Effects of electrical stimulation of the central nucleus of the amygdala on the in vivo electrophysiological activity of rat nigral dopaminergic neurons

✍ Scribed by Claude Rouillard; Arthur S. Freeman

• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: English
• Weight: 895 KB
• Volume: 21
• Category: Article
• ISSN: 0887-4476
• DOI: 10.1002/syn.890210410

✦ Synopsis

The central nucleus of the amygdala (CeA) receives a dopaminergic (DA) innervation from the midbrain. Among its many efferent projections, the CeA innervates the substantia nigra. The possibility that the CeA influences the activity of nigral DA neurons was evaluated. The effects of electrical stimulation of the CeA on the firing rate and pattern of nigral DA neurons were investigated in anesthetized rats. Poststimulus time histograms revealed that nigral DA cells were either inhibited (N = 151, excited (N = 13), or unresponsive (N = 17) to CeA stimulation (250 stimuli a t 0.5 Hz). The mean (2SEM) latency to inhibition (24 t 9 msec) was significantly shorter than that for excitation (65 ? 10 msec); the duration of inhibition (200 2 29 msec) was also significantly greater than the duration of excitation (86 t 11 msec) (P < 0.01 for both). DA cells that were excited had basal firing rates significantly lower than those of the inhibited or unresponsive cells ( P < 0.05). Preliminary data suggest that DA cell burst-firing increases or decreases, respectively, in association with stimulation-evoked increases or decreases in firing rate. The relatively long latencies for stimulation-evoked responses suggest that CeA projection neurons indirectly affect nigral DA neurons via polysynaptic pathways. These results demonstrate that the CeA has the ability to influence the activity of nigral DA neurons, consistent with the putative role of the CeA as a n interface between the limbic and extrapyramidal systems. Given the crucial role of the amygdala in anxiety states, these findings suggest that DA cell function may also be affected in such disorders. o 1995 Wiley-Liss, Inc.