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Restoring the Firing Activity of Ventral Tegmental Area Neurons by Lateral Hypothalamic Deep Brain Stimulation Following Morphine Administration in Rats Publisher Pubmed



Nikbakhtzadeh M1 ; Ashabi G1 ; Saadatyar R2 ; Doostmohammadi J3 ; Nekoonam S4 ; Keshavarz M1 ; Riahi E1
Authors
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Authors Affiliations
  1. 1. Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Department of Biomedical Engineering, School of Electrical Engineering, Iran University of Science and Technology, Tehran, Iran
  3. 3. Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Source: Physiology and Behavior Published:2023


Abstract

We have previously shown that high-frequency deep brain stimulation (DBS) of the lateral hypothalamus (LH) compromises morphine-induced addiction-like behavior in rats. The exact mechanism underlying this effect is not known. Here, we investigated the assumption that DBS in the LH influences the firing activity of neurons in the ventral tegmental area (VTA). To that end, male Wistar rats received morphine (5 mg/kg; s.c.) for three days and underwent extracellular single unit recording under general anesthesia one day later. During the recording, the rats received an intraoperative injection of morphine (5 mg/kg; s.c.) plus DBS in the LH (130 Hz pulse frequency, 150 μA amplitude, and 100 μs pulse width). One group of animals also received preoperative DBS after each morphine injection before the recording. The spiking frequency of VTA neurons was measured at three successive phases: (1) baseline (5–15 min); (2) DBS-on (morphine + DBS for 30 min); and (3) After-DBS (over 30 min after termination of DBS). Results showed that morphine suppressed the firing activity of a large population of non-DA neurons, whereas it activated most DA neurons. Intraoperative DBS reversed morphine suppression of non-DA firing, but did not alter the excitatory effect of morphine on DA neurons firing. With repeated preoperative application of DBS, non-DA neurons returned to the morphine-induced suppressive state, but DA neurons released from the excitatory effect of morphine. It is concluded that the development of morphine reward is associated with a hypoactivity of VTA non-DA neurons and a hyperactivity of DA neurons, and that DBS modulation of the spiking activity may contribute to the blockade of morphine addiction-like behavior. © 2023 Elsevier Inc.
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