Abstract:Background: Brain-derived neurotrophic factor (BDNF) plays important roles in neurotransmitter release and synaptic plasticity and has been hypothesized to be involved in the development and maintenance of addictive disorders. The objective of this study was to investigate alterations of BDNF expression in a non-substance-related addiction, i.e. pathological gambling (PG). Methods: Serum levels of BDNF were assessed in male patients with PG (n = 14) and healthy control subjects (n = 13) carefully matched for s… Show more
“…BDNF seems likely to play a role in addiction for other reasons also. For example, BDNF serum levels are increased in individuals with addictive behaviors such as pathological gambling (Geisel et al, 2012) and opiate dependence (Heberlein et al, 2011). Serum levels of BDNF are also elevated in naïve individuals following exposure to Δ 9 -tetrahydrocannabinol (THC), the main psychoactive component in marijuana, a commonly abused drug (D’Souza et al, 2009).…”
The neurotrophin BDNF and the steroid hormone estrogen exhibit potent effects on hippocampal neurons during development and in adulthood. BDNF and estrogen have also been implicated in the etiology of diverse types of neurological disorders or psychiatric illnesses, or have been discussed as potentially important in treatment. Although both are typically studied independently, it has been suggested that BDNF mediates several of the effects of estrogen in hippocampus, and that these interactions play a role in the normal brain as well as disease. Here we focus on the mossy fiber (MF) pathway of the hippocampus, a critical pathway in normal hippocampal function, and a prime example of a location where numerous studies support an interaction between BDNF and estrogen in the rodent brain. We first review the temporal and spatially-regulated expression of BDNF and estrogen in the MFs, as well as their receptors. Then we consider the results of studies that suggest that 17β-estradiol alters hippocampal function by its influence on BDNF expression in the MF pathway. We also address the hypothesis that estrogen influences hippocampus by mechanisms related not only to the mature form of BDNF, acting at trkB receptors, but also by regulating the precursor, proBDNF, acting at p75NTR. We suggest that the interactions between BDNF and 17β-estradiol in the MFs are potentially important in the normal function of the hippocampus, and have implications for sex differences in functions that depend on the MFs and in diseases where MF plasticity has been suggested to play an important role, Alzheimer’s disease, epilepsy and addiction.
“…BDNF seems likely to play a role in addiction for other reasons also. For example, BDNF serum levels are increased in individuals with addictive behaviors such as pathological gambling (Geisel et al, 2012) and opiate dependence (Heberlein et al, 2011). Serum levels of BDNF are also elevated in naïve individuals following exposure to Δ 9 -tetrahydrocannabinol (THC), the main psychoactive component in marijuana, a commonly abused drug (D’Souza et al, 2009).…”
The neurotrophin BDNF and the steroid hormone estrogen exhibit potent effects on hippocampal neurons during development and in adulthood. BDNF and estrogen have also been implicated in the etiology of diverse types of neurological disorders or psychiatric illnesses, or have been discussed as potentially important in treatment. Although both are typically studied independently, it has been suggested that BDNF mediates several of the effects of estrogen in hippocampus, and that these interactions play a role in the normal brain as well as disease. Here we focus on the mossy fiber (MF) pathway of the hippocampus, a critical pathway in normal hippocampal function, and a prime example of a location where numerous studies support an interaction between BDNF and estrogen in the rodent brain. We first review the temporal and spatially-regulated expression of BDNF and estrogen in the MFs, as well as their receptors. Then we consider the results of studies that suggest that 17β-estradiol alters hippocampal function by its influence on BDNF expression in the MF pathway. We also address the hypothesis that estrogen influences hippocampus by mechanisms related not only to the mature form of BDNF, acting at trkB receptors, but also by regulating the precursor, proBDNF, acting at p75NTR. We suggest that the interactions between BDNF and 17β-estradiol in the MFs are potentially important in the normal function of the hippocampus, and have implications for sex differences in functions that depend on the MFs and in diseases where MF plasticity has been suggested to play an important role, Alzheimer’s disease, epilepsy and addiction.
