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At least 127 records · Page 7Linked to original sources
PubMed2004

Bombesin/gastrin-releasing peptide receptors in the basolateral amygdala regulate memory consolidation.

Several receptor and intracellular signalling systems in the basolateral amygdala (BLA) regulate memory formation. In the present study, we show that bombesin/gastrin-releasing peptide (GRP) receptors in the BLA are involved in the consolidation of affectively motivated memory. Adult male rats were trained in a single-trial step-down inhibitory avoidance task and tested for retention 24 h later. Post-training systemic injection of the bombesin/GRP receptor antagonist (D-Tpi6, Leu13 psi[CH2NH]-Leu14) bombesin (6-14) (RC-3095) impaired memory retention. In rats implanted under thionembutal anaesthesia with guide cannulae aimed at the BLA, post-training bilateral infusion of RC-3095 into the BLA dose-dependently impaired retention. Pre-training unilateral muscimol inactivation of the BLA blocked the memory-impairing effect of post-training systemic administration of RC-3095. The results suggest that bombesin/GRP receptors in the BLA are involved in the consolidation of aversive memory, and the BLA mediates the memory-impairing effect of systemic bombesin/GRP receptor blockade.

Amygdala↗
PubMed2006

Stress reverses plasticity in the pathway projecting from the ventromedial prefrontal cortex to the basolateral amygdala.

We have previously shown that high-frequency stimulation to the basolateral amygdala (BLA) induces long-term potentiation (LTP) in the ventromedial prefrontal cortex (vmPFC) and that prior exposure to inescapable stress inhibits the induction of LTP in this pathway [Maroun & Richter-Levin (2003)J. Neurosci., 23, 4406-4409]. Here, we show that the reciprocal pathway projecting from the vmPFC to the BLA is resistant to the induction of LTP. Conversely, long-term depression (LTD) is robustly induced in the BLA in response to low-frequency stimulation to the vmPFC. Furthermore, prior exposure to inescapable stress reverses plasticity in this pathway, resulting in the promotion of LTP and the inhibition of LTD. Our findings suggest that, under normal and safe conditions, the vmPFC is unable to exert excitatory synaptic plasticity over the BLA; rather, LTD, which encodes memory of safety in the BLA, is favoured. Following stressful experiences, LTP in the BLA is promoted to encode memory of fear.

Amygdala↗
PubMed2000

Changes in functional connectivity in orbitofrontal cortex and basolateral amygdala during learning and reversal training.

Interconnections between orbitofrontal cortex (OFC) and basolateral amygdala (ABL) are critical for encoding and using associative information about the motivational significance of stimuli. Previously, we reported that neurons in OFC and ABL fired selectively to cues during odor discrimination learning and reversal training. Here we conducted an analysis of correlated firing in the cell pairs recorded in the previous study. Correlated firing during the intertrial intervals was compared across task phases during different phases of acquisition and reversal learning. Changes in correlated activity during initial learning and subsequent accurate performance on the discrimination problems closely resembled the changes in odor selectivity in OFC and ABL reported earlier. Increased correlated firing was most pronounced in OFC during accurate go, no-go performance in the postcriterion phase of performance, whereas correlated firing in ABL increased primarily during an earlier phase of learning. In contrast, findings during subsequent reversal training diverged from our earlier report in which odor selectivity diminished in OFC and reversed in ABL. When the reinforcement contingencies of the odors were reversed after the rat had learned the original associations, correlated firing further increased significantly in OFC but remained stable in ABL. This evidence that associative encoding increments with reversal learning in OFC suggests that the original associations, although not expressed as stimulus driven activity, may be maintained within the network as new associations are acquired.

Amygdala↗
PubMed2001

Long-term depression in the basolateral amygdala of the mouse involves the activation of interneurons.

