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At least 73 records · Page 4Linked to original sources
PubMed1999

Relationship of calcium-binding protein containing neurons and projection neurons in the rat basolateral amygdala.

Two-laser and two-color approaches were used to observe the colocalization of the calcium-binding proteins, calbindin D28k and parvalbumin, and the retrograde tracer, Fluoro-Gold (FG) in the basolateral amygdala of the rat. The study was performed on five adult rats into which FG was injected to the frontal association cortex. Then, the localization of the retrogradely labeled neurons in the basolateral amygdala was compared with the localization of the neurons labeled by calcium-binding proteins. The present study showed that most of the retrogradely labeled neurons in the posterior part of the basolateral amygdala are also calbindin-positive. Even though a lot of parvalbumin-positive endings were present at the surface of the retrogradely labeled cells, we did not observe the colocalization of the parvalbumin and projective neurons.

Amygdala↗
PubMedDate not supplied

Temporary basolateral amygdala lesions disrupt acquisition of socially transmitted food preferences in rats.

Lesions of the basolateral amygdala (BLA) have long been associated with abnormalities of taste-related behaviors and with failure in a variety of taste- and odor-related learning paradigms, including taste-potentiated odor aversion, conditioned taste preference, and conditioned taste aversion. Still, the general role of the amygdala in chemosensory learning remains somewhat controversial. In particular, it has been suggested that the amygdala may not be involved in a form of chemosensory learning that has recently received a substantial amount of study-socially transmitted food preference (STFP). Here, we provide evidence for this involvement by pharmacologically inactivating the basolateral amygdala bilaterally during STFP training. The same inactivation sites that impaired taste aversion learning eliminated the normally conditioned preference for a food smelled on a conspecific's breath. Impairments of learned preference persisted even in testing sessions in which BLA was not inactivated, and learning was normal when the BLA was inactivated only during testing sessions; thus, the impairment was a true acquisition deficit. In conjunction with previous results from other paradigms, therefore, our data suggest that the amygdala is vital for learning procedures involving pairings of potent and arbitrary chemosensory stimuli.

Amygdala↗
PubMed1993

Differential effects of excitotoxic lesions of the basolateral amygdala, ventral subiculum and medial prefrontal cortex on responding with conditioned reinforcement and locomotor activity potentiated by intra-accumbens infusions of D-amphetamine.

The experiments reported here have investigated the impact on reward-related processes of lesioning the basolateral amygdala, ventral subiculum and prelimbic cortex which represent the major limbic sources of afferents to the ventral striatum. The results showed that, while lesions of the prelimbic cortex were without effect on the approach to a CS predictive of sucrose reinforcement and the acquisition of a new response with conditioned reinforcement, lesions of the other two structures significantly impaired both responses. However, there were important differences between the effects of basolateral amygdala and ventral subiculum lesions. Thus, lesions of the ventral subiculum completely abolished the locomotor response to intra-accumbens infusions of D-amphetamine, in addition to blocking the potentiative effect of the same treatment on responding with conditioned reinforcement. Lesions of the basolateral amygdala, by contrast, reduced the control over behaviour by a conditioned reinforcer, but not the potentiation of that control by intra-accumbens D-amphetamine except at the highest dose. Moreover, the locomotor response to D-amphetamine-induced increases in dopamine in the nucleus accumbens was unaffected by amygdala lesions over the dose range blocked by ventral subiculum lesions. The results suggest a rather selective effect of amygdala-ventral striatal interactions on processes subserving conditioned reinforcement and a more fundamental influence of ventral subiculum-ventral striatal interactions in mediating the psychomotor stimulant effects of D-amphetamine.

Afferent Pathways↗
PubMed1997

Excitatory amino acid receptor antagonists block the cardiovascular and anxiety responses elicited by gamma-aminobutyric acidA receptor blockade in the basolateral amygdala of rats.

