Journal articles: 'Lateral nucleus accumbens'

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Wang, Dongmei, Jianjun Zhang, Yunjing Bai, Xigeng Zheng, Mirmohammadali M. Alizamini, Wen Shang, Qingxiong Yang, Ming Li, Yonghui Li, and Nan Sui. "Melanin-concentrating hormone in rat nucleus accumbens or lateral hypothalamus differentially impacts morphine and food seeking behaviors." Journal of Psychopharmacology 34, no. 4 (January 7, 2020): 478–89. http://dx.doi.org/10.1177/0269881119895521.

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Background: Identifying neural substrates that are differentially affected by drugs of abuse and natural rewards is key to finding a target for an efficacious treatment for substance abuse. Melanin-concentrating hormone is a polypeptide with an inhibitory effect on the mesolimbic dopamine system. Here we test the hypothesis that melanin-concentrating hormone in the lateral hypothalamus and nucleus accumbens shell is differentially involved in the regulation of morphine and food-rewarded behaviors. Methods: Male Sprague–Dawley rats were trained with morphine (5.0 mg/kg, subcutaneously) or food pellets (standard chow, 10–14 g) to induce a conditioned place preference, immediately followed by extinction training. Melanin-concentrating hormone (1.0 µg/side) or saline was infused into the nucleus accumbens shell or lateral hypothalamus before the reinstatement primed by morphine or food, and locomotor activity was simultaneously monitored. As the comparison, melanin-concentrating hormone was also microinjected into the nucleus accumbens shell or lateral hypothalamus before the expression of food or morphine-induced conditioned place preference. Results: Microinfusion of melanin-concentrating hormone into the nucleus accumbens shell (but not into the lateral hypothalamus) prevented the reinstatement of morphine conditioned place preference but had no effect on the reinstatement of food conditioned place preference. In contrast, microinfusion of melanin-concentrating hormone into the lateral hypothalamus (but not in the nucleus accumbens shell) inhibited the reinstatement of food conditioned place preference but had no effect on the reinstatement of morphine conditioned place preference. Conclusions: These results suggest a clear double dissociation of melanin-concentrating hormone in morphine/food rewarding behaviors and melanin-concentrating hormone in the nucleus accumbens shell. Melanin-concentrating hormone could be a potential target for therapeutic intervention for morphine abuse without affecting natural rewards.

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Taverna, Stefano, Barbara Canciani, and Cyriel M. A. Pennartz. "Dopamine D1-Receptors Modulate Lateral Inhibition Between Principal Cells of the Nucleus Accumbens." Journal of Neurophysiology 93, no. 3 (March 2005): 1816–19. http://dx.doi.org/10.1152/jn.00672.2004.

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One of the current hypotheses on dopamine in the physiology of motivation posits that this neurotransmitter regulates filtering and selection of inputs to the nucleus accumbens. The effects of dopamine (100 μM) and the D1-receptor agonist SKF 38393 (20–50 μM) on GABAergic synaptic transmission between pairs of principal cells of rat nucleus accumbens were studied by using simultaneous dual patch-clamp recordings in acutely prepared brain slices. Both compounds attenuated postsynaptic responses induced by presynaptic firing and this effect was reversed by the D1-receptor antagonist SCH 23390 (25 μM). This attenuating effect of dopamine D1-receptors may act to diminish competitive interactions between single projection neurons or ensembles in the nucleus accumbens.

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Sazdanovic, Maja, Predrag Sazdanovic, Ivana Zivanovic-Macuzic, Vladimir Jakovljevic, Dejan Jeremic, Amir Peljto, and Jovo Tosevski. "Neurons of human nucleus accumbens." Vojnosanitetski pregled 68, no. 8 (2011): 655–60. http://dx.doi.org/10.2298/vsp1108655s.

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Background/Aim. Nucleus accumbens is a part of the ventral striatum also known as a drug active brain region, especially related with drug addiction. The aim of the study was to investigate the Golgi morphology of the nucleus accumbens neurons. Methods. The study was performed on the frontal and sagittal sections of 15 human brains by the Golgi Kopsch method. We classified neurons in the human nucleus accumbens according to their morphology and size into four types: type I - fusiform neurons; type II - fusiform neurons with lateral dendrite, arising from a part of the cell body; type III - pyramidal-like neuron; type IV - multipolar neuron. The medium spiny neurons, which are mostly noted regarding to the drug addictive conditions of the brain, correspond to the type IV - multipolar neurons. Results. Two regions of human nucleus accumbens could be clearly recognized on Nissl and Golgi preparations each containing different predominant neuronal types. Central part of nucleus accumbens, core region, has a low density of impregnated neurons with predominant type III, pyramidal-like neurons, with spines on secondary branches and rare type IV, multipolar neurons. Contrary to the core, peripheral region, shell of nucleus, has a high density of impregnated neurons predominantly contained of type I and type IV - multipolar neurons, which all are rich in spines on secondary and tertiary dendritic branches. Conclusion. Our results indicate great morphological variability of human nucleus accumbens neurons. This requires further investigations and clarifying clinical significance of this important brain region.

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Swerdlow, Neal R., and George F. Koob. "Dopamine, schizophrenia, mania, and depression: Toward a unified hypothesis of cortico-striatopallido-thalamic function." Behavioral and Brain Sciences 10, no. 2 (June 1987): 197–208. http://dx.doi.org/10.1017/s0140525x00047488.

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AbstractConsiderable evidence from preclinical and clinical investigations implicates disturbances of brain dopamine (DA) function in the pathophysiology of several psychiatric and neurologic disorders. We describe a neural model that may help organize theseindependent experimental observations. Cortical regions classically associated with the limbic system interact with infracortical structures, including the nucleus accumbens, ventral pallidum, and dorsomedial nucleus of the thalamus. In our model, overactivity in forebrain DA systems results in the loss of lateral inhibitory interactions in the nucleus accumbens, causing disinhibition of pallidothalamic efferents; this in turn causes rapid changes and a loss of focused corticothalamic activity in cortical regions controlling cognitive and emotional processes. These effects might be manifested clinically by some symptoms of psychoses. Underactivity of forebrain DA results in excess lateral inhibition in the nucleus accumbens, causing tonic inhibition of pallidothalamic efferents; this perpetuates tonic corticothalamic activity and prevents the initiation of new activity in other critical cortical regions. These effects might be manifested clinically by some symptoms of depression. This model parallels existing explanations for the etiology of several movement disorders, and may lead to testable inferences regarding the neural substrates of specific psychopathologies.

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Lalonde, Robert, and Catherine Strazielle. "Neuroanatomical pathways underlying the effects of hypothalamo-hypophysial-adrenal hormones on exploratory activity." Reviews in the Neurosciences 28, no. 6 (July 26, 2017): 617–48. http://dx.doi.org/10.1515/revneuro-2016-0075.

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AbstractWhen injected via the intracerebroventricular route, corticosterone-releasing hormone (CRH) reduced exploration in the elevated plus-maze, the center region of the open-field, and the large chamber in the defensive withdrawal test. The anxiogenic action of CRH in the elevated plus-maze also occurred when infused in the basolateral amygdala, ventral hippocampus, lateral septum, bed nucleus of the stria terminalis, nucleus accumbens, periaqueductal grey, and medial frontal cortex. The anxiogenic action of CRH in the defensive withdrawal test was reproduced when injected in the locus coeruleus, while the amygdala, hippocampus, lateral septum, nucleus accumbens, and lateral globus pallidus contribute to center zone exploration in the open-field. In addition to elevated plus-maze and open-field tests, the amygdala appears as a target region for CRH-mediated anxiety in the elevated T-maze. Thus, the amygdala is the principal brain region identified with these three tests, and further research must identify the neural circuits underlying this form of anxiety.

