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At least 163 records · Page 9Linked to original sources
PubMed1999

Basolateral amygdala is involved in modulating consolidation of memory for classical fear conditioning.

Previous findings indicate that the basolateral amygdala complex of nuclei (BLC) is involved in modulating (i.e., enhancing or impairing) memory consolidation for aversive training such as inhibitory avoidance. The present study examined whether the BLC also modulates the consolidation of memory for classical fear conditioning in which a specific context is paired with footshock. Adult male rats with bilateral cannulae targeting the BLC were allowed, first, to habituate in a Y maze that had differently shaped and textured arms. On the next day the rats were placed in one maze arm (shock arm), and they received four unsignaled footshocks. In Experiment 1, immediately after the training some rats received BLC inactivation with lidocaine (10 microgram/0.2 microliter per side), and control rats received buffered saline. In Experiment 2, rats received immediate post-training intra-BLC infusions of the muscarinic receptor agonist oxotremorine (10 ng/0.2 microliter per side) or saline. On a 24 hr retention test each rat was placed in a "safe" arm of the maze and allowed to access all maze arms. Lidocaine-treated rats had impaired memory for the classical fear conditioning when they were compared with the saline-treated controls: they spent less time freezing, entered the shock arm more readily and more often, and spent more time in it. In contrast, oxotremorine-treated rats had a stronger memory for the context-footshock association as assessed by all measures of memory. Thus, post-training treatments affecting BLC function modulate memory for Pavlovian contextual fear conditioning in a manner similar to that found with other types of training.

Amygdala↗
PubMed2004

Basolateral amygdala dopamine receptor antagonism modulates initial reactivity to but not habituation of the acoustic startle response.

Although the basolateral amygdala (BLA) plays a role in the habituation to sensory stimuli, the receptor mechanisms mediating this process remain unclear. In the present study, we investigated the role of BLA dopamine (DA) in the habituation of the acoustic startle response (ASR) with intra-BLA infusions of DA receptor antagonists. Male Long Evans rats were subjected to startle pulses over two consecutive once-daily sessions. Prior to testing on Day 1, separate groups of animals received bilateral intra-BLA infusions of a D1 (SCH 23390: 0, 3.2, 6.4 microg per side) or a D2/D3 (raclopride: 0, 2.5, 5.0 microg per side) receptor antagonist. Animals were retested 24h later (Day 2) without prior drug infusion in order to assess possible treatment effects on within- and between-session habituation of the ASR. As expected, within- and between-session habituation was observed in vehicle-treated controls. Within-session habituation was also seen in SCH 23390- and raclopride-treated animals both on Day 1 as well as 24h later (Day 2). Evidence of between-session habituation was observed in SCH 23390-treated animals. However, compared to vehicle, intra-BLA SCH 23390 or raclopride attenuated the initial startle response on Day 1, but not Day 2. No evidence of between-session habituation was found in raclopride-treated animals, although this probably reflected the attenuated initial response to the startling stimulus on Day 1 rather than a reduced rate of habituation on Day 2. The present study suggests that while BLA DA is not involved in habituation of the ASR, it may mediate the perceived aversive nature of the initially startling stimuli.

Acoustic Stimulation↗
PubMed1984

Phasic activity of the basolateral amygdala, cingulate gyrus, and hippocampus during REM sleep in the cat.

We analyzed the electrical activity of the basolateral amygdala (BLA), anterior and posterior regions of the cingulate gyrus (A-CG and P-CG), the dorsal hippocampus (DH), the anterior ventral thalamic nucleus (AVTN), and the sensory motor cortex during the rapid eye movements and ponto-geniculo-occipital (PGO) activity of REM sleep in cats in chronic preparation. Polygraphic recordings and computational perievent averages using the phasic contractions of the lateral rectus muscle (LR) of the eyeball as the triggering signal of the analysis were performed. We observed biphasic potentials (200-300 ms) of variable amplitude, related to the phasic phenomena of REM sleep, in the BLA, A-CG, P-CG, DH, and AVTN. The latencies of the potentials of these regions were always greater than those of the geniculate PGO activities. We propose that the recorded limbic potentials resulted from propagation of PGO activity and that this phenomenon may reflect the limbic structure of the hallucinatory, vegetative, and emotional components of REM sleep.

Amygdala↗
PubMedDate not supplied

Basolateral amygdala lesions do not prevent memory of context-footshock training.

