Feldman’s Article Review
The article, “A neurobiological model for the effects of early brainstem functioning on the development of behavior and emotion regulation in infants: Implications for prenatal risk”, by Geva and Feldman (2008) proposes a theoretical model that employs the three observational levels to study prenatal risk. The study focuses on physiological control of cyclic processes and integration in the sensory-related to the brainstem, control of the capacities of emotion and attention involving the brainstem and limbic systems. The study also focuses on complex results involving the intactness of the brainstem, as well as the limbic system.
The study largely reviews previous studies as support to tackle its study topic. Studies indicate that at late gestation, substantial brainstem developmental transformations occur and, thus, prenatal and perinatal risk can affect the brainstem, as well as the heart and lung physiological homeostatic control. Brainstem dysfunction has been commonly observed in preterm infants. Myelination in the early maturation of the structures of the brainstem in preterm infants explicitly defines the possible links involving the brainstem dysfunction and vertical integration disruption risk.
Particular prenatal and perinatal vulnerabilities that affect myelination functions of the synapse in the brainstem are bound to affect adaptive self-control development. Studies on premature infants have shown a link between CNS defects and poor results. It has been determined that neuronal pathologies are detectable in the brainstem in about 71% of interventricular hemorrhagic infants. Moreover, MRI studies indicate broad brainstem involvement in this disorder. It is postulated that trauma in the early brainstem affects physiological control directly in the early stages of life. This may be evident in the autonomic nervous system, circadian control of arousal, and visceral homeostasis modulation. These brainstem-mediated systems indicate a link to emotional development and regulation of attention in infants.
Though brain trauma has been shown to resolve typically in the neonatal stage, its physiological, as well as behavioral effects can be evident than if one seeks the brainstem-mediated function mechanisms. After 3 months, development shifts to the sensory-specific attention during which adaptive coordination of alertness and distress during the processing of information is attained. Then the development extends to connectivity to the limbic system. No data has been provided regarding neuro-pathogenesis, resulting in dysregulation of emotions yet; despite rich information linking physiological control and results in preterm infants. A conceptual model has been used to describe the control of behavioral manifestations in the changes relating to neurobiological maturation due to time, neural activity, and stimulation exposure. Two paths are used to provide evidence of a direct and mediated relationship; a link between brainstem dysfunction and cognitive, as well as inhibitory control and a link between brainstem dysfunction and socio-emotional self-control.
The model of vertical-integration explains many vital issues including perinatal, as well as prenatal trauma and recovery. The model further explains the neurological foundation of emotions and self-control, as well as the results of environmental shaping of particular pathological processes in prenatal and perinatal stages. Therefore, this progression underscores the importance of evaluating brainstem dysfunctions as they can serve as vital pointers of the vulnerabilities of the emergence of the abilities of self-control. This study proposes an ABR assessment in premature infants in the neonatal stage because it comprises particular characteristics identifiable based on maturation.
The article concludes with a suggestion that early assessments of the brainstem and the other lower-level brain structures among the preterm births are vital and can be pointers of self-control deficiencies. This evaluation is specifically essential in infants born before full brainstem maturation. Determination of dysfunctions of the brainstem helps target infants vulnerable to self-control deficiencies and can permit interventions that will boost self-regulatory difficulties.
Jutras-Aswad, & DiNieri Article Review
The article, “Neurobiological consequences of maternal cannabis on human fetal development and its neuropsychiatric outcome” by Jutras-Aswad, and DiNieri (2009) seeks to review the neurobiological consequences that accompany exposure to developmental cannabinoid to the brain development during human fetal life. The chief psychoactive ingredient in cannabis is D9-tetrahydrocannabinol (THC), and studies show that a third of it is capable of traversing the placenta upon smoking cannabis. This causes worry for developing fetus due to maternal cannabis consumption.
This article hypothesizes that perinatal exposure to THC affects the fundamental process of development, specifically impairment of the connectivity between the regions of the brain important in mood, cognition, as well as motivation establishment. This renders the neural circuits susceptible to dysfunction in later life, which may affect sensitivity to events of development and stressors from the environment that can encourage neuropsychiatric disorders. To achieve the objective of this article, the authors drew evidence mostly from previous human neurobiological studies and a bit of study in animal models. The study is justified by the fact that despite numerous literature documenting adverse effects of cannabis use, information about neurobiological effects on the fetal development of the brain and this article adds to this limited literature.
