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Non-Synonyms (Similar-Sounding)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Medial forebrain bundle (B&K, p. 196): A set of fibers running from olfactory regions of the cerebrum through the hypothalamus into the midbrain and pons. Its function involves regulation of basic biological drives.
Varieties of learning and developmental theories of memory
Published in Romain Meeusen, Sabine Schaefer, Phillip Tomporowski, Richard Bailey, Physical Activity and Educational Achievement, 2017
Phillip Tomporowski, Daniel M. Pendleton, Bryan A. McCullick
The neurobiology of operant learning has been studied extensively. There are specific neural pathways that are involved in the recognition of environmental cues and the initiation of motor movements. Important for the present discussion are the neural pathways that are engaged as the reinforcing consequences of actions are experienced. Animal research conducted in the mid-1950s (Olds & Milner, 1954) revealed the ‘reward centres’ of the brain; that is, structures that are involved in establishing memories of actions that lead to reward or to punishers. The medial forebrain bundle is a network of axons, primarily dopaminergic in nature, that extend between the midbrain and the rostral basal forebrain. Various tracts project to the prefrontal cortex, limbic cortex, nucleus accumbens and the hippocampus and all play roles in reinforcement circuitry.
Central Stimulant Abuse: Neurochemistry and Pharmacotherapy
Published in Mark S. Gold, Marc Galanter, Barry Stimmel, Cocaine: Pharmacology, Addiction, and Therapy, 2014
Charles A. Dackis, Mark S. Gold, A.L.C. Pottash
In his classic studies in the 1950’s, Olds found that certain discrete brain regions, which he named “pleasure centers”,5 would support electrical self-stimulation in animals. Since that time, much research has been directed toward delineating the neurochemistry and neuroanatomy of endogenous reward systems in the brain. It is now apparent that central dopamine systems are intimately involved in these pathways.6 In particular, descending reward fibers from the lateral hypothalamus project via the medial forebrain bundle to the ventral tegmentum, where they appear to synapse with major dopamine cell groups.6, 7 In fact, the interruption of dopamine neurotransmission blocks electrical self-stimulation of the lateral hypothalamus.8 The ventral tegmentum in turn projects to several other striatal, limbic and cortical dopamine areas. Specific lesions of these dopamine-containing nuclei will block the direct self-administration of cocaine into these areas.9, 10, 11 Similarly, selective dopamine receptor antagonists reduce or eliminate cocaine self-administration by animals,12 and central stimulant euphoria in humans.13, 14 These and other findings6, 15 indicate that the activation of dopamine circuits appears to mediate cocaine reward in animals, and cocaine euphoria in humans.
Neurosurgery and neuromodulation for anorexia nervosa in the 21st century: a systematic review of treatment outcomes
Published in Eating Disorders, 2022
Stuart B. Murray, Michael Strober, Reza Tadayonnejad, Ausaf A. Bari, Jamie D. Feusner
The BNST is a small gray mater structure located in the stria terminalis—a bundle of axons which connect it to the amygdaloid nuclei, which is thought to be critically involved in stress response, reward processing, and goal-directed behaviors (Dumont, 2009). Two case studies to date have targeted the (BNST). The first study was a case study of a 58-year-old woman with a primary diagnosis of major depressive disorder, comorbid anxiety, and a 44-year history of relapsing and remitting AN, whose pre-operative AN treatment was unclear (Blomstedt et al., 2017). After initially undergoing bilateral DBS to the medial forebrain bundle, the patient noted reduced depressive symptoms, although no effect on AN symptoms. This treatment was terminated (and the device explanted) after 10 months due to blurred vision. At age 58, the patient underwent a second surgery, initiating DBS to the BNST. While formal measures of AN psychopathology were not recorded, the patient noted a complete remission of food-related anxiety, such that tube feeding could be discontinued. However, the authors noted that the patient continued to habitually eat only enough to maintain a minimally stable weight, even in the absence of fear or anxiety (Blomstedt et al., 2017).
MicroRNA-185 activates PI3K/AKT signalling pathway to alleviate dopaminergic neuron damage via targeting IGF1 in Parkinson’s disease
Published in Journal of Drug Targeting, 2021
Xiaocui Qin, Xia Zhang, Pinyu Li, Min Wang, Li Yan, Peiling Pan, Hailing Zhang, Xuejun Hong, Muxi Liu, Zeqing Bao
Rats were anaesthetised with pentobarbital sodium (50 µg/kg, Chemical Reagents Shanghai Co., Ltd., Shanghai, China) and fixed in a prone position in a stereoscopic locator (RWD Life Science Co., Shenzhen, China). The skin on the head was sterilised with 75% ethanol and cut with a sharp knife to expose the skull. Started from the anterior fontanelle, two points of the medial forebrain bundle were drilled based on the Paxinos & Watson mode, one was located at 4.4 mm posterior to the anterior fontanelle, 1.2 mm to the right of the midline, and 7.8 mm below the skull, while the other one at 4.0 mm posterior to the anterior fontanelle, 0.8 mm to the right of the midline, and 8.0 mm below the inner skull. The injection doses of 6-OHDA (Sigma-Aldrich) were 2.25 µL and 2.7 µL, respectively, and rats were injected with 6-OHDA at 1 µL/min for 5 min. The rats were kept warm after the operation and raised in cages with sufficient food and water (20–25 °C, lighting time of 8.00am–8.00pm). Penicillin was used to prevent infection for 3 d at 200,000 U per day. In the same way, 2.25 µL and 2.7 µL of normal saline were injected into the medial forebrain bundle of rats as a sham control [21].
Deep brain stimulation for the treatment of severe intractable anorexia nervosa
Published in British Journal of Neurosurgery, 2019
Michał Sobstyl, Angelika Stapińska-Syniec, Marlena Sokół-Szawłowska, Anna Kupryjaniuk
The last case report describing a patient with severe MDD and concomitant AN also provided good results for both psychiatric conditions.4 In this case, a 60-year-old woman had childhood-onset anxiety and AN, with anxiety symptoms associated with food intake, restricted eating, and later, purging. She suffered from MMD with severe anxiety.4 The authors used medial forebrain bundle (MFB) – a reward-based pathway structure for permanent stimulation. MDD and AN symptoms improved up to 24 months postoperatively. Due to stimulation-induced blurred vision, the patient was implanted with two electrodes targeting the bed nucleus of the stria terminalis, the structure regarded as the major output pathway of the amygdala regulating threat and anxiety.16 An additional 12 months of follow-up provided significant improvement in depressive symptoms, and the patient's anxiety regarding food and eating vanished.4 Tube feeding was discontinued with concomitant stable food intake. Despite these improvements, her BMI decreased from 16.2 to 14.3 kg/m2 at 36 months. This weight loss could be related to outdoor activities that were not possible to perform preoperatively. This case highlights the concept that influencing the underlying neurobiological mechanisms of AN is more effective than focusing on weight gain alone as an outcome measure.4