The present studies examined the effects of basolateral amygdala (BLA) lesions induced prior to or after context-footshock training on 48-h memory, using several retention measures. In experiment 1, male Sprague-Dawley rats with bilateral BLA lesions (NMDA, 12.5 mg/mL, 0.2 microL) were given footshock training in one compartment of a two-compartment alley. Rats were habituated to the alley and 24 h later were given two footshocks in the shock compartment. Retention was tested 48 h later, using latency to enter the shock compartment and time spent freezing as measures of memory. Two days later, they were tested again and received a footshock on each re-entry of the shock compartment prior to remaining in the safe compartment for 200 consecutive seconds. The BLA lesions did not block retention as assessed by freezing or number of re-entries of the shock compartment. In experiment 2, no prior habituation was given, and only one footshock was used for the training. BLA lesions did not block retention, as indicated by latencies to enter the shock compartment on a 48-h test or by number of entries of the shock compartment. Experiment 3 examined the effects of the GABAA agonist muscimol infused into the BLA prior to the 48-h retention test. The muscimol infusions decreased retention test entrance latencies but did not block retention as assessed by the number of subsequent entries of the shock compartment. These findings provide additional evidence that an intact BLA is not required for the acquisition or retention of context-footshock training.

Amygdala↗
PubMed2004

Role of basolateral amygdala dopamine in modulating prepulse inhibition and latent inhibition in the rat.

RATIONALE: The dopamine (DA) projection to the basolateral amygdala (BLA) modulates nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) DA transmission. Given the involvement of the BLA, and of NAc and mPFC DA, in select forms of information processing, we sought to determine the role of BLA DA in modulating prepulse inhibition (PPI) and latent inhibition (LI). OBJECTIVE: The effects of BLA D1 (SCH 23390) and D2/D3 (raclopride) receptor blockade on PPI and LI were examined. METHODS: Separate groups of male Long-Evans rats received bilateral intra-BLA infusions of SCH 23390 (3.2 or 6.4 microg/0.5 microl per side), raclopride (2.5 or 5.0 microg/0.5 microl per side) or saline prior to testing. In two experiments, the effects of BLA DA receptor antagonism on PPI of the acoustic startle response (ASR) and LI of conditioned taste aversion were determined. A control group received bilateral intra-striatal infusions of SCH 23390 or raclopride prior to PPI testing. RESULTS: Intra-BLA SCH 23390 or raclopride had no effect on the ASR. Intra-BLA SCH 23390 enhanced and raclopride disrupted PPI, both in a dose-related manner. Intra-striatal SCH 23390 or raclopride had no effect on PPI or ASR magnitude. Finally, BLA DA receptor blockade had no effect on LI. CONCLUSIONS: These results indicate that PPI is modulated by BLA DA and suggest that this modulation occurs independently of changes in NAc and/or mPFC DA transmission. They also suggest that BLA DA is not involved in modulating LI and add to evidence indicating that PPI and LI are mediated by different neural substrates.

Amygdala↗
PubMed2001

Histamine H3 receptor-mediated impairment of contextual fear conditioning and in-vivo inhibition of cholinergic transmission in the rat basolateral amygdala.

We investigated the effects of agents acting at histamine receptors on both, spontaneous release of ACh from the basolateral amygdala (BLA) of freely moving rats, and fear conditioning. Extensive evidence suggests that the effects of histamine on cognition might be explained by the modulation of cholinergic systems. Using the microdialysis technique in freely moving rats, we demonstrated that perfusion of the BLA with histaminergic compounds modulates the spontaneous release of ACh. The addition of 100 mm KCl to the perfusion medium strongly stimulated ACh release, whereas, 0.5 microm tetrodotoxin (TTX) inhibited spontaneous ACh release by more than 50%. Histaminergic H3 antagonists (ciproxifan, clobenpropit and thioperamide), directly administered to the BLA, decreased ACh spontaneous release, an effect fully antagonized by the simultaneous perfusion of the BLA with cimetidine, an H2 antagonist. Local administration of cimetidine alone increased ACh spontaneous release slightly, but significantly. Conversely, the administration of H1 antagonists failed to alter ACh spontaneous release. Rats receiving intra-BLA, bilateral injections of the H3 antagonists at doses similar to those inhibiting ACh spontaneous release, immediately after contextual fear conditioning, showed memory consolidation impairment of contextual fear conditioning. Post-training, bilateral injections of 50 microg scopolamine also had an adverse effect on memory retention. These observations provide the first evidence that histamine receptors are involved in the modulation of cholinergic tone in the amygdala and in the consolidation of fear conditioning.

