Gastrin-Releasing Peptide Signaling Plays a Limited and Subtle Role in Amygdala Physiology and Aversive Memory
Figure 1
The gastrin-releasing peptide receptor is expressed in interneurons in the lateral amygdala and affects amygdala physiology.
A) In situ hybridization of the GRPR in the amygdala. B) Binary version of A) that more clearly distinguishes the ISH signal (white dots), mainly in the lateral (LA) and basolateral (BLA) with only very few labeled cells in the central lateral (CeL) and central medial (CeM) nuclei. C) Higher power image showing ISH signal in neurons that were D) co-immunolabeled for eGFP being expressed under control of the GAD67 promoter. E) Sample recordings of spontaneous inhibitory postsynaptic currents recorded from LA pyramidal neurons in control conditions, in the presence of GRP and after addition of picrotoxin in slices made from WT and GRPR KO mice. The patch pipette contained high Cl− therefore IPSCs were inward at the holding potential of −70 mV. CNQX (20 µM) was present to block fast excitatory activity. Picrotoxin (100 µM) blocked all the inward currents confirming their inhibitory nature. F) Quantification of the results from 6 slices from WT and 4 slices from GRPR KO mice. G) Typical example of the most rostral and ventral in vivo recording position in the central medial nucleus of the amygdala. H) Cumulative frequency plot of CeM single unit activity from 12 WT and 12 GRPR KO mice. Inset shows a sample record.