Long-term depression (LTD) in the basolateral amygdala, following low frequency stimulation (1 Hz/900 pulses) of the lateral amygdala, was studied in an in vitro slice preparation of 2-3 weeks and 2-4 months old mice. Whole-cell patch-clamp recordings of neurons, visualized by means of infrared videomicroscopy, and extracellular field potential recordings were performed. Loading single neurons with the calcium chelator BAPTA (30 mM) did not reduce the excitatory postsynaptic currents following low frequency stimulation. However, buffering presynaptic calcium with BAPTA-AM, and application of the specific Ca2+/calmodulin-stimulated protein kinase II antagonist KN-62 (1-[N,O-bis(5-isoquinoline sulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperizine), blocked low frequency stimulation-induced LTD. The induction of LTD was reduced by the competitive N-methyl-D-aspartate receptor antagonist D-(-)-2-amino-5-phosphonopentanoic acid (50 microM), and blocked by the metabotropic glutamate receptor antagonist (-)-amino-4-carboxy-methyl-phenylacetic acid (1 mM), and by 5-hydroxytryptamine (5-HT; 30 microM) via the activation of 5-HT(1A) receptors. Also blocking GABA(A) receptor-mediated synaptic transmission with bicuculline (10 microM) or picrotoxin (20 microM) reduced the induction of LTD. Visually and electrophysiologically identified interneurons in slices from 2 weeks old mice, expressed in contrast to adult mice (2-4 months), pronounced LTD. Principal neurons showed only weak LTD after low frequency stimulation.A synopsis of these findings suggests a pivotal role of GABAergic interneurons and serotonergic afferents in the induction of LTD in the basolateral nucleus of the amygdala.

Aging↗
PubMed1996

Glutamate and aspartate immunoreactive neurons of the rat basolateral amygdala: colocalization of excitatory amino acids and projections to the limbic circuit.

The basolateral amygdala has projections to several structures that take part in the limbic cortico-striato-pallido-thalamic circuit, including the prefrontal cortex, ventral striatum, and mediodorsal thalamic nucleus. The present investigation used a technique that combines retrograde tract tracing with immunohistochemistry for glutamate and aspartate to determine if amygdaloid neurons projecting to different targets in the limbic circuit can be distinguished on the basis of their content of excitatory amino acids. Cell counts revealed that at least 85-95% of the neurons in the basolateral nucleus projecting to the prefrontal cortex or ventral striatum were pyramidal cells that exhibited glutamate or aspartate immunoreactivity. Colocalization studies indicated that 94-100% of aspartate-immunoreactive neurons in the basolateral nucleus were also glutamate positive and that 92-94% of glutamate-immunoreactive neurons were also aspartate positive. A small number of glutamate-positive pyramidal neurons in the anterior subdivision of the cortical nucleus were found to project to the mediodorsal thalamic nucleus. However, the great majority of amygdaloid neurons with projections to the mediodorsal nucleus did not exhibit glutamate or aspartate immunoreactivity. The absence of glutamate and aspartate immunoreactivity in these cells suggests that these neurons do not use excitatory amino acids as neurotransmitters. The finding of high levels of glutamate and aspartate in basolateral amygdaloid neurons projecting to the prefrontal cortex and ventral striatum is consistent with previous reports indicating that these neurons may use excitatory amino acids as neurotransmitters, but is not a definitive criterion for this determination.

Amygdala↗
PubMed2004

Parvalbumin-containing interneurons in the basolateral amygdala express high levels of the alpha1 subunit of the GABAA receptor.

The basolateral amygdala (ABL) is essential for the amnestic effects of benzodiazepines in aversive learning tasks. Because the alpha1 subunit of the gamma-aminobutyric acid (GABA)(A) receptor is critical for these amnestic actions, knowledge of the neuronal localization of this subunit in the ABL should contribute to an understanding of the candidate neuronal mechanisms involved. To examine this question, we used dual-labeling immunohistochemical techniques to study the localization of the alpha1 subunit in the ABL. Our results suggest that the alpha1 subunit of the GABA(A) receptor is localized primarily in GABAergic interneurons in the ABL at the somal level, although the intense neuropil staining in the lateral nucleus suggests that distal dendrites of pyramidal projection neurons in this nucleus may also contain high levels of the alpha1 subunit. The great majority of alpha1-immunoreactive interneurons also exhibit immunoreactivity for the beta2/3 subunits of the GABA(A) receptor. Parvalbumin-positive (PV+) interneurons are the main interneuronal subpopulation exhibiting alpha1 immunoreactivity, but some calretinin-positive interneurons also express this subunit. These data suggest that certain subpopulations of GABAergic interneurons in the ABL, especially PV+ cells, receive a robust GABAergic innervation. Because the most likely source of this innervation is intrinsic, these results suggest that PV+ interneurons could constitute an important component of interneuronal networks in the ABL. These networks may be critical for the generation of synchronized rhythmic oscillations involved in consolidation of emotional memories. The activation of alpha1-containing GABA(A) receptors in the ABL by benzodiazepines may disrupt rhythmic oscillations critical for memory consolidation.

Amygdala↗
PubMed2005

Role of the cholinergic system in the rat basolateral amygdala on morphine-induced conditioned place preference.