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Sazdanovic, Maja, Slobodanka Mitrovic, Milos Todorovic, Maja Vulovic, Dejan Jeremic, Zoran Milosavljevic, Predrag Sazdanovic, and Neda Ognjanovic. "Morphology of Human Nucleus Accumbens Neurons Based on the Immunohistochemical Expression of Gad67." Serbian Journal of Experimental and Clinical Research 17, no. 4 (December 1, 2016): 297–302. http://dx.doi.org/10.1515/sjecr-2016-0041.

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Abstract The nucleus accumbens is a part of the ventral striatum along with the caudate nucleus and putamen. The role of the human nucleus accumbens in drug addiction and other psychiatric disorders is of great importance. The aim of this study was to characterize medium spiny neurons in the nucleus accumbens according to the immunohistochemical expression of GAD67. This study was conducted on twenty human brains of both sexes between the ages of 20 and 75. The expression of GAD67 was assessed immunohistochemically, and the characterization of the neurons was based on the shape and size of the soma and the number of impregnated primary dendrites. We showed that neurons of the human nucleus accumbens expressed GAD67 in the neuron soma and in the primary dendrites. An analysis of the cell body morphology revealed the following four different types of neurons: fusiform neurons, fusiform neurons with lateral dendrites, pyramidal neurons and multipolar neurons. An immunohistochemical analysis showed a strong GAD67 expression in GABAergic medium spiny neurons, which could be classifi ed into four different types, and these neurons morphologically correlated with those described by the Golgi study.

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Whiting, Alexander C., Michael Y. Oh, and Donald M. Whiting. "Deep brain stimulation for appetite disorders: a review." Neurosurgical Focus 45, no. 2 (August 2018): E9. http://dx.doi.org/10.3171/2018.4.focus18141.

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The mechanisms of appetite disorders, such as refractory obesity and anorexia nervosa, have been vigorously studied over the last century, and these studies have shown that the central nervous system has significant involvement with, and responsibility for, the pathology associated with these diseases. Because deep brain stimulation has been shown to be a safe, efficacious, and adjustable treatment modality for a variety of other neurological disorders, it has also been studied as a possible treatment for appetite disorders. In studies of refractory obesity in animal models, the ventromedial hypothalamus, the lateral hypothalamus, and the nucleus accumbens have all demonstrated elements of success as deep brain stimulation targets. Multiple targets for deep brain stimulation have been proposed for anorexia nervosa, with research predominantly focusing on the subcallosal cingulate, the nucleus accumbens, and the stria terminalis and medial forebrain bundle. Human deep brain stimulation studies that focus specifically on refractory obesity and anorexia nervosa have been performed but with limited numbers of patients. In these studies, the target for refractory obesity has been the lateral hypothalamus, ventromedial hypothalamus, and nucleus accumbens, and the target for anorexia nervosa has been the subcallosal cingulate. These studies have shown promising findings, but further research is needed to elucidate the long-term efficacy of deep brain stimulation for the treatment of appetite disorders.

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Roik, Roman O., Andrei A. Lebedev, and Petr D. Shabanov. "The value of extended amygdala structures in emotive effects of narcogenic with diverse chemical structure." Research Results in Pharmacology 5, no. 3 (September 30, 2019): 11–19. http://dx.doi.org/10.3897/rrpharmacology.5.38389.

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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.

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Sasabayashi, Daiki, Yoichiro Takayanagi, Tsutomu Takahashi, Naoyuki Katagiri, Atsushi Sakuma, Chika Obara, Masahiro Katsura, et al. "Subcortical Brain Volume Abnormalities in Individuals With an At-risk Mental State." Schizophrenia Bulletin 46, no. 4 (March 12, 2020): 834–45. http://dx.doi.org/10.1093/schbul/sbaa011.

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Abstract Previous structural magnetic resonance imaging studies of psychotic disorders have demonstrated volumetric alterations in subcortical (ie, the basal ganglia, thalamus) and temporolimbic structures, which are involved in high-order cognition and emotional regulation. However, it remains unclear whether individuals at high risk for psychotic disorders with minimal confounding effects of medication exhibit volumetric changes in these regions. This multicenter magnetic resonance imaging study assessed regional volumes of the thalamus, caudate, putamen, nucleus accumbens, globus pallidus, hippocampus, and amygdala, as well as lateral ventricular volume using FreeSurfer software in 107 individuals with an at-risk mental state (ARMS) (of whom 21 [19.6%] later developed psychosis during clinical follow-up [mean = 4.9 years, SD = 2.6 years]) and 104 age- and gender-matched healthy controls recruited at 4 different sites. ARMS individuals as a whole demonstrated significantly larger volumes for the left caudate and bilateral lateral ventricles as well as a smaller volume for the right accumbens compared with controls. In male subjects only, the left globus pallidus was significantly larger in ARMS individuals. The ARMS group was also characterized by left-greater-than-right asymmetries of the lateral ventricle and caudate nucleus. There was no significant difference in the regional volumes between ARMS groups with and without later psychosis onset. The present study suggested that significant volume expansion of the lateral ventricle, caudate, and globus pallidus, as well as volume reduction of the accumbens, in ARMS subjects, which could not be explained only by medication effects, might be related to general vulnerability to psychopathology.

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Shabanov, Petr D., Andrei Andreevich Lebedev, Vitalii Ivanovich Morozov, and Sergei Vladimirivich Azarenko. "INTERACTION BETWEEN OREXIN AND OPIOIDS SYSTEMS OF THE STRUCTURES OF PARAAMYGDALAR COMPLEX IN THE REINFORCING EFFECTS OF SPONTANEOUS AND ACTIVATED SELF-STIMULATION OF THE LATERAL HYPOTHALAMUS." Bulletin of the Russian Military Medical Academy 19, no. 1 (December 15, 2017): 37–45. http://dx.doi.org/10.17816/brmma12163.

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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).

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Jones, D. L. "Central integration of cardiovascular and drinking responses elicited by central administration of angiotensin II: divergence of regulation by the ventral tegmental area and nucleus accumbens." Canadian Journal of Physiology and Pharmacology 64, no. 7 (July 1, 1986): 1011–16. http://dx.doi.org/10.1139/y86-172.

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Previous studies had implicated the involvement of the ventral tegmental area and its dopamine projections to the nucleus accumbens in goal-directed behavior. This study investigated whether or not the GABAergic inputs to the ventral tegmental area and, in turn, dopaminergic input to the nucleus accumbens from the ventral tegmental area modify drinking and cardiovascular responses elicited by central administration of angiotensin II. Injections of 25 ng of angiotensin II into a lateral cerebral ventricle of the rat elicited water intakes averaging 7–8 mL in 15 min with latencies usually less than 3 min. Pretreatment of the nucleus accumbens with spiperone, a dopamine antagonist, or the ventral tegmental area with γ-amino butyric acid (GABA) produced dose-dependent reductions in water intake and number of laps taken while increasing the latency to drink. The spiperone injection did not alter the pressor response. On the other hand, the GABA injections attenuated the pressor responses to central angiotensin II administration. These findings suggest that GABA input to the ventral tegmental area modifies both the cardiovascular and drinking responses elicited following central administration of angiotensin II. However, the dopamine projections to the nucleus accumbens appear to be involved only in the drinking responses elicited by central injections of angiotensin II. Divergence for the coordination of the skeletal motor behavioral component and the cardiovascular component elicited by central administration of angiotensin II must occur before the involvement of these dopamine pathways.