Blockade of gamma-aminobutyric acid (GABAA) receptors in the anterior basolateral amygdala (BLA) with bicuculline methiodide results in an increase in heart rate, blood pressure and "anxiety" in rats. Glutamate receptors in the BLA are also reported to be involved in eliciting anxiety responses. The purpose of this study was to investigate the interaction between GABAergic inhibition and glutamatergic excitation in the BLA. Male Wistar rts were implanted with femoral arterial catheters and bilateral chronic microinjection cannulae into the BLA. Each animal was injected with either artificial cerebrospinal fluid (100 nl), bicuculline methiodide (10 pmol/100 nl) or bicuculline methiodide + one dose of an antagonist of either the N-methyl-D-aspartate receptor [AP5 (20 and 100 pmol) and dizocilpine (25 and 125 pmol)] or the non-N-methyl-D-aspartate ionotropic receptor [CNQX (10 and 50 pmol) and GYKI 52466 (50 and 250 pmol)]. Increases in heart rate, blood pressure and "anxiety" (as measured in the social interaction test) observed in rats after bicuculline methiodide injections into the BLA were blocked in a dose dependent manner with the concurrent injections of either N-methyl-D-aspartate or non-N-methyl-D-aspartate antagonists, suggesting that activation of both subtypes of glutamate ionotropic receptors may be necessary for the responses elicited by GABAA receptor blockade in the basolateral amygdala.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2006

Pyramidal cells of the rat basolateral amygdala: synaptology and innervation by parvalbumin-immunoreactive interneurons.

The generation of emotional responses by the basolateral amygdala is determined largely by the balance of excitatory and inhibitory inputs to its principal neurons, the pyramidal cells. The activity of these neurons is tightly controlled by gamma-aminobutyric acid (GABA)-ergic interneurons, especially a parvalbumin-positive (PV(+)) subpopulation that constitutes almost half of all interneurons in the basolateral amygdala. In the present semiquantitative investigation, we studied the incidence of synaptic inputs of PV(+) axon terminals onto pyramidal neurons in the rat basolateral nucleus (BLa). Pyramidal cells were identified by using calcium/calmodulin-dependent protein kinase II (CaMK) immunoreactivity as a marker. To appreciate the relative abundance of PV(+) inputs compared with excitatory inputs and other non-PV(+) inhibitory inputs, we also analyzed the proportions of asymmetrical (presumed excitatory) synapses and symmetrical (presumed inhibitory) synapses formed by unlabeled axon terminals targeting pyramidal neurons. The results indicate that the perisomatic region of pyramidal cells is innervated almost entirely by symmetrical synapses, whereas the density of asymmetrical synapses increases as one proceeds from thicker proximal dendritic shafts to thinner distal dendritic shafts. The great majority of synapses with dendritic spines are asymmetrical. PV(+) axon terminals form mainly symmetrical synapses. These PV(+) synapses constitute slightly more than half of the symmetrical synapses formed with each postsynaptic compartment of BLa pyramidal cells. These data indicate that the synaptology of basolateral amygdalar pyramidal cells is remarkably similar to that of cortical pyramidal cells and that PV(+) interneurons provide a robust inhibition of both the perisomatic and the distal dendritic domains of these principal neurons.

Amygdala↗
PubMed2005

Attraction to sexual pheromones and associated odorants in female mice involves activation of the reward system and basolateral amygdala.