Acetylcholine↗
PubMedDate not supplied

Modulation of memory consolidation by the basolateral amygdala or nucleus accumbens shell requires concurrent dopamine receptor activation in both brain regions.

Previous findings indicate that the basolateral amygdala (BLA) and the nucleus accumbens (NAc) interact in influencing memory consolidation. The current study investigated whether this interaction requires concurrent dopamine (DA) receptor activation in both brain regions. Unilateral, right-side cannulae were implanted into the BLA and the ipsilateral NAc shell or core in male Sprague-Dawley rats ( approximately 300 g). One week later, the rats were trained on an inhibitory avoidance (IA) task and, 48 h later, they were tested for retention. Drugs were infused into the BLA and NAc shell or core immediately after training. Post-training intra-BLA infusions of DA enhanced retention, as assessed by latencies to enter the shock compartment on the retention test. Infusions of the general DA receptor antagonist cis-Flupenthixol (Flu) into the NAc shell (but not the core) blocked the memory enhancement induced by the BLA infusions of DA. In the reverse experiment, post-training intra-NAc shell infusions of DA enhanced retention and Flu infusions into the BLA blocked the enhancement. These findings indicate that BLA modulation of memory consolidation requires concurrent DA receptor activation in the NAc shell but not the core. Similarly, NAc shell modulation of memory consolidation requires concurrent DA receptor activation in the BLA. Together with previous findings, these results suggest that the dopaminergic innervation of the BLA and NAc shell is critically involved in the modulation of memory consolidation.

Amygdala↗
PubMed2003

Basolateral amygdala neurons encode cocaine self-administration and cocaine-associated cues.

Electrophysiological recording procedures were used to examine basolateral amygdala (BLA) cell firing during cocaine self-administration and relative to response-independent presentations of cocaine-associated stimuli. Of 72 neurons (n = 10 rats), 31 cells (43%) were classified as phasically active, exhibiting one of three types of patterned discharges relative to the drug-reinforced response, similar to that previously described for nucleus accumbens (Acb) neurons (Carelli, 2002). Briefly, neurons exhibited increased firing rates within seconds preceding the response [termed preresponse (PR)], increased activity within seconds after the response [termed reinforcement excitation (RFe)] or an inhibition in cell firing before and/or after the response for intravenous cocaine [termed reinforcement inhibition (RFi)]. To examine the responsiveness of these same neurons to cocaine-associated stimuli, the stimulus "probe" procedure was used. Specifically, probe trials (18-20) were presented in which the audiovisual (tone-house light) stimulus associated with intravenous cocaine delivery during self-administration was randomly presented by the computer, interspersed between reinforced lever press responses. Neurons classified as type PR or type RFi were not activated by the stimulus. In contrast, neurons that exhibited increased firing immediately after the response (type RFe neurons) were significantly activated by the audiovisual cue. These findings are discussed with respect to the role of the BLA in cocaine addiction as well as previous studies characterizing Acb cell firing during cocaine self-administration.

Acoustic Stimulation↗
PubMed1998

Overtraining does not mitigate contextual fear conditioning deficits produced by neurotoxic lesions of the basolateral amygdala.

The influence of overtraining on the magnitude of fear-conditioning deficits produced by neurotoxic lesions of the basolateral amygdala (BLA) was examined. Either 1 d before or 1 week after the administration of neurotoxic BLA lesions, rats received either 1 or 25 conditioning trials consisting of the delivery of unsignaled foot shock in a novel observation chamber; freezing served as the measure of conditional fear. In this conditioning paradigm, asymptotic performance is reached in five conditioning trials, and 25 conditioning trials constitutes an overtraining procedure. The results revealed that overtraining does not affect the magnitude of the contextual freezing deficits produced by post-training BLA lesions. Similarly, overtraining did not influence the level of reacquisition obtained by rats with post-training BLA lesions after 10 reacquisition trials. A similar pattern of results was observed in rats with pretraining BLA lesions. Neurotoxic BLA lesions did not alter either motor activity or shock reactivity. These results indicate that overtraining does not limit the important role of the BLA in the acquisition and expression of contextual fear conditioning.

Amygdala↗
PubMed1995

Comparative ultrastructural localization of the NMDAR1 glutamate receptor in the rat basolateral amygdala and bed nucleus of the stria terminalis.