The effects of intra-basolateral amygdala (intra-BLA) injections of physostigmine, atropine, nicotine and/or mecamylamine on morphine-induced conditioned place preference (CPP) in rats was investigated by using an unbiased 3-day schedule of place conditioning design. Animals that received 3 daily injections of morphine (0.5-10 mg/kg) subcutaneously (s.c.) or saline (1.0 ml/kg, s.c.) showed a significant preference for compartment paired with morphine. The maximum response was observed with 7.5 mg/kg of the opioid. Administration of the anticholinesterase drug, physostigmine (1, 3 and 5 microg/rat) with an ineffective dose of morphine (0.5 mg/kg) elicited a significant CPP. Injections of antimuscarinic receptor agent, atropine (1, 4 and 7 microg/rat) dose-dependently inhibited the morphine (7.5 mg/kg)-induced place preference. The injections of nicotine (0.75, 1 and 2 microg/rat) potentiated the morphine (0.5 mg/kg)-induced place preference, while the nicotinic receptor antagonist, mecamylamine (1, 3 and 6 microg/rat) dose-dependently inhibited the morphine (7.5 mg/kg)-induced place preference. Furthermore, administration of atropine (7 microg/rat) but not mecamylamine (6 microg/rat) reduced the response induced by different doses of physostigmine plus morphine. Moreover, mecamylamine (6 microg/rat) but not atropine (7 microg/rat) reduced the response induced by different doses of nicotine plus morphine. It is concluded that the muscarinic and nicotinic receptor mechanisms in the BLA may be involved in the acquisition of morphine-induced place preference.

Amygdala↗
PubMed1999

Bombesin microinjection into the basolateral amygdala influences feeding behavior in the rat.

It has been demonstrated that the basolateral amygdala (ABL) represents a satiety mechanism. Experimental data indicate that peripheral or central applications of neuropeptide bombesin (BN) and BN-like peptides inhibit feeding. Since the amygdala (AMY) is rich in BN-like immunoreactive elements, the present study was performed to determine whether 10 or 40 ng doses of BN microinjected bilaterally into the ABL could modify solid food intake. Twenty nanograms of BN (10 ng per injection site) in 24-h deprived rats caused transient inhibition of food intake and 80 ng resulted in a significant reduction of food consumption for 1 h. This inhibitory effect of BN on feeding was eliminated by prior BN antagonist treatment. Results of behavioral tests showed that BN microinjections into the ABL specifically reduced food intake without altering behavioral patterns or influencing the body temperature. Present results suggest that BN-like peptides may act as a complex satiety signal in the ABL.

Amygdala↗
PubMed1992

Kindling-induced long-lasting changes in synaptic transmission in the basolateral amygdala.

1. Intracellular current-clamp recordings were obtained from neurons of the basolateral amygdala (BLA) in an in vitro slice preparation from control and kindled animals. Postsynaptic potentials, elicited by stimulation of the stria terminalis (ST) or lateral amygdaloid nucleus (LA), were used to investigate the role of excitatory and inhibitory amino acid transmission in kindling-induced epileptiform activity. The contributions of glutamatergic and GABAergic receptor subtypes were analyzed by use of the non-N-methyl-D-aspartate (non-NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the NMDA antagonist DL-2-amino-5-phosphonovaleric acid (APV), and the GABAA antagonist bicuculline methiodide (BMI). 2. The synaptic waveform evoked in control neurons consisted of an excitatory postsynaptic potential (EPSP), a fast inhibitory postsynaptic potential (f-IPSP), and a slow inhibitory postsynaptic potential (s-IPSP). Stimulation of the ST or LA pathways evoked a burst-firing response in BLA neurons contralateral from the site of stimulation of kindled animals. 3. APV (50 microM) reduced, but CNQX (10 microM) completely blocked, the burst-firing response in BLA neurons from kindled animals and bicuculline-induced bursting in control neurons. 4. Kindling significantly increased the amplitude of both the slow NMDA- and the fast non-NMDA-receptor-mediated components of synaptic transmission (s- and f-EPSPs, respectively). Furthermore, the stimulus intensities required to evoke EPSPs just subthreshold for action potential generation were significantly lower in slices from kindled animals. 5. In kindled neurons no significant change was observed in the membrane input resistance and resting membrane potential or in the number of action potentials elicited in response to depolarizating current injection. 6. Kindling resulted in a pathway-specific loss of ST- and LA-evoked feedforward GABAergic synaptic transmission and of spontaneous IPSPs. In the same BLA neurons, direct GABAergic inhibition via stimulation of the LA was not affected by kindling. 7. The enhanced glutamatergic transmission was not due to disinhibition, because, in the presence of BMI (and CNQX to prevent BMI-induced bursting), the s-EPSP amplitude was still greater in kindled than in control neurons. 8. These results provide evidence that the epileptiform activity observed in BLA neurons after kindling results from an increase in excitatory NMDA- and non-NMDA-receptor-mediated glutamatergic transmission and a decrease in inhibitory gamma-aminobutyric acid (GABA)-receptor-mediated transmission; the enhanced excitatory transmission cannot be accounted for by reduced inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1999