Adult female mice are innately attracted to non-volatile pheromones contained in male-soiled bedding. In contrast, male-derived volatiles become attractive if associated with non-volatile attractive pheromones, which act as unconditioned stimulus in a case of Pavlovian associative learning. In this work, we study the chemoinvestigatory behaviour of female mice towards volatile and non-volatile chemicals contained in male-soiled bedding, in combination with the analysis of c-fos expression induced by such a behaviour to clarify: (i) which chemosensory systems are involved in the detection of the primary attractive non-volatile pheromone and of the secondarily attractive volatiles; (ii) where in the brain male-derived non-volatile and volatile stimuli are associated to induce conditioned attraction for the latter; and (iii) whether investigation of these stimuli activates the cerebral reward system (mesocorticolimbic system including the prefrontal cortex and amygdala), which would support the view that sexual pheromones are reinforcing. The results indicate that non-volatile pheromones stimulate the vomeronasal system, whereas air-borne volatiles activate only the olfactory system. Thus, the acquired preference for male-derived volatiles reveals an olfactory-vomeronasal associative learning. Moreover, the reward system is differentially activated by the primary pheromones and secondarily attractive odorants. Exploring the primary attractive pheromone activates the basolateral amygdala and the shell of nucleus accumbens but neither the ventral tegmental area nor the orbitofrontal cortex. In contrast, exploring the secondarily attractive male-derived odorants involves activation of a circuit that includes the basolateral amygdala, prefrontal cortex and ventral tegmental area. Therefore, the basolateral amygdala stands out as the key centre for vomeronasal-olfactory associative learning.

Amygdala↗
PubMed2002

Glucocorticoids alter calcium conductances and calcium channel subunit expression in basolateral amygdala neurons.

Glucocorticoid hormones, which are released in high amounts after stress, enter the brain where they bind to intracellular receptors that are abundant in limbic areas, in particular the hippocampus and amygdala nuclei. Behavioural studies indicate that glucocorticoids modulate learning and memory processes via receptors in the hippocampus and amygdala. So far, the effects of glucocorticoids on amygdala neurons have not been investigated at the cellular and molecular level. We report here that in vitro application of glucocorticoids for 20 min increases 1-4 h later the amplitude of sustained, high-voltage-activated calcium currents in principal neurons of the basolateral amygdala. In contrast, the transient, low-voltage-activated currents were decreased. We examined whether these functional changes in calcium conductance were accompanied by transcriptional regulation of calcium channel subunits. Analysis of the RNA - collected after recording and then linearly amplified - revealed that glucocorticoid-mediated increases in sustained calcium currents are associated with a parallel shift in the relative expression of the alpha1 subunit constituting the pore of the sustained, high-voltage-activated (L-type) calcium channel. These data indicate that glucocorticoids, probably by selectively targeting genes encoding calcium channel subunits, largely alter the calcium influx into basolateral amygdala neurons. These actions could modify amygdala network function and thus contribute to the behavioural effects exerted by the stress hormones via the basolateral amygdala.

Amygdala↗
PubMed2005

Reconditioning of heroin place preference requires the basolateral amygdala.

To investigate the role of the basolateral amygdala (BLA) in the reacquisition of heroin seeking, we studied the effect of BLA inactivation after heroin re-exposure in the presence of drug-conditioned cues. We employed a heroin conditioned place preference task [Leri F, Rizos Z, 2005. Reconditioning of drug-related cues: a potential contributor to relapse after drug re-exposure. Pharmacol Biochem Behav 2005;80:621-30.], where after initial conditioning and subsequent extinction, rats received a single reconditioning session (explicit compartment-heroin re-pairing), followed by a test of heroin seeking 24 h later. Rats were infused with GABA(A)/GABA(B) agonists (muscimol and baclofen, 0.03 and 0.3 nmol, respectively/0.3 microl) or vehicle, either 15 min or 6 h following the heroin reconditioning session. Animals that received vehicle infusions, whether they were given 15 min or 6 h following reconditioning, showed a significant preference for the heroin-paired compartment 24 h later. However, inactivation of the BLA 15 min post-reconditioning, but not 6 h following reconditioning, completely blocked the reacquisition of heroin seeking. These results suggest that the BLA plays an important role in a putative learning process initiated by drug re-exposure which may underlie the process of relapse.

Amygdala↗
PubMed2006

Vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat.