The N-methyl-D-aspartate (NMDA)-type glutamate receptor in the basolateral amygdala (BLA) has been implicated in activity-dependent plasticity important for cortically evoked acquisition of fear-potentiated startle response. We examined the ultrastructural immunoperoxidase labeling of the R1 subunit of the NMDA receptor in the BLA of adult rats to determine the potential cellular and subcellular sites mediating the effects generated by NMDA activation. The localization was compared with that seen in the bed nucleus of the stria terminalis (BNST), the major efferent pathway from the central nucleus of the amygdala, which has a more pronounced involvement in autonomic function. Electron microscopy established that in the BLA, 68.4% (n = 177) of the profiles showing NMDAR1-like immunoreactivity (NMDAR1-LI) were dendrites, and 19.8% were distal tips of astrocytic processes. In contrast, profiles containing NMDAR1-LI (n = 262) in the BNST were more equally distributed between dendrites (37.4%) and axons (38.2%). The subcellular localization of NMDAR1 immunoreactivity was, however, similar in both regions. Our findings provide the first ultrastructural evidence that glutamate may prominently act through NMDAR1 receptors to elicit postsynaptic actions on intrinsic neurons in the BLA and BNST. The results also indicate that, in the BLA, the NMDAR1 receptor plays an important role in astrocytic function, whereas the receptor is more preferentially a presynaptic modulator in axons which terminate in or pass through the BNST.

Amygdala↗
PubMed1992

In vivo kindling does not alter afterhyperpolarizations (AHPs) following action potential firing in vitro in basolateral amygdala neurons.

Kindling in vivo results in enhanced glutamatergic synaptic transmission and epileptiform bursting in vitro in neurons of the basolateral amygdala (BLA). We tested the hypothesis that reduction of intrinsic inhibitory mechanisms, such as the slow- and medium-afterhyperpolarizations (s-AHPs, m-AHPs), contributes to the enhanced neuronal excitability observed in kindling-induced epileptogenesis using intracellular recording methodology. In these studies, neurons were recorded from the BLA contralateral to the kindling site. AHPs following depolarizing current-induced (100 ms, 1 nA) action potentials were recorded from BLA neurons of control and kindled animals. We found no difference in the amplitude of the s-AHP and m-AHP, or the duration of the s-AHP between control and kindled neurons. In addition, kindling did not alter the distribution of accommodating/non-accommodating BLA neurons (as assessed from neuronal responses during long (500 ms) depolarizing current injection). It is concluded that an alteration in the neuronal network within the BLA rather than a blockade of an intrinsic inhibitory mechanism underlies the enhanced excitability recorded in BLA neurons following kindling.

Action Potentials↗
PubMed2005

NMDA receptor antagonists antagonize the facilitatory effects of post-training intra-basolateral amygdala NMDA and physostigmine on passive avoidance learning.

In the present study, the effects of post-training intra-basolateral amygdala (BLA) injection of an N-methyl-d-aspartate (NMDA) receptor agonist and competitive or noncompetitive antagonists, on memory retention of passive avoidance learning was measured in the presence and absence of physostigmine in rats. Intra-BLA administration of lower doses of NMDA (10(-5) and 10(-4) microg/rat) did not affect memory retention, although higher doses of the drug (10(-3), 10(-2) and 10(-1) microg/rat) increased memory retention. The greatest response was obtained with 10(-1) microg/rat of the drug. The different doses of the competitive NMDA receptor antagonist DL-AP5 (1, 3.2 and 10 microg/rat) and noncompetitive NMDA receptor antagonist MK-801 (0.5, 1 and 2 microg/rat) decreased memory retention in rats dose dependently. Both competitive and noncompetitive NMDA receptor antagonists reduced the effect of NMDA (10(-2) microg/rat). In another series of experiments, intra-BLA injection of physostigmine (2, 3 and 4 microg/rat) improved memory retention. Post-training co-administration of lower doses of NMDA (10(-5) and 10(-4) microg/rat) and physostigmine (1 microg/rat), doses which were ineffective when given alone, significantly improved the retention latency. The competitive and noncompetitive NMDA receptor antagonists, DL-AP5 and MK-801, decreased the effect of physostigmine (2 microg/rat). Atropine decreased memory retention by itself and potentiated the response to DL-AP5 and MK-801. It may be concluded that amygdalar NMDA receptor mechanisms interact with cholinergic systems in the modulation of memory.