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Lorrain, Daniel S., Jon V. Riolo, Leslie Matuszewich, and Elaine M. Hull. "Lateral Hypothalamic Serotonin Inhibits Nucleus Accumbens Dopamine: Implications for Sexual Satiety." Journal of Neuroscience 19, no. 17 (September 1, 1999): 7648–52. http://dx.doi.org/10.1523/jneurosci.19-17-07648.1999.

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Colle, Lois M., and Roy A. Wise. "Effects of nucleus accumbens amphetamine on lateral hypothalamic brain stimulation reward." Brain Research 459, no. 2 (September 1988): 361–68. http://dx.doi.org/10.1016/0006-8993(88)90653-1.

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Burke, Dennis A., and Veronica A. Alvarez. "Serotonin receptors contribute to dopamine depression of lateral inhibition in the nucleus accumbens." Cell Reports 39, no. 6 (May 2022): 110795. http://dx.doi.org/10.1016/j.celrep.2022.110795.

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Onténiente, Brigitte, Hervé Simon, Khalid Taghzouti, Michel Geffard, Michel Le Moal, and André Calas. "Dopamine-GABA interactions in the nucleus accumbens and lateral septum of the rat." Brain Research 421, no. 1-2 (September 1987): 391–96. http://dx.doi.org/10.1016/0006-8993(87)91315-1.

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Ren, Shuancheng, Yaling Wang, Faguo Yue, Xiaofang Cheng, Ruozhi Dang, Qicheng Qiao, Xueqi Sun, et al. "The paraventricular thalamus is a critical thalamic area for wakefulness." Science 362, no. 6413 (October 25, 2018): 429–34. http://dx.doi.org/10.1126/science.aat2512.

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Clinical observations indicate that the paramedian region of the thalamus is a critical node for controlling wakefulness. However, the specific nucleus and neural circuitry for this function remain unknown. Using in vivo fiber photometry or multichannel electrophysiological recordings in mice, we found that glutamatergic neurons of the paraventricular thalamus (PVT) exhibited high activities during wakefulness. Suppression of PVT neuronal activity caused a reduction in wakefulness, whereas activation of PVT neurons induced a transition from sleep to wakefulness and an acceleration of emergence from general anesthesia. Moreover, our findings indicate that the PVT–nucleus accumbens projections and hypocretin neurons in the lateral hypothalamus to PVT glutamatergic neurons’ projections are the effector pathways for wakefulness control. These results demonstrate that the PVT is a key wakefulness-controlling nucleus in the thalamus.

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Maruani, Julia, and Pierre A. Geoffroy. "Multi-Level Processes and Retina–Brain Pathways of Photic Regulation of Mood." Journal of Clinical Medicine 11, no. 2 (January 16, 2022): 448. http://dx.doi.org/10.3390/jcm11020448.

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Light exerts powerful biological effects on mood regulation. Whereas the source of photic information affecting mood is well established at least via intrinsically photosensitive retinal ganglion cells (ipRGCs) secreting the melanopsin photopigment, the precise circuits that mediate the impact of light on depressive behaviors are not well understood. This review proposes two distinct retina–brain pathways of light effects on mood: (i) a suprachiasmatic nucleus (SCN)-dependent pathway with light effect on mood via the synchronization of biological rhythms, and (ii) a SCN-independent pathway with light effects on mood through modulation of the homeostatic process of sleep, alertness and emotion regulation: (1) light directly inhibits brain areas promoting sleep such as the ventrolateral preoptic nucleus (VLPO), and activates numerous brain areas involved in alertness such as, monoaminergic areas, thalamic regions and hypothalamic regions including orexin areas; (2) moreover, light seems to modulate mood through orexin-, serotonin- and dopamine-dependent pathways; (3) in addition, light activates brain emotional processing areas including the amygdala, the nucleus accumbens, the perihabenular nucleus, the left hippocampus and pathways such as the retina–ventral lateral geniculate nucleus and intergeniculate leaflet–lateral habenula pathway. This work synthetizes new insights into the neural basis required for light influence mood

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He, Zi-Xuan, Ke Xi, Kai-Jie Liu, Mei-Hui Yue, Yao Wang, Yue-Yue Yin, Lin Liu, et al. "A Nucleus Accumbens Tac1 Neural Circuit Regulates Avoidance Responses to Aversive Stimuli." International Journal of Molecular Sciences 24, no. 5 (February 22, 2023): 4346. http://dx.doi.org/10.3390/ijms24054346.

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Neural circuits that control aversion are essential for motivational regulation and survival in animals. The nucleus accumbens (NAc) plays an important role in predicting aversive events and translating motivations into actions. However, the NAc circuits that mediate aversive behaviors remain elusive. Here, we report that tachykinin precursor 1 (Tac1) neurons in the NAc medial shell regulate avoidance responses to aversive stimuli. We show that NAcTac1 neurons project to the lateral hypothalamic area (LH) and that the NAcTac1→LH pathway contributes to avoidance responses. Moreover, the medial prefrontal cortex (mPFC) sends excitatory inputs to the NAc, and this circuit is involved in the regulation of avoidance responses to aversive stimuli. Overall, our study reveals a discrete NAc Tac1 circuit that senses aversive stimuli and drives avoidance behaviors.

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Zheng, Huiyuan, Michele Corkern, Irina Stoyanova, Laurel M. Patterson, Rui Tian, and Hans-Rudolf Berthoud. "Appetite-inducing accumbens manipulation activates hypothalamic orexin neurons and inhibits POMC neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 6 (June 1, 2003): R1436—R1444. http://dx.doi.org/10.1152/ajpregu.00781.2002.

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Corticolimbic circuits involving the prefrontal cortex, amygdala, and ventral striatum determine the reward value of food and might play a role in environmentally induced obesity. Chemical manipulation of the nucleus accumbens shell (AcbSh) has been shown to elicit robust feeding and Fos expression in the hypothalamus and other brain areas of satiated rats. To determine the neurochemical phenotype of hypothalamic neurons receiving input from the AcbSh, we carried out c-Fos/peptide double-labeling immunohistochemistry in various hypothalamic areas known to contain feeding peptides, from rats that exhibited a significant feeding response after AcbSh microinjection of the GABAA agonist muscimol. In the perifornical area, a significantly higher percentage of orexin neurons expressed Fos after muscimol compared with saline injection. In contrast, Fos expression was not induced in melanin-concentrating hormone and cocaine-amphetamine-related transcript (CART) neurons. In the arcuate nucleus, Fos activation was significantly lower in neurons coexpressing CART and proopiomelanocortin, and there was a tendency for higher Fos expression in neuropeptide Y neurons. In the paraventricular nucleus, no significant activation of oxytocin and CART neurons was found. Thus AcbSh manipulation may elicit food intake through coordinated stimulation of hypothalamic neurons expressing orexigenic peptides and suppression of neurons expressing anorexigenic peptides. However, activation of many neurons not expressing these peptides suggests that additional peptides/transmitters in the lateral hypothalamus and accumbens projections to other brain areas might also be involved.

