Evoked potentials recorded from slices of pigeon hippocampus were reversibly attenuated by 2 mM kynurenic acid. High frequency stimulation (3 x 200 Hz for 1 sec, with 1 sec intervals) evoked a persistent increase in the evoked potential, lasting in a nondecremental form for at least 2 hr. This incre
Induction of long-term potentiation in the basolateral amygdala does not depend on NMDA receptor activation
β Scribed by Dr. Paul F. Chapman; Lisa L. Bellavance
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 932 KB
- Volume
- 11
- Category
- Article
- ISSN
- 0887-4476
No coin nor oath required. For personal study only.
β¦ Synopsis
Long-term potentiation (LTP) can be induced in the lateral and basolat-era1 amygdala by stimulating synaptic afferents in the external capsule (EC). We examined the sensitivity of amygdaloid LTP to the NMDA receptor antagonist 2-amino-5phosphonopentanoate (AP5), which is known to block LTP induction in the Schaffer collateraYCA1 synapses in the hippocampus. While relatively high concentrations (100 pM) of DL-AP~ 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 pM, a concentration sufficient to block both synaptic responses mediated by NMDA receptors and LTP induction in the hippocampus and neocortex, AF'5 did not affect the probability of inducing LTP in the amygdala. Application of 10 pM 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 pM 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. o 1992 Wiley-Liss. Inc.
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