Sensory Enrichment Therapy
Scientific research shows environmental enrichment improves the brain’s ability to overcome addiction
We believe sensory enrichment could help in the following areas:
- Fewer withdrawals symptoms,
- Fewer clients wanting to leave against professional advice,
- Improved mood regulation during and post treatment,
and even possibly
- Long term recovery with a lower rate of relapse.
How it works!
Environmental Enrichment is a field of neuroscience that studies the impact of sensory, motor, cognitive and social experiences on brain development and brain function.
Neuroplasticity, or the lifelong ability of the brain to create more neurons, more connections, and more supportive tissue, and to re-balance neurotransmitters is now widely understood.
Sensory Enrichment Therapy is a new evidence-based treatment modality that was developed by translating the protocols used in the science lab into short, fun, hands-on experiences that people can do from home and in residential programs to trigger the brain’s plasticity mechanisms.
It has been validated in randomized controlled trials with children with developmental disorders including autism spectrum disorder. Children who followed the program were 6 times more likely to achieve clinically significant gains compared to their peers who only followed standard care.
Environmental enrichment reduces heroin seeking following incubation of craving in both male and female rats
Eddy D. Barrera, Lacey Loughlin, Stephen Greenberger, Scott Ewing, Priscila Hachimine, Robert Ranaldi
Contemporary treatments for heroin use disorder demonstrate only limited efficacy when the goals are long term abstinence and prevention of relapse. We have demonstrated that environmental enrichment (EE) reduces cue-induced heroin reinstatement in male rats. The present study is an attempt to extend the “anti-relapse” effects of EE to female rats and to periods where incubation of craving is hypothesized to occur.
This experiment implemented a 3-phase procedure. In Phase 1, male and female rats were trained to self-administer heroin for 15 days. Phase 2 consisted of a 3- or 15-day forced abstinence (FA) period. In Phase 3 half of the rats were placed into EE and the other half in non-EE housing and subsequently tested for responding in extinction (no heroin or cues) for 15 days followed by a cue-induced reinstatement test.
We found that rats in the 15 days FA condition showed significantly enhanced drug seeking during extinction, irrespective of sex. We also found that EE significantly reduced this effect. During reinstatement, EE significantly reduced drug seeking in male and female rats and in both 3- and 15-day FA groups.
EE, with or without prolonged FA, effectively reduced heroin seeking in male and female rats. These findings indicate that EE can reduce drug-seeking in males and females and when putative incubation of craving (i.e., prolonged abstinence period) has occurred and suggest that it may aid in the development of future long-term behavioral treatments for individuals at risk for heroin relapse.
Environmental Enrichment Modulates Drug Addiction and Binge-Like Consumption of Highly Rewarding Substances: A Role for Anxiety and Compulsivity Brain Systems?
Rodríguez-Ortega E, Cubero I.
Drug addiction is a chronic disorder comprising components of both impulsivity and compulsivity in the so called “addiction cycle” which develops over time from early non-dependent, repetitive, binge-consumption to later post-dependent compulsive consumption. Thus, frequent binge-like intake is a typical pattern of excessive drug intake characteristic of the pre-dependent phase of the addiction cycle, which represent an important risk factor to develop addiction in vulnerable individuals. In this framework, it is of paramount interest to further understand the earliest stage of the addiction cycle so novel approaches would emerge aimed to control repetitive episodes of binge-consumption in non-dependent subjects, protecting vulnerable individuals from transition to dependence.
Environmental enrichment (EE) is a preclinical animal model in which animals are housed under novel, social enriched conditions, which allows exercising and provides sensory and cognitive stimulation.
EE promotes important improvements for a variety of cognitive processes and clear therapeutic and protective effects preventing ethanol (EtOH) and drug addiction as well.
Interestingly, recent observations suggest that EE might additionally modulate binge-like intake of highly palatable caloric substances, including EtOH, which suggests the ability of EE to regulate consumption during the initial stage of the addiction cycle.
We have proposed that EE protective and therapeutic effects on binge-consumption of palatable substances might primarily be mediated by the modulatory control that EE exerts on anxiety and impulsivity/compulsivity traits, which are all risk factors favoring transition to drug addiction.
Environmental enrichment reverses increased addiction risk caused by prenatal ethanol exposure
Wang R, Hausknecht KA, Shen YL, Haj-Dahmane S, Vezina P, Shen RY
Prenatal ethanol exposure (PE) leads to multiple cognitive and behavioral deficits including increased drug addiction risk. Previous studies have shown that the rearing environment plays a significant role in addiction propensity.
In the present study, we investigated if environmental enrichment during development could be effective in lowering the PE-induced increase in addiction risk.