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Lecourtier, Lucas, Alicia DeFrancesco, and Bita Moghaddam. "Differential tonic influence of lateral habenula on prefrontal cortex and nucleus accumbens dopamine release." European Journal of Neuroscience 27, no. 7 (April 2008): 1755–62. http://dx.doi.org/10.1111/j.1460-9568.2008.06130.x.

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Maldonado-Irizarry, CS, CJ Swanson, and AE Kelley. "Glutamate receptors in the nucleus accumbens shell control feeding behavior via the lateral hypothalamus." Journal of Neuroscience 15, no. 10 (October 1, 1995): 6779–88. http://dx.doi.org/10.1523/jneurosci.15-10-06779.1995.

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Knowlton, Christopher J., Tabea Ines Ziouziou, Niklas Hammer, Jochen Roeper, and Carmen C. Canavier. "Inactivation mode of sodium channels defines the different maximal firing rates of conventional versus atypical midbrain dopamine neurons." PLOS Computational Biology 17, no. 9 (September 17, 2021): e1009371. http://dx.doi.org/10.1371/journal.pcbi.1009371.

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Two subpopulations of midbrain dopamine (DA) neurons are known to have different dynamic firing ranges in vitro that correspond to distinct projection targets: the originally identified conventional DA neurons project to the dorsal striatum and the lateral shell of the nucleus accumbens, whereas an atypical DA population with higher maximum firing frequencies projects to prefrontal regions and other limbic regions including the medial shell of nucleus accumbens. Using a computational model, we show that previously identified differences in biophysical properties do not fully account for the larger dynamic range of the atypical population and predict that the major difference is that originally identified conventional cells have larger occupancy of voltage-gated sodium channels in a long-term inactivated state that recovers slowly; stronger sodium and potassium conductances during action potential firing are also predicted for the conventional compared to the atypical DA population. These differences in sodium channel gating imply that longer intervals between spikes are required in the conventional population for full recovery from long-term inactivation induced by the preceding spike, hence the lower maximum frequency. These same differences can also change the bifurcation structure to account for distinct modes of entry into depolarization block: abrupt versus gradual. The model predicted that in cells that have entered depolarization block, it is much more likely that an additional depolarization can evoke an action potential in conventional DA population. New experiments comparing lateral to medial shell projecting neurons confirmed this model prediction, with implications for differential synaptic integration in the two populations.

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Yamada, Hiroki, Takahiro Takeda, Toshiki Uchihara, Shizuko Sato, Susumu Kirimura, Yuka Hirota, Makoto Kodama, et al. "Macroscopic Localized Subicular Thinning as a Potential Indicator of Amyotrophic Lateral Sclerosis." European Neurology 79, no. 3-4 (2018): 200–205. http://dx.doi.org/10.1159/000487992.

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Subicular degeneration occurs in amyotrophic lateral sclerosis (ALS) patients. However, it was unknown whether microscopic subicular degeneration could be observed as macroscopic changes and whether these changes were associated with the transactive-response DNA binding protein 43 kDa (TDP-43) pathology. Topographic differences between subicular degeneration caused by ALS and Alzheimer disease (AD) had also not been characterized. Here we investigated the subiculum and related areas in autopsied brains from 3 ALS and 3 AD patients. Macroscopic subicular thinning and corresponding astrocytosis were pronounced in ALS compared to AD. This thinning was frequently accompanied by TDP-43 pathology in the transentorhinal cortex and nucleus accumbens. The preferential susceptibility of the perforant pathway to TDP-43 deposition may be an underlying cause of subicular thinning in ALS.

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Serra, Carlo, Kevin Akeret, Nicolai Maldaner, Victor E. Staartjes, Luca Regli, Gerasimos Baltsavias, and Niklaus Krayenbühl. "A White Matter Fiber Microdissection Study of the Anterior Perforated Substance and the Basal Forebrain: A Gateway to the Basal Ganglia?" Operative Neurosurgery 17, no. 3 (November 24, 2018): 311–20. http://dx.doi.org/10.1093/ons/opy345.

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Abstract BACKGROUND Studies detailing the anatomy of the basal forebrain (BF) from a neurosurgical perspective are missing. OBJECTIVE To describe the anatomy of the BF and of the anterior perforated substance (APS), the BF emphasizing surgical useful anatomical relationship between surface landmarks and deep structures. METHODS White matter fiber microdissection was performed on 5 brain specimens to analyze the topographic anatomy of the APS and expose layer-by-layer fiber tracts and nuclei of the BF. RESULTS The APS, as identified anatomically, surgically, and neuroradiologically, has clear borders measured 23.3 ± 3.4 mm (19-27) in the mediolateral and 12.5 ± 1.2 mm (11-14) in the anteroposterior directions. A detailed stratigraphy of the BF was performed from the APS up to basal ganglia and thalamus allowing identification and dissection of the main components of the BF (septum, nucleus accumbens, amygdala, innominate substance) and its white matter tracts (band of Broca, extracapsular thalamic peduncle, ventral amygdalohypothalamic fibers). The olfactory trigone together with diagonal gyrus and the APS proper is a relevant superficial landmark for the basal ganglia (inferior to the nucleus accumbens, lateral to the caudate head, and medial to the lentiform nucleus). CONCLUSION The findings in our study supplement available anatomic knowledge of APS and BF, providing reliable landmarks for precise topographic diagnosis of BF lesions and for intraoperative orientation. Surgically relevant relationships between surface and deep anatomic structures are highlighted offering thus a contribution to neurosurgeons willing to perform surgery in this delicate area.

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Chen, Li, and Daniel J. Lodge. "The lateral mesopontine tegmentum regulates both tonic and phasic activity of VTA dopamine neurons." Journal of Neurophysiology 110, no. 10 (November 15, 2013): 2287–94. http://dx.doi.org/10.1152/jn.00307.2013.

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Anatomic studies have demonstrated that the mesolimbic dopamine system receives a substantial afferent input from a variety of regions ranging from the prefrontal cortex through to the brain stem. However, how these afferents regulate dopamine neuron activity is still largely unknown. The mesopontine tegmentum provides a significant input to ventral tegmental area (VTA) dopamine neurons, and it has been demonstrated that discrete subdivisions within this region differentially alter dopamine neuron activity. Thus the laterodorsal tegmental nucleus provides a tonic input essential for maintaining burst firing of dopamine neurons, whereas the pedunculopontine tegmental (PPTg) nucleus regulates a transition from single-spike firing to burst firing. In contrast, the recently identified rostromedial tegmental nucleus provides an inhibitory input to the VTA and decreases spontaneous dopamine neuron activity. Here, we demonstrate that an area adjacent to the PPTg regulates both population activity as well as burst firing of VTA dopamine neurons. Specifically, N-methyl-d-aspartic acid (NMDA) activation of the lateral mesopontine tegmentum produces an increase in the number of spontaneously active dopamine neurons and an increase in the average percentage of burst firing of dopamine neurons. This increase in neuronal activity was correlated with extracellular dopamine efflux in the nucleus accumbens, as measured by in vivo microdialysis. Taken together, we provide further evidence that the mesopontine tegmentum regulates discrete dopamine neuron activity states that are relevant for the understanding of dopamine system function in both normal and disease states.