Modulation of basolateral amygdala neuronal firing and afferent drive by dopamine receptor activation in vivo.

The basolateral amygdala (BLA) is implicated in responding to affective stimuli. Dopamine (DA) is released in the BLA during numerous conditions; however, the neurophysiological effects of DA in the BLA have not been examined in depth. In this study, the effects of DA receptor manipulation on spontaneous and afferent-driven neuronal firing were examined using in vivo extracellular single-unit recordings in parallel with systemic and iontophoretic drug application, and stimulation of the substantia nigra/ventral tegmental area in the rat. The effects of DA receptor activation in the BLA were found to depend on the characteristics of the BLA neuron examined, causing an increase in the firing rate of putative interneurons and a decrease in the firing of identified projection neurons. Additionally, DA receptor activation attenuated short-latency spikes evoked by electrical stimulation of prefrontal cortical and mediodorsal thalamic inputs to the BLA while potentiating the responses evoked by electrical stimulation of sensory association cortex. DA receptor activation can thus attenuate BLA projection neuron firing via two mechanisms: (1) by a direct inhibition, and (2) by indirect actions mediated via activation of BLA interneurons. This is hypothesized to lead to a global filtration of weaker inputs. Moreover, DA potentiates sensory inputs and attenuates medial prefrontal cortex inputs to the BLA. Conditions in which DA is released in the BLA, such as during the presentation of an affective stimulus, will lead to a potentiation of the strongest sensory input and a dampening of cortical inhibition over the BLA, thus augmenting the response to affective sensory stimuli.

Afferent Pathways↗
PubMed1993

Absence of amnestic effect of an anxiolytic 5-HT3 antagonist (BRL 46470A) injected into basolateral amygdala, as opposed to diazepam.

This experiment compares the effects of microinjections into the basolateral amygdala nucleus of diazepam (DZP) and a new 5-HT3 receptor antagonist, BRL 46470A, on acquisition and retention of an inhibitory avoidance tasks by rats. The animals were microinjected with DZP or BRL 46470A between 10 and 15 min before the learning trial. Retention testing 48 h later showed impaired retention in animals injected with DZP but not with BRL 46470A. These results show that BRL 46470A, a compound suggested to have anxiolytic effects does not induce amnesia. This evidence for a possible dissociation between anxiety-reducing and memory-disrupting effects of a drug has implications, for one, for the understanding of the neuronal substrates mediating these effects, and secondly, for the search for anxiolytic agents devoid of undesirable side effects on memory processes.

Amnesia↗
PubMed2006

Glucocorticoid receptors and beta-adrenoceptors in basolateral amygdala modulate synaptic plasticity in hippocampal dentate gyrus, but not in area CA1.

The basolateral amygdala (BLA) is a key structure in a memory-modulatory system that regulates stress and stress hormones (glucocorticoid and noradrenaline) effects on hippocampal functioning. We have shown previously that priming the amygdala differentially affects plasticity in the hippocampal dentate gyrus (DG) and CA1, and mimicked acute stress effect on plasticity in these two subregions. In the present study, we investigated the mechanisms that mobilize the BLA to differentially alter plasticity in DG and CA1. Glucocorticoid receptors antagonist RU 38486 or beta-adrenoceptor antagonist propranolol were microinfused in the BLA, 10 min prior to BLA activation-induced modulation of long-term potentiation (LTP) in DG and CA1. The results showed that neither glucocorticoid nor noradrenergic transmissions in the BLA are necessary for LTP induction and for the impairing effect of amygdala activation on CA1 LTP. In contrast, blockade of glucocorticoid or noradrenergic transmission in BLA, increased baseline synaptic transmission in the DG, but suppressed the enhancing effect of BLA activation on DG LTP. These findings provide further evidence for a differential amygdala control of hippocampal subregions as well as for differential memory processes involving CA1 and DG. They also provide insight into how stress hormones exert their actions on the circuits involved in these processes.