To simulate heavy drinking during pregnancy in humans, pregnant Sprague-Dawley rats received ethanol (6 g/kg/day) or vehicle through intragastric gavage on gestation days 8–20. After weaning, the offspring were reared in either an enriched environment (EE) including neonatal handling and complex housing or an impoverished environment (IE) consisting of barren, single housing. Adult male offspring were then tested for locomotion, performance on the elevated plus maze, and amphetamine self-administration under a progressive ratio reinforcement schedule.
Overall, EE rats, compared to IE rats, showed reduced locomotor activity in a novel environment and lower levels of anxiety, irrespective of prenatal treatments. Prenatal ethanol exposure increased amphetamine self-administration at both doses tested (0.02 and 0.05 mg/kg/infusion) and in each case EE relative to IE reversed this effect.
These findings suggest that postnatal environmental complexity plays a determining role in addiction risk after PE.
Exposure to environmental enrichment attenuates addiction-like behavior and alters molecular effects of heroin self-administration in rats.
Additive Effects of Physical Exercise and Environmental Enrichment on Adult Hippocampal Neurogenesis in Mice
Fabel K, Wolf SA, Ehninger D, Babu H, Leal-Galicia P, Kempermann G.
Voluntary physical exercise (wheel running, RUN) and environmental enrichment both stimulate adult hippocampal neurogenesis but do so by different mechanisms. RUN induces precursor cell proliferation, whereas ENR exerts a survival-promoting effect on newborn cells. In addition, continued RUN prevented the physiologically occurring age-related decline in precursor cell in the dentate gyrus but did not lead to a corresponding increase in net neurogenesis.
We hypothesized that in the absence of appropriate cognitive stimuli the potential for neurogenesis could not be realized but that an increased potential by proliferating precursor cells due to RUN could actually lead to more adult neurogenesis if an appropriate survival-promoting stimulus follows the exercise.
We thus asked whether a sequential combination of RUN and ENR (RUNENR) would show additive effects that are distinct from the application of either paradigm alone.
We found that the effects of 10 days of RUN followed by 35 days of ENR were additive in that the combined stimulation yielded an approximately 30% greater increase in new neurons than either stimulus alone, which also increased neurogenesis.
Surprisingly, this result indicates that although overall the amount of proliferating cells in the dentate gyrus is poorly predictive of net adult neurogenesis, an increased neurogenic potential nevertheless provides the basis for a greater efficiency of the same survival-promoting stimulus.
We thus propose that physical activity can “prime” the neurogenic region of the dentate gyrus for increased neurogenesis in the case the animal is exposed to an additional cognitive stimulus, here represented by the enrichment paradigm.
Transcriptomics of Environmental Enrichment Reveals a Role for Retinoic Acid Signaling in Addiction
Zhang Yafang, Kong Fanping, Crofton Elizabeth J., Dragosljvich Steven N., Sinha Mala, Li Dingge, Fan Xiuzhen, Koshy Shyny, Hommel Jonathan D., Spratt Heidi M., Luxon Bruce A., Green Thomas A.
There exists much variability in susceptibility/resilience to addiction in humans.
The environmental enrichment paradigm is a rat model of resilience to addiction-like behavior, and understanding the molecular mechanisms underlying this protective phenotype may lead to novel targets for pharmacotherapeutics to treat cocaine addiction.
We investigated the differential regulation of transcript levels using RNA sequencing of the rat nucleus accumbens after environmental enrichment/isolation and cocaine/saline self-administration. Ingenuity Pathways Analysis and Gene Set Enrichment Analysis of 14,309 transcripts demonstrated that many biofunctions and pathways were differentially regulated. New functional pathways were also identified for cocaine modulation (e.g., Rho GTPase signaling) and environmental enrichment (e.g., signaling of EIF2, mTOR, ephrin).
However, one novel pathway stood out above the others, the retinoic acid (RA) signaling pathway. The RA signaling pathway was identified as one likely mediator of the protective enrichment addiction phenotype, an interesting result given that nine RA signaling-related genes are expressed selectively and at high levels in the nucleus accumbens shell (NAcSh).
Subsequent knockdown of Cyp26b1 (an RA degradation enzyme) in the NAcSh of rats confirmed this role by increasing cocaine self-administration as well as cocaine seeking. These results provide a comprehensive account of enrichment effects on the transcriptome and identify RA signaling as a contributing factor for cocaine addiction.
Short-term environmental enrichment is sufficient to counter stress-induced anxiety and associated structural and molecular plasticity in basolateral amygdala
A. Ashokan, A. Hegde, R. Mitra
Moderate levels of anxiety enable individual animals to cope with stressors through avoidance, and could be an adaptive trait. However, repeated stress exacerbates anxiety to pathologically high levels.
Dendritic remodeling in the basolateral amygdala is proposed to mediate potentiation of anxiety after stress. Similarly, modulation of brain-derived neurotrophic factor is thought to be important for the behavioral effects of stress.
In the present study, we investigate if relatively short periods of environmental enrichment in adulthood can confer resilience against stress-induced anxiety and concomitant changes in neuronal arborisation and brain derived neurotrophic factor within basolateral amygdala.