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Stellar, James R., and Dale Corbett. "Regional neuroleptic microinjections indicate a role for nucleus accumbens in lateral hypothalamic self-stimulation reward." Brain Research 477, no. 1-2 (January 1989): 126–43. http://dx.doi.org/10.1016/0006-8993(89)91400-5.

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Hirunagi, Kanjun, Elke Rommel, Andreas Oksche, and Horst W. Korf. "Vasoactive intestinal peptide-immunoreactive cerebrospinal fluid-contacting neurons in the reptilian lateral septum nucleus accumbens." Cell & Tissue Research 274, no. 1 (October 1993): 79–90. http://dx.doi.org/10.1007/bf00327988.

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Urstadt, K. R., S. F. Zaidi, P. Kally, and B. G. Stanley. "Lateral hypothalamic NMDA and GABAA receptors mediate feeding elicited by ipsilateral nucleus accumbens shell inhibition." Appetite 57 (July 2011): S45. http://dx.doi.org/10.1016/j.appet.2011.05.286.

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Rada, P., S. Tucci, E. Murzi, and L. Hernández. "Extracellular glutamate increases in the lateral hypothalamus and decreases in the nucleus accumbens during feeding." Brain Research 768, no. 1-2 (September 1997): 338–40. http://dx.doi.org/10.1016/s0006-8993(97)00788-9.

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Mungarndee, Suriyaphun S., Robert F. Lundy, and Ralph Norgren. "Expression of Fos during sham sucrose intake in rats with central gustatory lesions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 3 (September 2008): R751—R763. http://dx.doi.org/10.1152/ajpregu.90344.2008.

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For humans and rodents, ingesting sucrose is rewarding. This experiment tested the prediction that the neural activity produced by sapid sucrose reaches reward systems via projections from the pons through the limbic system. Gastric cannulas drained ingested fluid before absorption. For 10 days, the rats alternated an hour of this sham ingestion between sucrose and water. On the final test day, half of them sham drank water and the other half 0.6 M sucrose. Thirty minutes later, the rats were killed and their brains immunohistochemically stained for Fos. The groups consisted of controls and rats with excitotoxic lesions in the gustatory thalamus (TTA), the medial (gustatory) parabrachial nucleus (PBN), or the lateral (visceral afferent) parabrachial nucleus. In controls, compared with water, sham ingesting sucrose produced significantly more Fos-positive neurons in the nucleus of the solitary tract, PBN, TTA, and gustatory cortex (GC). In the ventral forebrain, sucrose sham licking increased Fos in the bed nucleus of the stria terminalis, central nucleus of amygdala, and the shell of nucleus accumbens. Thalamic lesions blocked the sucrose effect in GC but not in the ventral forebrain. After lateral PBN lesions, the Fos distributions produced by distilled H2O or sucrose intake did not differ from controls. Bilateral medial PBN damage, however, eliminated the sucrose-induced Fos increase not only in the TTA and GC but also in the ventral forebrain. Thus ventral forebrain areas associated with affective responses appear to be activated directly by PBN gustatory neurons rather than via the thalamocortical taste system.

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Radakovic, Ratko, Vaisakh Puthusseryppady, Emma Flanagan, Matthew C. Kiernan, Eneida Mioshi, and Michael Hornberger. "Frontostriatal grey matter atrophy in amyotrophic lateral sclerosis A visual rating study." Dementia & Neuropsychologia 12, no. 4 (December 2018): 388–93. http://dx.doi.org/10.1590/1980-57642018dn12-040008.

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ABSTRACT Amyotrophic lateral sclerosis (ALS) is characterised by frontostriatal grey matter changes similar to those in frontotemporal dementia (FTD). However, these changes are usually detected at a group level, and simple visual magnetic resonance imaging (MRI) cortical atrophy scales may further elucidate frontostriatal changes in ALS. Objective: To investigate whether frontostriatal changes are detectable using simple visual MRI atrophy rating scales applied at an individual patient level in ALS. Methods: 21 ALS patients and 17 controls were recruited and underwent an MRI scan. Prefrontal cortex sub-regions of the medial orbitofrontal cortex (MOFC), lateral orbitofrontal cortex (LOFC) and anterior cingulate cortex (ACC), striatal sub-regions of the caudate nucleus (CN) and nucleus accumbens (NAcc) were rated using visual grey matter atrophy 5-point Likert scales. Results: Significantly higher atrophy ratings in the bilateral MOFC only in ALS patients versus controls was observed (p<.05). Patients with greater MOFC atrophy had significantly higher atrophy of the CN (p<.05) and LOFC (p<.05). Conclusion: Use of simple visual atrophy rating scales on an individual level reliably detects frontostriatal deficits specific to ALS, showing MOFC atrophy differences with associated CN and LOFC atrophy. This is an applicable method that could be used to support clinical diagnosis and management.

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Bychkov, Eugenii R., Andrei A. Lebedev, Nikolai S. Efimov, Artyem S. Kryukov, Inessa V. Karpova, Sarng S. Pyurveev, Andrei V. Droblenkov, and Petr D. Shabanov. "Features of the involvement of the dopamine and serotonin brain systems in positive and negative emotional states in rats." Reviews on Clinical Pharmacology and Drug Therapy 18, no. 2 (August 16, 2020): 123–30. http://dx.doi.org/10.17816/rcf182123-130.

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The aim was to study the effect of rewarding and aversive stimulation of lateral hypothalamus on the turnover of monoamines in the terminal structures of the mesocorticolimbic and nigrostriatal systems: the nucleus accumbens (NAc) and striatum (St). The Wistar male rats were implanted electrodes in the lateral hypothalamus and further trained in self-stimulation test. Animals were also selected on aversive emotional reactions were observed after pressing the pedal for self-stimulation. Subsequently, forced stimulation was performed for 5 minutes and the animals were decapitated. The content of norepinephrine, dopamine (DA) and its metabolites 3,4-dioxiphenylacetic acid (DOPАС) and homovanilinic acid, serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in the nucleus accumbens and striatum were determined by high performance liquid chromatography with electrochemical detection. Positive and aversive stimulation of lateral hypothalamus decreased the level of DA in the NAc, however, only stimulation of the positive emotiogenic zone increased the DA and 5-HT turnover in the NAc, as evidenced by an increase in the DOPАС/DA and 5-HIAA/SER ratios, respectively. Rewarding and aversive stimulation decreased the level of 5-HT in St, however, only rewarding stimulation decreased the St level of 5-HIAA compared to control and animals with aversive stimulation. Rewarding stimulation increased the turnover of serotonin in St, as evidenced by the increase of 5-HIAA/5-HT ratios. The activity of the noradrenergic system did not change after rewarding and aversive stimulation. Thus, both rewarding and aversive electrical stimulation increases the turnover of DA and 5-HT in NAc and St. However, these changes are more significant after rewarding stimulation. DA turnover increases more in NAc, and 5-HT turnover in St. The data obtained indicate the specificity of the dopaminergic and serotonergic involvement for the formation of a modality of emotional reactions. Data may provide guidance for developing treatment strategies for neuropsychiatric diseases related to the malfunction of the reward system.

