens between the terminal field from neurons originating in the amygdala and neurons which project to the lateral hypothalamus. In addition, neurons in the basolateral amygdala appear to make synaptic contact with neurons in the nucleus accumbens that project to the lateral hypothalamic area.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed2002

Cholinergic activation of the basolateral amygdala regulates unlearned freezing behavior in rats.

Recent evidence suggests that the basolateral amygdala (BLA) is involved in the expression of freezing behavior in rats. This study investigated the effects of unilateral phthalic acid (PA) lesions of the nucleus basalis magnocellularis (NBM) on fear-motivated behavior in response to a natural predator-stimulus. Such lesions preferentially disrupt the cholinergic projection to the BLA. Rats were placed in a chamber containing either real or fake cat hair, and the amount of time spent freezing and the number of contacts made with the stimulus were measured. Compared with Sham control rats, the PA NBM-lesioned rats displayed significantly less freezing in the presence of the cat hair. Both the Sham and lesioned rats made fewer contacts with the real than the fake cat hair. Pre-testing intra-BLA infusion of the direct muscarinic cholinergic agonist oxotremorine ipsilateral to the PA NBM-lesion attenuated the freezing deficit. The indirect non-specific cholinergic agonist physostigmine increased the time spent freezing in Sham rats, but did not attenuate the freezing deficit in the NBM-lesioned rats. Sham and NBM-lesioned rats given oxotremorine infusions made fewer contacts with either the real or the fake cat hair. The PA NBM-lesion did not affect open field activity. These findings indicate that muscarinic cholinergic activation in the BLA from the NBM influences fear-motivated freezing behavior.

Amygdala↗
PubMed1996

Retrograde abolition of conditional fear after excitotoxic lesions in the basolateral amygdala of rats: absence of a temporal gradient.

The role of the basolateral amygdala (LA) in the acquisition and expression of Pavlovian fear conditioning was examined in 80 rats. Excitotoxic lesions were made in the BLA using N-methyl-D-aspartate 7 days before or 1, 14, or 28 days after Pavlovian fear conditioning. Conditioning consisted of three pairings of a tone with an aversive footshock in a novel chamber, and freezing behavior served as an index of conditional fear. BLA lesions abolished conditional freezing to both the contextual and acoustic conditional stimuli at all training-to-lesion intervals, and the magnitude of the impairment did not vary as a function of the training-to-lesion interval. Reacquisition training elevated levels of freezing in rats with BLA lesions but did not reduce the magnitude of their deficit in relation to that of controls. These results reveal that neurons in the BLA have an enduring role in the expression of conditional fear.

Amygdala↗
PubMed2002

Lesions of the nucleus basalis magnocellularis induced by 192 IgG-saporin block memory enhancement with posttraining norepinephrine in the basolateral amygdala.

Extensive evidence indicates that drugs and stress hormones act in the basolateral amygdala (BLA) to modulate memory consolidation. The BLA projects to the nucleus basalis magnocellularis (NBM), which sends broad cholinergic projections to the neocortex. NBM-cortex projections have been implicated in learning, memory storage, and plasticity. The current study investigated whether the cholinergic NBM-cortex projections are involved in BLA-mediated modulation of memory consolidation. Bilateral cholinergic cell lesions of the NBM were induced in rats with infusions of 192 IgG-saporin (0.1 microg/0.5 microl per side). Additionally, cannulae were implanted bilaterally in the BLA. One week after surgery, the rats were trained in an inhibitory avoidance task and, immediately after training, norepinephrine (0.3 microg, 1.0 microg, or 3.0 microg in 0.2 microl) or vehicle (PBS) was infused bilaterally into the BLA. Norepinephrine infusions produced a dose-dependent enhancement of 48-h retention (0.3 microg and 1.0 microg doses enhanced) in nonlesioned rats but did not affect retention in NBM-lesioned rats. Choline acetyltransferase assays of frontal and occipital cortices confirmed the NBM lesions. These findings indicate that cholinergic NBM-cortex projections are required for BLA-mediated modulation of memory consolidation.

Amygdala↗