scholarly journals The value of extended amygdala structures in emotive effects of narcogenic with diverse chemical structure

2019 ◽  
Vol 5 (3) ◽  
pp. 11-19
Author(s):  
Roman O. Roik ◽  
Andrei A. Lebedev ◽  
Petr D. Shabanov

Introduction: Studies on the mechanisms of the reinforcing action of opioid and non-opioid narcotics confirmed the existence in the brain of a specialized system named the extended amygdala. Materials and methods: To clarify the value of the extended amygdala structures (bed nucleus, central nucleus of the amygdala and nucleus accumbens shell) in the mechanisms of unconditioned and conditioned reinforcement activated by various narcogenic, this paper carried out a neuropharmacological analysis of these effects, using blockade of dopamine receptors, GABA, opioids and CRF receptors within these brain structures, as well as an analysis of behavioral responses by self-stimulation (unconditioned reinforcement) and conditioned place preference (CPP) (conditioned reinforcement). Results and discussion: The central amygdala and the bed nucleus have a controlling influence on the hypothalamus, which is predominantly of CRF-, GABA- and dopaminergic nature. Through D1 dopamine receptors,, a direct positive (activating) effect on the lateral hypothalamus is made. The D2 receptor blockade of the nucleus accumbens prevents narcogenic from exerting the reinforcing properties, which are primarily stimulating. The blockade of the D1 receptors of the nucleus accumbens by SCH-23390 prevents the expression of unconditioned and conditioned reinforcing properties of predominantly opiates and opioids. The blockade of GABAA receptors in the nucleus accumbens with bicuculline prevents the manifestation of the primary and secondary reinforcing properties (CPP) of psychostimulant drugs (amphetamine), without affecting the effects of opiates and opioids (fentanyl and leu-enkephalin). Conclusion: The pharmacological analysis proves that CRF, dopamine and GABA receptors are most important for the correction of reinforcement activated by various narcogenic.

1999 ◽  
Vol 877 (1 ADVANCING FRO) ◽  
pp. 461-485 ◽  
Author(s):  
G. CHIARA ◽  
G. TANDA ◽  
V. BASSAREO ◽  
F. PONTIERI ◽  
E. ACQUAS ◽  
...  

Neuroscience ◽  
2015 ◽  
Vol 295 ◽  
pp. 243-251 ◽  
Author(s):  
S.R. Hauser ◽  
G.A. Deehan ◽  
R. Dhaher ◽  
C.P. Knight ◽  
J.A. Wilden ◽  
...  

2017 ◽  
Vol 19 (1) ◽  
pp. 37-45
Author(s):  
Petr D Shabanov ◽  
Andrei Andreevich Lebedev ◽  
Vitalii Ivanovich Morozov ◽  
Sergei Vladimirivich Azarenko

Male Wistar rats were implanted bipolar electrodes into the lateral hypothalamus to study self-stimulation reaction in the Skinner box and microcannulas into the right lateral ventricle and structutes of the paraamygdalar complex (bed nucleus of stria terminalis, central nucleus of amygdala or nucleus accumbens) to study central effects of orexin (5 µg in 5 µl i. v. for an injection) on the reinforcing properties of pharmacological drugs. Intraperitoneal administration of trimeperidine (3 mg/kg), a synthetic opioid, was shown to increase self-stimulation of the lateral hypothalamus in the Skinner box (number of pedal pressings for 10 min) by 51.8%, and sulpiride (5 mg/kg, a small dose), an antagonist of D2 dopamine receptors, did not change but in the large dose (20 mg/kg) decreased self-stimulation by 49.3% (a number of pedal pressings, or self-stimulation frequency within 10 min). At the same time, SB-408124, an antagonist of OX1R receptors and its combination with orexin did not change self-stimulation indexes after intrastructural administration into the bed nucleus of stria terminalis, central nucleus of amygdala or nucleus accumbens. On the background of blockade of OX1R receptors by SB-408124 (1 µg for all structures) trimeperidine reduced their activating action on self-stimulation reaction. Sulpiride (5 mg/kg i. p., a dose not affecting self-stimulation reaction) blocked activating action of trimeperidine after blockade OX1R receptors by SB-408124 (1 µg). The data obtained can suggest that OX1R receptors participate in the reinforcing effects of synthetic opioid trimeperidine and the blockade of them by SB-408124 potentiate antagonist effects of sulpiride on self-stimulation (4 tables, bibliography: 23 refs).


2018 ◽  
Author(s):  
Juyoen Hur ◽  
Claire M. Kaplan ◽  
Jason F. Smith ◽  
Daniel E. Bradford ◽  
Andrew S. Fox ◽  
...  

ABSTRACTAlcohol abuse is common, imposes a staggering burden on public health, and is challenging to treat, underscoring the need to develop a deeper understanding of the underlying neurobiology. When administered acutely, ethyl alcohol reduces threat reactivity in humans and other animals, and there is growing evidence that threat-dampening and related negative reinforcement mechanisms support the etiology and recurrence of alcohol and other kinds of substance misuse. Converging lines of evidence motivate the hypothesis that these effects are mediated by the central extended amygdala (EAc)—including the central nucleus of the amygdala (Ce) and bed nucleus of the stria terminalis (BST)—but the relevance of this circuitry to acute alcohol effects in humans remains poorly understood. Using a single-blind, randomized-groups design, multiband imaging data were acquired from 49 social drinkers while they performed an fMRI-optimized emotional-faces/places paradigm after consuming alcohol or placebo. Relative to placebo, alcohol significantly dampened reactivity to threat-related emotional faces in the BST. To rigorously assess potential regional differences in activation, data were extracted from anatomically defined Ce and BST regions-of-interest. Analyses revealed a similar pattern of dampening across the two regions. In short, alcohol acutely dampens reactivity to threat-related faces in humans and it does so similarly across the two major divisions of the EAc. These observations provide a framework for understanding the translational relevance of addiction models derived from work in rodents, inform on-going debates about the functional organization of the EAc, and set the stage for bi-directional translational models aimed at developing improved treatment strategies for alcohol abuse and other addictions.


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