Amygdala↗
PubMedDate not supplied

Lasting increases in basolateral amygdala activity after emotional arousal: implications for facilitated consolidation of emotional memories.

Manipulations that reduce or enhance the activity of basolateral amygdala (BLA) neurons in the minutes to hours after training have been shown to respectively impair or facilitate retention on the inhibitory avoidance task. Although this suggests that BLA activity is altered after emotional arousal, such changes have not been directly demonstrated. To test this, we devised a feline analog of the inhibitory avoidance task and recorded BLA unit activity before and after a single inescapable footshock. Single-unit recordings revealed that the firing rate of many BLA neurons gradually increased after the footshock, peaking 30-50 min post-shock and then subsiding to baseline levels 2 h later. During this period of increased activity, the discharges of simultaneously recorded BLA cells were more synchronized than before the shock. Although it was known that pairing innocuous (conditioned stimulus, CS) and noxious stimuli modifies the responsiveness of BLA neurons to the CS, our results constitute the first demonstration that emotional arousal produces lasting increases in the spontaneous firing rates of BLA neurons. We propose that these changes in BLA activity may promote Hebbian interactions between coincident but spatially distributed activity patterns in BLA targets, facilitating the consolidation of emotional memories.

Action Potentials↗
PubMed1998

Mechanisms underlying the enhancement of excitatory synaptic transmission in basolateral amygdala neurons of the kindling rat.

To elucidate the mechanism underlying epileptiform discharges in kindled rats, synaptic responses in kindled basolateral amygdala neurons in vitro were compared with those from control rats by using intracellular and whole cell patch-clamp recordings. In kindled neurons, electrical stimulation of the stria terminalis induced epileptiform discharges. The resting potential, apparent input resistance, current-voltage relationship of the membrane, and the threshold, amplitude, and duration of action potentials in kindled neurons were not different from those in control neurons. The electrical stimulation of stria terminalis elicited excitatory postsynaptic potentials (EPSPs) and DL-2-amino-5-phosphonopentanoic acid (AP5)-sensitive and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)-sensitive excitatory postsynaptic currents (EPSCs). The amplitude of evoked EPSPs and of evoked AP5-sensitive and CNQX-sensitive EPSCs were enhanced markedly, whereas fast and slow inhibitory postsynaptic potentials (IPSPs) induced by electrical stimulation of lateral amygdaloid nucleus were not significantly different. The rise time and the decay time constant of the evoked CNQX-sensitive EPSCs were shortened, whereas the rise time of the evoked AP5-sensitive EPSCs was shortened, but the decay time constants were not significantly different. In both tetrodotoxin (TTX)-containing medium and low Ca2+ and TTX-containing medium, the frequency and amplitude of spontaneous EPSCs were increased in kindled neurons. These increases are presumably due to nearly synchronous multiquantal events resulted from the increased probability of Glu release at the nerve terminals. The rise time of evoked CNQX- and AP5-sensitive EPSCs and the decay time constant of evoked CNQX-sensitive EPSCs were shortened, suggesting that excitatory synapses at the proximal dendrite and/or the soma in kindled neurons may contribute more effectively to generate evoked EPSCs than those at distal dendrites. In conclusion, the increases in the amplitudes of spontaneous and evoked EPSCs and in the frequency of spontaneous EPSCs may contribute to the epileptiform discharges in kindled neurons.

2-Amino-5-phosphonovalerate↗
PubMed2005

Retrograde endocannabinoid signaling in a postsynaptic neuron/synaptic bouton preparation from basolateral amygdala.

Retrograde synaptic signaling by endogenous cannabinoids (endocannabinoids) is a recently discovered form of neuromodulation in the brain. In the basolateral amygdala (BLA), endocannabinoid signaling has been implicated in learning and memory, specifically in extinction of aversive memories. To examine retrograde endocannabinoid signaling in this brain region, BLA neurons were freshly isolated using an enzyme-free procedure. These isolated neurons retain attached functional excitatory and inhibitory synaptic boutons. Spontaneous GABAergic IPSCs (sIPSCs) were isolated from these freshly isolated neurons and a 4 s step of depolarization from -60 to 0 mV produced suppression of sIPSC frequency and amplitude. A similar depolarization-induced suppression of inhibition (DSI) was observed in neurons in BLA slices. DSI in the single-cell preparation was abolished by the CB1 receptor antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide, and DSI duration was shortened in the presence of 2-methyl-6-(phenylethynyl) pyridine, an mGluR5 (metabotropic glutamate receptor 5) antagonist. The initial decrease in sIPSCs induced by the DSI procedure was greatly attenuated in recordings with 20 mm BAPTA containing postsynaptic internal solution, but a delayed-onset decrease was observed under this recording condition. A CB1 agonist decreased sIPSC frequency and amplitude, whereas CB1 antagonists increased these responses. The antagonist-induced increase was abolished in 20 mm BAPTA-filled cells. These data provide solid evidence for retrograde endocannabinoid signaling in the BLA and also indicate that this retrograde signaling requires only a postsynaptic neuron and attached synaptic boutons.