The basal forebrain (BF) plays a role in behavioral and cortical arousal, attention, learning, and memory. It has been suggested that cholinergic BF neurons co-release glutamate, and some cholinergic BF neurons have been reported to contain vesicular glutamate transporter 3 (VGLUT3). We examined the distribution and projections of BF cholinergic neurons containing VGLUT3, by using dual-label immunofluorescence for choline acetyltransferase (ChAT) and VGLUT3, in situ hybridization, and retrograde tracing. Neurons immunoreactive (+) or containing mRNAs for both ChAT and VGLUT3 were mainly localized to the ventral pallidum and more caudal BF regions; the co-immunoreactive neurons represented 31% of cholinergic neurons in the ventral pallidum and 5-9% more caudally. Examination of cholinergic axon terminals in known target areas of BF projections indicated that the basolateral amygdaloid nucleus contained numerous terminals co-immunoreactive for ChAT and VGLUT3, whereas sampled areas of the olfactory bulb, neocortex, hippocampus, reticular thalamic nucleus, and interpeduncular nucleus were devoid of double-labeled terminals. The basolateral amygdala is innervated by cholinergic BF neurons lacking low-affinity p75 nerve growth factor receptors; many ChAT+VGLUT3+ BF neurons were immunonegative to this receptor. Twenty-five to 79% of ChAT+VGLUT3+ neurons in different BF regions were retrogradely labeled from the basolateral amygdala, up to 52% (ventral pallidum) of the retrogradely labeled ChAT+ neurons were VGLUT3+, and the largest number of amygdala-projecting ChAT+VGluT3+ neurons was found in the ventral pallidum. These findings indicate that BF cholinergic neurons containing VGLUT3 project to the basolateral amygdala and suggest that these neurons might have the capacity to release both acetylcholine and glutamate.

Amygdala↗
PubMed2005

Long-term kindling of the basolateral amygdala impairs copulatory behavior in male rats.

This experiment examined the consequences of long-term kindling of the basolateral amygdala on male sexual behavior and the frequency of both spontaneous wet dog shakes (WDS) and those induced by the 5-HT2A receptor agonist DOI. Results demonstrated that following 60 stimulations of the left basolateral amygdala over a 4-week period, male Long-Evans rats exhibited decrements in every aspect of sexual behavior. Specifically, latencies to mount, intromit and ejaculate were all prolonged following long-term kindling, and ejaculation frequencies were significantly reduced. Furthermore, spontaneous peri-copulatory WDS were increased in kindled rats, suggesting a possible role of the 5-HT2A receptor. However, countering this suggestion, there were no differences between sham and kindled rats on WDS induced by the 5-HT2A receptor agonist DOI. These results suggest that kindled rats may exhibit elevated levels of endogenous serotonin during exposure to a female rat, which would attenuate copulatory behavior, while concurrently increasing WDS expression.

Amphetamines↗
PubMed1995

Footshock facilitates the expression of aversively motivated memory in rats given post-training amygdala basolateral complex lesions.

We previously reported that increased training in an escape task partially attenuates the memory impairment produced by large amygdala lesions induced 1 week following training. The present study examined the effect of amount of preoperative training on the retention of rats with lesions restricted to the amygdala basolateral complex. Rats received 1 or 10 training trials in a footshock-motivated escape task and 1 week later sham lesions or neurotoxic lesions of the basolateral complex. Four days after recovery from the surgery they were tested for inhibitory avoidance retention and then 2 days later given continuous multiple trial inhibitory avoidance training (CMIA) in the same apparatus. The basolateral complex lesions significantly decreased the retention latencies of rats given 1 or 10 trials. However, following administration of footshock on the CMIA task, the performance of the lesioned rats reflected the degree of preoperative escape training. The basolateral complex lesions also increased open field locomotor activity, an effect that may have contributed to the shorter retention latencies in lesioned animals. These findings indicate that an intact amygdala basolateral complex is not critical for the retention of the escape training.

Amygdala↗
PubMed1979

Differential effects of basolateral amygdala lesions on behavior, corticosterone, and prolactin responses.