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Salomons, Tim V., Robin Nusslock, Allison Detloff, Tom Johnstone, and Richard J. Davidson. "Neural Emotion Regulation Circuitry Underlying Anxiolytic Effects of Perceived Control over Pain." Journal of Cognitive Neuroscience 27, no. 2 (February 2015): 222–33. http://dx.doi.org/10.1162/jocn_a_00702.

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Anxiolytic effects of perceived control have been observed across species. In humans, neuroimaging studies have suggested that perceived control and cognitive reappraisal reduce negative affect through similar mechanisms. An important limitation of extant neuroimaging studies of perceived control in terms of directly testing this hypothesis, however, is the use of within-subject designs, which confound participants' affective response to controllable and uncontrollable stress. To compare neural and affective responses when participants were exposed to either uncontrollable or controllable stress, two groups of participants received an identical series of stressors (thermal pain stimuli). One group (“controllable”) was led to believe they had behavioral control over the pain stimuli, whereas another (“uncontrollable”) believed they had no control. Controllable pain was associated with decreased state anxiety, decreased activation in amygdala, and increased activation in nucleus accumbens. In participants who perceived control over the pain, reduced state anxiety was associated with increased functional connectivity between each of these regions and ventral lateral/ventral medial pFC. The location of pFC findings is consistent with regions found to be critical for the anxiolytic effects of perceived control in rodents. Furthermore, interactions observed between pFC and both amygdala and nucleus accumbens are remarkably similar to neural mechanisms of emotion regulation through reappraisal in humans. These results suggest that perceived control reduces negative affect through a general mechanism involved in the cognitive regulation of emotion.

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Hagan, Mary M., Stephen C. Benoit, Paul A. Rushing, Laurel M. Pritchard, Stephen C. Woods, and Randy J. Seeley. "Immediate and Prolonged Patterns of Agouti-Related Peptide-(83–132)-Induced c-Fos Activation in Hypothalamic and Extrahypothalamic Sites*." Endocrinology 142, no. 3 (March 1, 2001): 1050–56. http://dx.doi.org/10.1210/endo.142.3.8018.

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Abstract Several lines of evidence substantiate the important role of the central nervous system melanocortin 3- and 4-receptor (MC3/4-R) system in the control of food intake and energy balance. Agouti-related peptide (AgRP), an endogenous antagonist of these receptors, produces a robust and unique pattern of increased food intake that lasts up to 7 days after a single injection. Little is known about brain regions that may mediate this powerful effect of AgRP on food intake. To this end we compared c-Fos-like immunoreactivity (c-FLI) in several brain sites of rats injected intracerebroventricularly with 1 nmol AgRP-(83–132) 2 and 24 h before death and compared c-FLI patterns to those induced by another potent orexigenic peptide, neuropeptide Y (NPY). Although both NPY and AgRP induced c-FLI in hypothalamic areas, AgRP also produced increased c-FLI in the accumbens shell and lateral septum. Although NPY elicited no changes in c-FLI 24 h after administration, AgRP induced c-FLI in the accumbens shell, nucleus of the solitary tract, central amygdala, and lateral hypothalamus. These results indicate that an NPY-like hypothalamic circuit mediates the short-term effects of AgRP, but that the unique sustained effect of AgRP on food intake involves a complex circuit of key extrahypothalamic reward and feeding regulatory nuclei.

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Gruber, Aaron J., Elizabeth M. Powell, and Patricio O'Donnell. "Cortically Activated Interneurons Shape Spatial Aspects of Cortico-Accumbens Processing." Journal of Neurophysiology 101, no. 4 (April 2009): 1876–82. http://dx.doi.org/10.1152/jn.91002.2008.

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Basal ganglia circuits are organized as parallel loops that have been proposed to compete in a winner-take-all fashion to determine the appropriate behavioral outcome. However, limited experimental support for strong lateral inhibition mechanisms within striatal regions questions this model. Here, stimulation of the prefrontal cortex (PFC) using naturally occurring bursty patterns inhibited firing in most nucleus accumbens (NA) projection neurons. When an excitatory response was observed for one stimulation site, neighboring PFC sites evoked inhibition in the same neuron. Furthermore, PFC stimulation activated interneurons, and PFC-evoked inhibition was blocked by GABAA antagonists in corticoaccumbens slice preparations. Thus bursting PFC activity recruits local inhibition in the NA, shaping responses of projection neurons with a topographical arrangement that allows inhibition among parallel corticoaccumbens channels. The data indicate a high order of information processing within striatal circuits that should be considered in models of basal ganglia function and disease.

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Quiñones-Hinojosa, Alfredo, Brian E. Derrick, Edwin J. Barea-Rodriguez, Patricia H. Janak, and Joe L. Martinez. "Long-term potentiation at the lateral perforant path-nucleus accumbens synapse in the rat in vivo." Psychobiology 26, no. 3 (September 1998): 169–75. http://dx.doi.org/10.3758/bf03330605.

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West, Thomas E. G., and Roy A. Wise. "Effects of naltrexone on nucleus accumbens, lateral hypothalamic and ventral tegmental self-stimulation rate—frequency functions." Brain Research 462, no. 1 (October 1988): 126–33. http://dx.doi.org/10.1016/0006-8993(88)90594-x.

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Oterdoom, D. L. Marinus, Gertjan van Dijk, Martijn H. P. Verhagen, V. Carel R. Jiawan, Gea Drost, Marloes Emous, André P. van Beek, and J. Marc C. van Dijk. "Therapeutic potential of deep brain stimulation of the nucleus accumbens in morbid obesity." Neurosurgical Focus 45, no. 2 (August 2018): E10. http://dx.doi.org/10.3171/2018.4.focus18148.

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OBJECTIVEMorbid obesity is a growing problem worldwide. The current treatment options have limitations regarding effectiveness and complication rates. New treatment modalities are therefore warranted. One of the options is deep brain stimulation (DBS) of the nucleus accumbens (NAC). This review aims to summarize the current knowledge on NAC-DBS for the treatment of morbid obesity.METHODSStudies were obtained from multiple electronic bibliographic databases, supplemented with searches of reference lists. All animal and human studies reporting on the effects of NAC-DBS on body weight in morbidly obese patients were included. Articles found during the search were screened by 2 reviewers, and when deemed applicable, the relevant data were extracted.RESULTSFive relevant animal experimental papers were identified, pointing toward a beneficial effect of high-frequency stimulation of the lateral shell of the NAC. Three human case reports show a beneficial effect of NAC-DBS on body weight in morbidly obese patients.CONCLUSIONSThe available literature supports NAC-DBS to treat morbid obesity. The number of well-conducted animal studies, however, is very limited. Also, the optimal anatomical position of the DBS electrode within the NAC, as well as the optimal stimulation parameters, has not yet been established. These matters need to be addressed before this strategy can be considered for human clinical trials.

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Marcos, José Luis, Rossy Olivares-Barraza, Karina Ceballo, Melisa Wastavino, Víctor Ortiz, Julio Riquelme, Jonathan Martínez-Pinto, Pablo Muñoz, Gonzalo Cruz, and Ramón Sotomayor-Zárate. "Obesogenic Diet-Induced Neuroinflammation: A Pathological Link between Hedonic and Homeostatic Control of Food Intake." International Journal of Molecular Sciences 24, no. 2 (January 11, 2023): 1468. http://dx.doi.org/10.3390/ijms24021468.