Adrenergic beta-Antagonists↗
PubMed2005

Histaminergic modulation of excitatory synaptic transmission in the rat basolateral amygdala.

The effects of histamine on excitatory synaptic transmission between the external capsule and basolateral amygdala (BLA) were examined using intracellular and field potential recordings in rat amygdala slices. Bath application of histamine (20 microM) suppressed intracellular excitatory postsynaptic potentials (EPSPs; 70.3+/-5.1% of control amplitude) in 43 of 64 BLA neurons, and potentiated EPSPs (341+/-81% of control amplitude) in 21 neurons, without changing resting membrane potential or input resistance. The histamine-induced suppression of EPSPs was accompanied by an increase in paired-pulse facilitation of the slopes of EPSPs, suggesting a presynaptic locus of the action. The suppressive effect could be blocked by the selective H3 antagonist thioperamide, and mimicked by the selective H3 agonist R-alpha-methylhistamine, indicating that the suppressive effect is mediated by the presynaptic H3 receptor. The potentiating effect of histamine on EPSPs was not accompanied by the change of paired-pulse facilitation and was not affected by the presence of H1, H2 or H3 receptor antagonists. In addition, the effective concentration of agonist to produce 50% of maximal response (EC50) of the potentiating action of histamine is 49 nM, much lower than the EC50 (470 nM) of the H3 receptor-mediated suppressive effect characterized here. These observations suggest a novel, high affinity and postsynaptically mediated effect of histamine. In extracellular recordings, histamine, at low concentration (200 nM), consistently potentiated field potentials. At high concentration (20 microM), histamine suppressed field potentials, but potentiated field potentials when H3 receptors were blocked. Taken together, these results revealed that histamine, via the presynaptic H3 receptor and a currently unknown mechanism, decreases or increases excitatory synaptic transmission in the BLA respectively. This specific histaminergic modulation of neuronal activity in the amygdala may play an important role in amygdala-mediated physiological and pathophysiological processes, such as fear, emotional learning and memory, temporal lobe epilepsy, and affective disorders.

2-Amino-5-phosphonovalerate↗
PubMed2006

Enhancement of extinction memory consolidation: the role of the noradrenergic and GABAergic systems within the basolateral amygdala.

Evidence from previous studies indicates that the noradrenergic and GABAergic influences within the basolateral amygdala (BLA) modulate the consolidation of memory for fear conditioning. The present experiments investigated whether the same modulatory influences are involved in regulating the extinction of fear-based learning. To investigate this issue, male Sprague Dawley rats implanted with unilateral or bilateral cannula aimed at the BLA were trained on a contextual fear conditioning (CFC) task and 24 and 48 h later were given extinction training. Immediately following each extinction session they received intra-BLA infusions of the GABAergic antagonist bicuculline (50 ng), the beta-adrenocepter antagonist propranolol (500 ng), bicuculline with propranolol, norepinephrine (NE) (0.3, 1.0, and 3.0 microg), the GABAergic agonist muscimol (125 ng), NE with muscimol or a control solution. To investigate the involvement of the dorsal hippocampus (DH) as a possible target of BLA activation during extinction, other animals were given infusions of muscimol (500 ng) via an ipsilateral cannula implanted in the DH. Bilateral BLA infusions of bicuculline significantly enhanced extinction, as did infusions into the right, but not left BLA. Propranolol infused into the right BLA together with bicuculline blocked the bicuculline-induced memory enhancement. Norepinephrine infused into the right BLA also enhanced extinction, and this effect was not blocked by co-infusions of muscimol. Additionally, muscimol infused into the DH did not attenuate the memory enhancing effects of norepinephrine infused into the BLA. These findings provide evidence that, as with original CFC learning, noradrenergic activation within the BLA modulates the consolidation of CFC extinction. The findings also suggest that the BLA influence on extinction is not mediated by an interaction with the dorsal hippocampus.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

High potency of the orally-active NMDA-receptor antagonist CGP 40 116 in inhibiting excitatory postsynaptic potentials of rat basolateral amygdala neurones in vitro.