The present experiment examines hormone-behavior relationships following manipulation of the amygdala. Affective behavior and levels of corticosterone and prolactin were compared in rats with lesions of the basolateral amygdala and in nonlesioned and sham-operated controls. Animals with lesions of the basolateral amygdala were found to be hyperreactive and to have normal resting levels of corticosterone and prolactin but potentiated corticosterone responses to stress. Normal prolactin stress responses were unaltered by the lesion. The results are discussed in relation to behavioral and endocrine changes seen following other limbic system lesions.

Amygdala↗
PubMed1992

Induction of long-term potentiation in the basolateral amygdala does not depend on NMDA receptor activation.

Long-term potentiation (LTP) can be induced in the lateral and basolateral amygdala by stimulating synaptic afferents in the external capsule (EC). We examined the sensitivity of amygdaloid LTP to the NMDA receptor antagonist 2-amino-5-phosphonopentanoate (AP5), which is known to block LTP induction in the Schaffer collateral/CA1 synapses in the hippocampus. While relatively high concentrations (100 microM) of DL-AP5 were effective in preventing LTP induction in the lateral and basolateral amygdala in vitro, the same concentrations also significantly depressed synaptic responses to low-frequency stimulation. Furthermore, at 50 microM, a concentration sufficient to block both synaptic responses mediated by NMDA receptors and LTP induction in the hippocampus and neocortex, AP5 did not affect the probability of inducing LTP in the amygdala. Application of 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), which blocks non-NMDA excitatory amino acid receptors, reduced the monosynaptic response to EC stimulation by 85%. The remaining CNQX-insensitive response did not appear to be mediated by NMDA-type receptors, since it was not reduced by 50 or 100 microM AP5, and showed none of the voltage sensitivity characteristic of NMDA responses. These data suggest that while the induction of LTP in the amygdala produced by EC stimulation is blocked by high doses of AP5, plasticity at these synapses probably does not require activation of NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1997

Bicuculline administration into basolateral amygdala facilitates trace conditioning of odor aversion in the rat.

This study investigated the effect of bicuculline methiodide (BMI) microinjection into basolateral amygdala (BLA) on conditioned odor aversion. Bilateral injections of BMI (39 or 59 pmol/0.2 microliter) or artificial CSF were done in the BLA 5 min after the presentation of the conditioned stimulus (water intake at an almond-scented tube). This was followed 30 min later by lithium chloride-induced toxicosis. Whereas under these experimental conditions control rats (CSF injected) did not develop a conditioned odor aversion, BMI-treated rats (59 pmol) did so, suggesting that the blockade of GABAA receptors facilitated this learning. This facilitation was unlikely due to an unconditioned action of BMI, as a group microinjected with 59 pmol of BMI but not intoxicated did not display conditioned aversion. This result suggest that blockade of the GABAA receptors can prolong the olfactory trace duration, making it accessible to association with delayed toxicosis. Combined with previous results, these data support the hypothesis that the GABAergic system of the basolateral amygdala exerts control over the duration of a short-term odor trace in our conditioned odor aversion paradigms.

Amygdala↗
PubMed2005

Anxiolytic and anxiogenic effects of kindling--role of baseline anxiety and anatomical location of the kindling electrode in response to kindling of the right and left basolateral amygdala.

Effects of kindling of right and left basolateral amygdala (BLA) on plus maze anxiety was studied. Using a validated retest paradigm, it was possible to retest rats in the plus maze without increasing anxiety on retest. This permitted determining prekindling baseline levels of plus maze anxiety. Right BLA kindling of high baseline anxiety rats was anxiolytic one week after kindling. Right BLA kindling of low baseline anxiety rats was anxiogenic. In addition, left BLA kindling was either anxiogenic or without effect on plus maze anxiety, depending on baseline anxiety. Effects in left BLA differ from previous work showing anxiolytic effects of left BLA kindling. The discrepancy could be explained in part by prekindling baseline anxiety. These findings require modification of the previous conclusion that left hemisphere (left BLA) kindling is anxiolytic and right BLA kindling is anxiogenic in the plus maze. Rather the hemisphere difference may be due to an interaction between baseline anxiety level and kindling. If true, anxious disposition in rodents may interact with amygdala kindling to change amygdala function differently. Kindling and baseline anxiety effects on other behaviors (such as risk assessment and resistance to capture) are also described. Present data in the light of past studies suggest both premorbid anxiety state and location of the kindling electrode contribute to the effects of kindling on behavior.