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Obesity-induced neuroinflammation is a chronic aseptic central nervous system inflammation that presents systemic characteristics associated with increased pro-inflammatory cytokines such as interleukin 1 beta (IL-1β) and interleukin 18 (IL-18) and the presence of microglia and reactive astrogliosis as well as the activation of the NLRP3 inflammasome. The obesity pandemic is associated with lifestyle changes, including an excessive intake of obesogenic foods and decreased physical activity. Brain areas such as the lateral hypothalamus (LH), lateral septum (LS), ventral tegmental area (VTA), and nucleus accumbens (NAcc) have been implicated in the homeostatic and hedonic control of feeding in experimental models of diet-induced obesity. In this context, a chronic lipid intake triggers neuroinflammation in several brain regions such as the hypothalamus, hippocampus, and amygdala. This review aims to present the background defining the significant impact of neuroinflammation and how this, when induced by an obesogenic diet, can affect feeding control, triggering metabolic and neurological alterations.

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Tandon, Shashank, Kristen A. Keefe, and Sharif A. Taha. "Mu opioid receptor signaling in the nucleus accumbens shell increases responsiveness of satiety-modulated lateral hypothalamus neurons." European Journal of Neuroscience 45, no. 11 (May 4, 2017): 1418–30. http://dx.doi.org/10.1111/ejn.13579.

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Vásquez, Bélgica, and Mario Cantín. "Factors and Mechanisms Involved in Eating Behavior: a Current Status at Molecular Biology." International Journal of Medical and Surgical Sciences 1, no. 2 (October 26, 2018): 191–99. http://dx.doi.org/10.32457/ijmss.2014.023.

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By studying the human genome and advances in molecular biology, currently can predict interactions between the genome and food components in order to obtain information about the role of diet in maintaining health and in the prevention, initiation, development and progression or severity of a disease like obesity. The aim of this review was to present the current understanding of the factors that normally regulate eating behavior alteration, and the mechanisms involved and associated with molecular biology. About 42 genes related to the regulation of feeding, expressing at the nucleus accumbens, ventral tegmental area, nucleus of the solitary tract, the lateral hypothalamus, arcuate nucleus, paraventricular, ventromedial and dorsomedial hypothalamus. There are specific brain mechanisms that regulate hunger and satiety, which would be in constant interaction with mechanisms known as "wanting" and "liking" circuits modulated by reward, pleasure and addiction. The phenotypic expression of eating behavior is complex by genetic variability, whose behavior is defined by the interaction of genetic condition (innate), environmental experience and learning (acquired characteristics), which structured eating behavior. Altering the genes and circuits involved would be involved as a cause in eating disorders.

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Hauptman, Jason S., Antonio A. F. DeSalles, Randall Espinoza, Mark Sedrak, and Warren Ishida. "Potential surgical targets for deep brain stimulation in treatment-resistant depression." Neurosurgical Focus 25, no. 1 (July 2008): E3. http://dx.doi.org/10.3171/foc/2008/25/7/e3.

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Object The goal of this study was to evaluate the definition of treatment-resistant depression (TRD), review the literature regarding deep brain stimulation (DBS) for TRD, and identify potential anatomical and functional targets for future widespread clinical application. Methods A comprehensive literature review was performed to determine the current status of DBS for TRD, with an emphasis on the scientific support for various implantation sites. Results The definition of TRD is presented, as is its management scheme. The rationale behind using DBS for depression is reviewed. Five potential targets have been identified in the literature: ventral striatum/nucleus accumbens, subgenual cingulate cortex (area 25), inferior thalamic peduncle, rostral cingulate cortex (area 24a), and lateral habenula. Deep brain stimulation electrodes thus far have been implanted and activated in only the first 3 of these structures in humans. These targets have proven to be safe and effective, albeit in a small number of cases. Conclusions Surgical intervention for TRD in the form of DBS is emerging as a viable treatment alternative to existing modalities. Although the studies reported thus far have small sample sizes, the results appear to be promising. Various surgical targets, such as the subgenual cingulate cortex, inferior thalamic peduncle, and nucleus accumbens, have been shown to be safe and to lead to beneficial effects with various stimulation parameters. Further studies with larger patient groups are required to adequately assess the safety and efficacy of these targets, as well as the optimal stimulation parameters and long-term effects.

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Poplyak, Mariya Olegovna, Artem Gennad’evich Trufanov, Aleksandr Vasil’evich Temniy Aleksandr Vasil’evich Temniy, Aleksandr Yur’evich Efimtsev, Oleg Borisovich Chakchir, Alexei Vladimirovich Miheev, Dmitrij Igorevich Skulyabin, et al. "Subcortical lesions in various phenotypes of multiple sclerosis and their prognostic significance." Vestnik nevrologii, psihiatrii i nejrohirurgii (Bulletin of Neurology, Psychiatry and Neurosurgery), no. 5 (April 18, 2021): 346 (404)—357 (411). http://dx.doi.org/10.33920/med-01-2105-03.

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Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease that affects the central nervous system, mainly in young people, and leads to inevitable disability. The purpose of the study is to determine the degree of involvement of subcortical structures in the pathological process in multiple sclerosis and to assess their prognostic significance. 80 patients with relapsing-remitting (n=48) and secondary progressive (n=32) phenotypes of MS were examined; the control group consisted of 20 healthy people of the corresponding age and gender. Clinical assessment was carried out on the following scales: EDSS, MSSS, MMSE, FAB, MoCA, SDMT, Beck’s test and HADS. All patients underwent MRI of the brain and MR-morphometry using the Freesurfer 6.0 software. In patients with multiple sclerosis, the neurodegenerative process is represented by a decrease in the volumes of the caudate nucleus and putamen, an increase in the volume of the third and lateral ventricles, an increase in CSF volume, and the presence of «black holes». The volume of the third and lateral ventricles, as well as the volume of CSF (general neurodegeneration), depends on the duration of the disease. The degree of disability (EDSS) is influenced by the volumes of the caudate nucleus, globus pallidus, nucleus accumbens, and brainstem. In turn, cognitive decline is influenced by the volume of the thalamus, basal nuclei, brainstem, the volume of the lateral ventricles, and a decrease in the volume of the white matter and cerebellar cortex. Thus, dynamic assessment and monitoring of the volume of subcortical structures of the brain using MR-morphometry can act as a prognostic factor in the transition of the relapsing-relapsing phenotype of multiple sclerosis to the secondary progressive phenotype. English version of this article on pp. 404-411 is available at URL: https://panor.ru/articles/subcortical-brain-lesions-in-different-phenotypes-of-multiple-sclerosis-and-their-prognostic-significance/63941.html

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Ciriello, John, and Michael B. Gutman. "Functional identification of central pressor pathways originating in the subfornical organ." Canadian Journal of Physiology and Pharmacology 69, no. 7 (July 1, 1991): 1035–45. http://dx.doi.org/10.1139/y91-154.