Conventional intracellular recordings were used to monitor postsynaptic potentials of basolateral amygdala neurones (BLA) in brain slices comprising the BLA, the entorhinal cortex (EC) and the hippocampus, in which the EC-BLA connections were preserved. Stimulation of the BLA with a bipolar electrode elicited complex postsynaptic potentials consisting of alpha-amino-3-hydroxy-5-methyl-isoxazoleproprionic acid (AMPA) receptor-mediated fast excitatory postsynaptic potentials (fast EPSPs), gamma-amino-butyric acid [GABA(A)] receptor-mediated fast inhibitory postsynaptic potentials (fast IPSPs) and GABAB receptor-mediated slow IPSPs. Bath application of 10 microM of the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and of 10 microM of the GABA(A) receptor antagonist bicuculline methiodide (BMI) revealed a N-methyl-D-aspartate (NMDA) receptor-mediated slow EPSPs, which was occasionally followed by a GABAB receptor-mediated slow IPSPs. Under these conditions, the log concentration-response curve for D-(E)-2-amino-4-methyl-5-phosphono-3-pentanoic acid (CGP 40 116), a newly developed drug with proposed NMDA-receptor antagonist properties, was compared to that obtained with the 'classic' antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP5) in inhibiting the NMDA-mediated postsynaptic potentials. CGP 40 116 (IC50: 130 nM) was over 30 times more potent than D-AP5 (IC50: 4100 nM) in reducing NMDA-mediated slow EPSP. In conclusion, the present study indicates that CGP 40 116, a new orally-active NMDA antagonist, shows a very high potency on NMDA receptors in the amygdala and may therefore be a valuable tool for studying the behavioural effect of NMDA-receptor mediated transmission in this structure.

2-Amino-5-phosphonovalerate↗
PubMed2002

17beta-Estradiol reduces excitatory postsynaptic potential (EPSP) amplitude in rat basolateral amygdala neurons.

We examined the actions of estrogen on excitatory synaptic transmission in the basolateral amygdala (BLA), a brain region involved in learning, emotions, and the effects of stress. Intracellular recordings of monosynaptic excitatory postsynaptic potentials (EPSPs) were obtained from BLA neurons in a slice preparation. Bath application of 17beta-estradiol (2 micro M) reduced EPSP amplitude by an average of 77%. This reduction was readily reversed by washing with control saline and was not mimicked by the inactive isomer 17 alpha-estradiol. Other passive and active properties of BLA neurons were unaffected by 17beta-estradiol. The observed EPSP reduction is in sharp contrast to the potentiation of EPSPs by estrogen observed in other brain regions.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1999

Priming stimulation in the basolateral amygdala modulates synaptic plasticity in the rat dentate gyrus.

We investigated the effects of basolateral amygdala (BLA) priming on long-term potentiation (LTP) in the dentate gyrus (DG). In the control animals, the induction of high-frequency stimulation (HFS) to the perforant path (PP) resulted in hippocampal LTP at all the time intervals tested. A priming stimulation to the BLA prior to the application of HFS to the PP resulted in the enhancement of the excitatory post-synaptic potential (EPSP)-LTP and population spike (PS)-LTP in the DG from 90-min post-HFS onwards. These findings suggest that the amygdala has a potential role in the modulation of some aspects of memory that are mediated by the hippocampus.

Action Potentials↗
PubMed2004

Role of the basolateral amygdala in the storage of fear memories across the adult lifetime of rats.

The basolateral amygdala (BLA) is intimately involved in the development of conditional fear. Converging lines of evidence support a role for this region in the storage of fear memory but do not rule out a time-limited role in the memory consolidation. To examine this issue, we assessed the stability of BLA contribution to fear memories acquired across the adult lifetime of rats. Fear conditioning consisted of 10 tone-shock pairings in one context (remote memory), followed 16 months later by 10 additional tone-shock pairings with a novel tone in a novel context (recent memory). Twenty-four hours after recent training, rats were given NMDA or sham lesions of the BLA. Contextual and tone freezing were independently assessed in individual test sessions. Sham-lesioned rats showed high and comparable levels of freezing across all context and tone tests. In contrast, BLA-lesioned rats displayed robust freezing deficits across both recent and remote tests. Subsequent open-field testing revealed no effects of BLA lesions on activity patterns in a dark open field or during bright light exposure. Lesioned rats were able to reacquire normal levels of context-specific freezing after an overtraining procedure (76 unsignaled shocks). Together, these findings indicate that BLA lesions do not disrupt freezing behavior by producing hyperactivity, an inability to suppress behavior, or an inability to freeze. Rather, the consistent pattern of freezing deficits at both training-to-lesion intervals supports a role for the BLA in the permanent storage of fear memory.

Acoustic Stimulation↗