Amygdala↗
PubMed2000

NMDA-Receptor-dependent synaptic activation of voltage-dependent calcium channels in basolateral amygdala.

Afferent stimulation of pyramidal cells in the basolateral amygdala produced mixed excitatory postsynaptic potentials (EPSPs) mediated by N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors during whole cell current-clamp recordings. In the presence of GABA(A) receptor blockade, the mixed EPSPs recruited a large "all-or-none" depolarizing event. This recruited event was voltage dependent and had a distinct activation threshold. An analogous phenomenon elicited by exogenous glutamate in the presence of tetrodotoxin (TTX) was blocked by Cd(2+), suggesting that the event was a Ca(2+) spike. Selective glutamatergic blockade revealed that these Ca(2+) spikes were recruited readily by single afferent stimulus pulses that elicited NMDA EPSPs. In contrast, non-NMDA EPSPs induced by single stimuli failed to elicit the Ca(2+) spike even at maximal stimulus intensities although these non-NMDA EPSPs depolarized the soma more effectively than mixed EPSPs. Elongation of non-NMDA EPSPs by cyclothiazide or brief trains of stimulation were also unable to elicit the Ca(2+) spike. Blockade of K(+) channels with intracellular Cs(+) enabled single non-NMDA EPSPs to activate the Ca(2+) spike. The finding that voltage-dependent calcium channels are activated preferentially by NMDA-receptor-mediated EPSPs provides a mechanism for NMDA-receptor-dependent plasticity independent of Ca(2+) influx through the NMDA receptor.

2-Amino-5-phosphonovalerate↗
PubMed2006

Extinction is not a sufficient condition to prevent fear memories from undergoing reconsolidation in the basolateral amygdala.

Consolidated memories when reactivated may return to a state that requires protein synthesis in order to be restabilized (reconsolidation). It has been shown in a variety of systems that if reactivation induces significant extinction then extinction is the protein synthesis dependent memory state, rather than reconsolidation. Thus, extinction consolidation may prevent the memory from undergoing reconsolidation. We investigated whether such an interaction also exists between extinction and reconsolidation of fear memories within the amygdala, by using a within subjects experimental design. We found that inhibition of protein synthesis in the basolateral amygdala (BLA) impaired reconsolidation for both the briefly reactivated and extinguished fear memories suggesting that extinction is not a sufficient condition to prevent induction of reconsolidation in the amygdala. These findings demonstrate that extinction consolidation does not always interact with reconsolidation. Therefore, under these conditions, extinction is not a boundary condition on reconsolidation of fear memories in the basolateral amygdala.

Acoustic Stimulation↗
PubMed2002

Posttraining intra-basolateral amygdala scopolamine impairs food- and amphetamine-induced conditioned place preferences.

The present study investigated the role of cholinergic muscarinic receptor function within the basolateral amygdala memory in the consolidation of conditioned place preference (CPP) memory. Adult male Long-Evans rats were confined to treatment- or nontreatment-paired compartments for 30 min on 4 alternating days. After training, rats received intrabasolateral amygdala infusions of scopolamine (2.5 microg or 5.0 microg/0.5 microl) or saline. The rats were then given a 20-min test session, and the time spent in each of the compartments was recorded. Immediate posttraining (but not delayed 2 hr) scopolamine (5.0 microg) blocked acquisition of food- and amphetamine-induced CPPs. The findings indicate a time-dependent role for basolateral amygdala muscarinic receptors in memory consolidation underlying CPPs for natural and drug rewards.

Amphetamine↗