“…Several studies have reported that BDNF is elevated in patients with pathological gambling ( Angelucci et al., 2013 ; Choi et al., 2016 ; Geisel, Panneck, Hellweg, Wiedemann, & Müller, 2015 ). Researchers have suggested that the increased BDNF in pathological gamblers is related to altered dopaminergic transmission in the ventral tegmental area and nucleus accumbens, which are central components of the brain’s reward system ( Geisel, Banas, Hellweg, & Müller, 2012 ; Pu, Liu, & Poo, 2006 ).…”
Background and aimsThis study aimed to evaluate the association between the severity of pathological gambling, serum brain-derived neurotrophic factor (BDNF) level, and the characteristics of quantitative electroencephalography (EEG) in patients with gambling disorder.MethodsA total of 55 male patients aged 18–65 with gambling disorder participated. The severity of pathological gambling was assessed with the nine-item Problem Gambling Severity Index from the Canadian Problem Gambling Index (CPGI-PGSI). The Beck Depression Inventory and Lubben Social Network Scale were also assessed. Serum BDNF levels were assessed from blood samples. The resting-state EEG was recorded while the eyes were closed, and the absolute power of five frequency bands was analyzed: delta (1–4 Hz), theta (4–8 Hz), alpha (8–12 Hz), beta (12–30 Hz), and gamma (30–50 Hz).ResultsSerum BDNF level was positively correlated with theta power in the right parietal region (P4, r = .403, p = .011), beta power in the right parietal region (P4, r = .456, p = .010), and beta power in the right temporal region (T8, r = .421, p = .008). Gambling severity (CPGI-PGSI) was positively correlated with absolute beta power in the left frontal region (F7, r = .284, p = .043) and central region [(C3, r = .292, p = .038), (C4, r = .304, p = .030)].ConclusionsThese findings support the hypothesis that right-dominant lateralized correlations between BDNF and beta and theta power reflect right-dominant brain activation in addiction. The positive correlations between beta power and the severity of gambling disorder may be associated with hyperexcitability and increased cravings. These findings contribute to a better understanding of brain-based electrophysiological changes and BDNF levels in patients with pathological gambling.
“…While the reward deficiency hypothesis states that addiction is associated with diminished striatal value signals ( 16 ), an idea supported by some studies ( 17 – 19 ), other studies have found the opposite effect ( 20 , 21 ). PG has been associated with higher levels of brain-derived neurotrophic factor (BDNF), which regulates midbrain dopamine release ( 22 , 23 ). This effect was not associated with addiction severity ( 22 ).…”
Section: Introductionmentioning
confidence: 99%
“…PG has been associated with higher levels of brain-derived neurotrophic factor (BDNF), which regulates midbrain dopamine release ( 22 , 23 ). This effect was not associated with addiction severity ( 22 ). Monetary rewards might affect the reward system of PGs differently depending on the context and that the relation to non-monetary rewards is important.…”
Addiction and pathological gambling (PG) have been consistently associated with high impulsivity and a steep devaluation of delayed rewards, a process that is known as temporal discounting (TD). Recent studies indicated that enhanced episodic future thinking (EFT) results in less impulsive TD in healthy controls (HCs). In a separate line of research, it has been suggested that non-linearities in time perception might contribute to reward devaluation during inter-temporal choice. Therefore, in addition to deficits in valuation processes and executive control, impairments in EFT and non-linearities in time perception have been hypothesized to contribute to steep TD in addiction. In this study, we explore such a potential association of impairments in EFT and time perception with steep TD in PG. We investigated 20 PGs and 20 matched HCs. TD was assessed via a standard computerized binary choice task. EFT was measured using a variation of the Autobiographical Memory Interview by Levine et al. (1). Time perception was assessed with a novel task, utilizing a non-linear rating procedure via circle-size adjustments. Groups did not differ in baseline EFT. In both groups, a power law accounted time perception best, and the degree of non-linearity in time perception correlated with discounting across groups. A multiple regression analysis across all predictors and covariates revealed that only group status (PG/HC) and depression were significantly associated with discounting behavior such that PG increased TD and depression attenuated TD. Our findings speak against the idea that steep TD in PG is due to a skewed perception of time or impairments in EFT, at least under the present task conditions. The lack of overall group differences in EFT does not rule out the possibility of more complex interactions of EFT and decision-making. These interactions might be diminished in pathological gambling or addiction more generally, when other task configurations are used.
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