Glutamatergic transmission in the nucleus of the solitary tract modulates memory through influences on amygdala noradrenergic systems.
The authors examined whether glutamate release from the vagus nerve onto the nucleus of the solitary tract (NTS) is one mechanism by which the vagus influences memory and neural activity in limbic structures. Rats trained to drink from a spout were given a footshock (0.35 mA) on Day 5 after approaching the spout. Phosphate-buffered saline or 5.0, 50.0, or 100.0 nmol/0.5 microl glutamate was then infused into the NTS. Glutamate (5.0 or 50.0 nmol) significantly enhanced memory on the retention test. In Experiment 2, this effect was attenuated by blocking noradrenergic receptors in the amygdala with propranolol (0.3 microg/0.5 microl). Experiment 3 used in vivo microdialysis to determine whether footshock plus glutamate (50.0 nmol) alters noradrenergic output in the amygdala. These treatments caused a significant and long-lasting increase in amygdala noradrenergic concentrations. The results indicate that glutamate may be one transmitter that conveys the effects of vagal activation on brain systems that process memory.
Miyashita
Teiko
T
Department of Psychology, University of Virginia, Charlottesville 22904-4400, USA.
Williams
Cedric L
CL
D000344:Afferent Pathways / Q000502:physiology; D000679:Amygdala / Q000502:physiology*; D000818:Animals; D003214:Conditioning, Classical / Q000502:physiology; D005239:Fear / Q000502:physiology; D018698:Glutamic Acid / Q000502:physiology*; D008297:Male; D011939:Mental Recall / Q000502:physiology*; D009638:Norepinephrine / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012153:Retention, Psychology / Q000502:physiology; D017552:Solitary Nucleus / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology
D018698:Glutamic Acid; D009638:Norepinephrine