Two weeks of environmental enrichment countermanded the propensity of increased anxiety following chronic immobilization stress. Environmental enrichment concurrently reduced dendritic branching and spine density of projection neurons of the basolateral amygdala. Moreover, stress increased abundance of BDNF mRNA in the basolateral amygdala in agreement with the dendritic hypertrophy post-stress and role of BDNF in promoting dendritic arborisation.
In contrast, environmental enrichment prevented stress-induced rise in the BDNF mRNA abundance. Gain in body weights and adrenal weights remained unaffected by exposure to environmental enrichment.
These observations suggest that a short period of environmental enrichment can provide resilience against maladaptive effects of stress on hormonal, neuronal and molecular mediators of anxiogenesis.
Synaptic mechanism underlying serotonin modulation of transition to cocaine addiction
Li Y,Simmler L, Van Zessen R,
Flakowski J, Wan J, Deng F, Li Y, Nautiyal K, Pascoli v, Lüscher C
Over time, about 20% of chronic cocaine users lose control and become addicted. There are indications that the differential efficacy of the brain serotonin (5-HT) system may be involved in the vulnerability to drug addiction.
However, the relevant circuits and underlying cellular processes remain elusive. Li et al. discovered a synaptic mechanism in mice that underlies the modulatory role of 5-HT in reducing the likelihood of transition to compulsion and eventually addiction (see the Perspective by Miyazaki and Miyazaki). Cocaine binds to 5-HT transporters to block 5-HT reuptake. The elevated extracellular 5-HT activates 5-HT1B receptors and causes presynaptic depression of a projection from the orbitofrontal cortex to the dorsal striatum. These changes reduce the likelihood of inducing postsynaptic potentiation at these synapses, which ultimately drives compulsion. —PRS
Serotonin can prevent the development of compulsive cocaine seeking in mice.
Compulsive drug use despite adverse consequences defines addiction. While mesolimbic dopamine signaling is sufficient to drive compulsion, psychostimulants such as cocaine also boost extracellular serotonin (5-HT) by inhibiting reuptake. We used SERT Met172 knockin (SertKI) mice carrying a transporter that no longer binds cocaine to abolish 5-HT transients during drug self-administration. SertKI mice showed an enhanced transition to compulsion. Conversely, pharmacologically elevating 5-HT reversed the inherently high rate of compulsion transition with optogenetic dopamine self-stimulation. The bidirectional effect on behavior is explained by presynaptic depression of orbitofrontal cortex–to–dorsal striatum synapses induced by 5-HT via 5-HT1B receptors. Consequently, in projection-specific 5-HT1B receptor knockout mice, the fraction of individuals compulsively self-administering cocaine was elevated.
Characterization of the brain functional architecture of psychostimulant withdrawal using single-cell whole brain imaging
Adam Kimbrough, Marsida Kallupi, Lauren C. Smith, Sierra Simpson, Andres Collazo and Olivier George
Numerous brain regions have been identified as contributing to withdrawal behaviors, but unclear is the way in which these brain regions as a whole lead to withdrawal. The search for a final common brain pathway that is involved in withdrawal remains elusive. To address this question, we implanted osmotic minipumps containing either saline, nicotine (24 mg/kg/day), cocaine (60 mg/kg/day), or methamphetamine (4 mg/kg/day) for 1 week in male C57BL/6J mice. After 1 week the minipumps were removed and brains collected 8 hours (saline, nicotine and cocaine) or 12 hours (methamphetamine) after removal. We then performed single-cell whole-brain imaging of neural activity during the withdrawal period when brains were collected. We used hierarchical clustering and graph theory to identify similarities and differences in brain functional architecture. Although methamphetamine and cocaine shared some network similarities, the main common neuroadaptation between these psychostimulant drugs was a dramatic decrease in modularity, with a shift from a cortical- to subcortical-driven network, including a decrease in total hub brain regions. These results demonstrate that psychostimulant withdrawal produces the drug-dependent remodeling of functional architecture of the brain and suggest that the decreased modularity of brain functional networks and not a specific set of brain regions may represent the final common pathway associated with withdrawal.
A key aspect of treating drug abuse is understanding similarities and differences of how drugs of abuse affect the brain. In the present study we examined how the brain is altered during withdrawal from psychostimulants. We found that each drug produced a unique pattern of activity in the brain, but that brains in withdrawal from cocaine and methamphetamine shared similar features. Interestingly, we found the major common link between withdrawal from all psychostimulants, when compared to controls, was a shift in the broad organization of the brain in the form of reduced modularity. Reduced modularity has been shown in several brain disorders, including traumatic brain injury, and dementia, and may be the common link between drugs of abuse.
We are looking for addiction recovery treatment centers interested in working with us to create the next-generation residential programs.
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