Amygdala↗
PubMed2001

Rats with basolateral amygdala lesions show normal increases in conditioned stimulus processing but reduced conditioned potentiation of eating.

Rats with neurotoxic lesions of basolateral amygdala (ABL) and control rats showed comparable enhancement of attentional processing of a visual stimulus when its predictive value was altered. In contrast, lesioned rats showed less potentiation of eating than did control rats when food was available during presentations of a conditioned stimulus that was previously paired with food. When considered together with previous data, these results indicate a double dissociation between effects of lesions of the ABL and of the amygdala central nucleus on phenomena related to attentional processing and the acquisition of motivational value.

Amygdala↗
PubMed2006

Disrupting reconsolidation of conditioned withdrawal memories in the basolateral amygdala reduces suppression of heroin seeking in rats.

Recent data from our laboratory have demonstrated that appetitive drug memories undergo protein synthesis-dependent reconsolidation in the basolateral amygdala (BLA), an area important in the formation of emotional memories. We here investigated the importance of the BLA in the reconsolidation of opiate conditioned withdrawal memories. Rats with bilateral cannulas implanted in the BLA were trained to respond for heroin (0.12 mg/kg, i.v.) under a seeking-taking schedule, which required responding on a seeking lever to gain the opportunity to self-administer heroin by a single response on a taking lever. After induction of opiate dependence with subcutaneously implanted, heroin-filled osmotic minipumps (3 mg x kg(-1) x d(-1) heroin), rats received five consecutive pairings of a conditioned stimulus (CS) (tone, light, and odor compound) paired with naloxone (0.10 mg/kg, s.c.)-precipitated withdrawal. We replicated our previous findings that heroin seeking is suppressed in the presence of the withdrawal-associated CS. However, infusion of Zif268 antisense oligodeoxynucleotide into the BLA before reactivation of the CS-withdrawal association abolished this conditioned suppression in a reactivation-dependent manner. We also report that reconsolidation of CS-withdrawal memories upregulates Zif268 protein in the basolateral but not central nucleus of the amygdala and that Zif268 knockdown occurs selectively in the BLA. These results demonstrate that drug withdrawal memories undergo protein synthesis-dependent reconsolidation in the BLA and suggest a common mechanism for the reconsolidation of both appetitive and aversive drug memories.

Amygdala↗
PubMedDate not supplied

GluR5 kainate receptor mediated synaptic transmission in rat basolateral amygdala in vitro.

A non-NMDA and non-AMPA receptor mediated excitatory synaptic response was identified in intracellularly recorded basolateral amygdala (BLA) neurons in an in vitro slice preparation. Synaptic potentials were evoked by stimulation of either the external capsule (EC) or basal amygdala (BA). NMDA and GABA(A) receptors were blocked by inclusion of 100 microM (+/-)-2-amino-5-phosphonopentanoic acid and 10 microM bicuculline in the perfusion solution. The AMPA receptor-selective allosteric antagonists GYKI 52466 (50 microM) and GYKI 53655 (50 microM) partially suppressed depolarizing synaptic responses evoked by single shock EC stimulation, but fully blocked synaptic responses evoked by BA stimulation. In recordings carried out in the presence of the AMPA receptor antagonists, EC stimulation with pulse trains (5-8 pulses at 50-100 Hz) evoked a large increase in the amplitude of synaptic responses. The AMPA receptor-independent component of the train-induced synaptic response had a null potential near 0 mV. Such AMPA receptor-independent, train-evoked synaptic responses were largely blocked by the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM; 85 +/- 4%). In addition, the responses were blocked by the GluR5-selective kainate receptor antagonist LY293558 (10 microM; 95 +/- 2%). These results indicate that a component of the EC (but not the BA) synaptic response is mediated by kainate receptors containing the GluR5 subunit.

6-Cyano-7-nitroquinoxaline-2,3-dione↗