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The functional projections from pressor sites in the subfornical organ (SFO) were identified using the 2-deoxyglucose (2-DG) autoradiographic method in urethane-anesthetized, sinoaortic-denervated rats. Autoradiographs of brain and spinal cord sections taken from rats whose SFO was continuously stimulated electrically for 45 min with stereotaxically placed monopolar electrodes (150 μA, 1.5-ms pulse duration, 15 Hz) following injection of tritiated 2-DG were compared with control rats that received intravenous infusions of pressor doses of phenylephrine to mimic the increase in arterial pressure observed during SFO stimulation. Comparisons were also made to autoradiographs from rats in which the ventral fornical commissure (CFV), just dorsal to the SFO, was electrically stimulated. The pressor responses during either electrical stimulation of the SFO or intravenous infusion of phenylephrine were similar in magnitude. On the other hand, stimulation of the CFV did not elicit a significant pressor response. Electrical stimulation of the SFO increased 2-DG uptake, in comparison to the phenylephrine-infused rats, in the nucleus triangularis, septofimbrial nucleus, lateral septal nucleus, nucleus accumbens, bed nucleus of the stria terminalis, dorsal and ventral nucleus medianus (median preoptic nucleus), paraventricular nucleus of the thalamus, hippocampus, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus of the hypothalamus, and the intermediolateral nucleus of and central autonomic area of the thoracic spinal cord. In contrast, in rats whose CFV was stimulated, these nuclei did not demonstrate changes in 2-DG uptake compared with control animals that received pressor doses of phenylephrine. These data have demonstrated some of the components of the neural circuitry likely involved in mediating the pressor responses to stimulation of the SFO and the corrective responses to activation of the SFO by disturbances to circulatory and fluid balance homeostasis.Key words: cardiovascular reflex pathways, drinking, median preoptic nucleus, osmoreceptors, paraventricular nucleus of the hypothalamus, supraoptic nucleus.

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Lee, Hye-Jung, Bombi Lee, Sun-Hye Choi, Dae-Hyun Hahm, Mi-Rye Kim, Pyung-Ui Roh, Kwang-Ho Pyun, Gregory Golden, Chae-Ha Yang, and Insop Shim. "Electroacupuncture Reduces Stress-Induced Expression of c-Fos in the Brain of the Rat." American Journal of Chinese Medicine 32, no. 05 (January 2004): 795–806. http://dx.doi.org/10.1142/s0192415x04002405.

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We have previously shown that electroacupuncture (EA) at Shaohai and Neiguan ( HT 3- PC 6) points significantly attenuated stress-induced peripheral responses, including increases in blood pressure, heart rate and plasma catecholamines. In this study, we examined the central effect of EA on the expression of c-fos, one of the immediate-early genes in the brain of rats subjected to immobilization stress. Immobilization stress (180 minutes) preferentially produced a significant increase in Fos-like immunoreactivity (FLI) in stress-relevant regions including the paraventricular hypothalamic nucleus (PVN), arcuate nucleus (ARN), supraoptic nucleus (SON), suprachiasmatic nucleus (SCN), medial amygdaloid nucleus (AMe), bed nucleus of the stria terminalis (BST), hippocampus, lateral septum (LS), nucleus accumbens, and the locus coeruleus (LC). EA (3 Hz, 0.2 ms rectangular pulses, 20 mA) at HT 3- PC 6 on the heart and pericardium channels for 30 minutes during stress, significantly attenuated stress-induced FLI in the parvocellular PVN, SON, SCN, AMe, LS and the LC. However, EA stimulations at HT 3- PC 6 had no effect on FLI in the magnocelluar PVN, ARN, BST or the hippocampus. EA stimulation at HT 3- PC 6 had a greater inhibitory effect on stress-induced FLI than that at TE 5- LI 11, the triple energizer and large intestine meridian, or non-acupoints. These results demonstrated that EA attenuated stress-induced c-fos expression in brain areas. These results suggest that decreased c-fos expression in hypothalamic and LC neurons, among stress-related areas, may reflect the integrative action of acupuncture in stress response.

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Fraser, Kurt M., and Patricia H. Janak. "Long-lasting contribution of dopamine in the nucleus accumbens core, but not dorsal lateral striatum, to sign-tracking." European Journal of Neuroscience 46, no. 4 (August 2017): 2047–55. http://dx.doi.org/10.1111/ejn.13642.

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Stratford, Thomas R., and David Wirtshafter. "Evidence that the nucleus accumbens shell, ventral pallidum, and lateral hypothalamus are components of a lateralized feeding circuit." Behavioural Brain Research 226, no. 2 (January 2012): 548–54. http://dx.doi.org/10.1016/j.bbr.2011.10.014.

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Lerma-Cabrera, Jose M., Francisca Carvajal, Gabriela Chotro, Mirari Gaztañaga, Montserrat Navarro, Todd E. Thiele, and Inmaculada Cubero. "MC4-R signaling within the nucleus accumbens shell, but not the lateral hypothalamus, modulates ethanol palatability in rats." Behavioural Brain Research 239 (February 2013): 51–54. http://dx.doi.org/10.1016/j.bbr.2012.10.055.

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Kirouac, G. J., and P. K. Ganguly. "Topographical organization in the nucleus accumbens of afferents from the basolateral amygdala and efferents to the lateral hypothalamus." Neuroscience 67, no. 3 (August 1995): 625–30. http://dx.doi.org/10.1016/0306-4522(95)00013-9.

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Bystrowska, Beata, Małgorzata Frankowska, Irena Smaga, Ewa Niedzielska-Andres, Lucyna Pomierny-Chamioło, and Małgorzata Filip. "Cocaine-Induced Reinstatement of Cocaine Seeking Provokes Changes in the Endocannabinoid and N-Acylethanolamine Levels in Rat Brain Structures." Molecules 24, no. 6 (March 21, 2019): 1125. http://dx.doi.org/10.3390/molecules24061125.

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There is strong support for the role of the endocannabinoid system and the noncannabinoid lipid signaling molecules, N-acylethanolamines (NAEs), in cocaine reward and withdrawal. In the latest study, we investigated the changes in the levels of the above molecules and expression of cannabinoid receptors (CB1 and CB2) in several brain regions during cocaine-induced reinstatement in rats. By using intravenous cocaine self-administration and extinction procedures linked with yoked triad controls, we found that a priming dose of cocaine (10 mg/kg, i.p.) evoked an increase of the anadamide (AEA) level in the hippocampus and prefrontal cortex only in animals that had previously self-administered cocaine. In the same animals, the level of 2-arachidonoylglycerol (2-AG) increased in the hippocampus and nucleus accumbens. Moreover, the drug-induced relapse resulted in a potent increase in NAEs levels in the cortical areas and striatum and, at the same time, a decrease in the tissue levels of oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) was noted in the nucleus accumbens, cerebellum, and/or hippocampus. At the level of cannabinoid receptors, a priming dose of cocaine evoked either upregulation of the CB1 and CB2 receptors in the prefrontal cortex and lateral septal nuclei or downregulation of the CB1 receptors in the ventral tegmental area. In the medial globus pallidus we observed the upregulation of the CB2 receptor only after yoked chronic cocaine treatment. Our findings support that in the rat brain, the endocannabinoid system and NAEs are involved in cocaine induced-reinstatement where these molecules changed in a region-specific manner and may represent brain molecular signatures for the development of new treatments for cocaine addiction.

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Journal articles on the topic 'Lateral nucleus accumbens'

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