Endocannabinoids (ECB) signaling fundamentally occurs at the synapse with an explicit continuum of the deed from the establishment of the synapse in early synaptic function neurodevelopment in the adult brain. eCBs exert their impacts mainly through the cannabinoid CB1 (emerges in early brain developments) and CB2 receptors and GPR55. Besides the CB1R, the THC and eCBs, as well, work as ligands for other receptors like the CB2R (limited to the marginal immune system, and partly in microglia cells). THC activates GPR55 directly.
This study used human postmortem of the brain of the fetus of mid-gestational maternal subjects exposed to cannabis that had begun showing early insights to the molecular, as well as the biochemical changes. The study did not determine substantial changes in the expression of CB1R mRNA in all the areas investigated because of cannabis use. In the rodent models, no alterations to CB1R mRNA were observed due to THC exposure, despite other studies indicating there are alterations. The authors, nevertheless, state that it is still not yet possible to rule out the potential CB1R function coupling impairment since THC results in brain down-regulation and desensitization that is dependent on the region, as well as the time. There is still limited study on this topic, thus the authors have recommended dipper research.
Dopamine regulates the actions disrupted due to THC exposure. Many studies indicate that exposure to cannabis hampers dopamine system maturation. Evidence depicts that a strong interaction of ECB and opioid networks is related to reward and behaviors of addiction. Data suggests that exposure to cannabis in ontogeny affects some endogenous opioid network components in the limbic structures, which persist into adulthood. Maternal THC exposure reduces serotonin and can contribute to dysregulation of moods and depression abnormalities. Studies have also indicated that the use of cannabis in women resulted in long-term abnormalities in behavior and cognitive development in their offspring.
The article closes with a conclusion that the impact of cannabis on the developmental brain, behavior, and mental health is yet to be fully understood because of the scantiness of scientific research on this topic, thus a recommendation for further research to increase insight on existing data is called for.
Schepis, Adinoff, & Rao, Article Review
The article, “Neurobiological process in adolescent addictive disorders” by Schepis, Adinoff, and Rao (2008) tries to define the etiological factors of addiction in adolescents and the existing evidence that incriminate diverse means in development. The adolescent stage is vulnerable to substance experimentation, which is associated with increased adulthood substance use disorder (SUD) rates. Factors of neurobiological development, including normative (frontal-limbic connections that are immature, underdeveloped frontal lobe) and non-normative (poorer serotonergic function, the atypical function of the hypothalamic-pituitary-adrenal axis), can predispose adolescents to susceptibility to SUD since this is a stage of immense neurobiological transformations.
Substance use is very costly to society, and it is evident that this is a common phenomenon among youths; about 60% of drug abusers are initiated to substance abuse before or at the age of 18 years. For cigarettes and alcohol, the rate is about 80%. Moreover, early substance use increases the chances of using other substances and the progression to SUD in adulthood. This study is, thus, rightly justified on the basis that to limit these high costs, morbidity, as well as mortality because of addiction, prevention or early management of substance use is indispensable, but this is only possible when there is an understanding of the addiction pathophysiology in adolescents. This is what this article seeks to study.
This study purely derives from diverse previous researches. Specifically, the study targets factors related to or leading to diagnosable intensity of substance use as opposed to factors leading to experimental use solely. In the neuroscience of adolescent development, the study reviewed studies conducted on animals and humans. Findings indicate that adolescence is the stage of highest neural growth, transformation, and maturation. This is where completion of development of executive (neurocognitive) functions is reached, and this is dependent on myelination, as well as synaptic pruning. Myelination permits faster processing and circuit concentration to respond to rapid environmental dictates. In synaptic pruning, connections responsible for responding to the environment are sustained and strengthened and the others are eliminated.
Adolescents experience dramatic changes in almost all neurotransmitter systems, but relevant to SUD development, alterations in dopamine (DA) (important mesolimbic pathway). DA is released in response to environmental forces like food, drugs, and water. Studies in animals and humans show that DA receptors reach climax early in development and are removed in adolescence. The maturation of cannabinoid, GABAergic and glutaminergic systems also occur concurrently with DA systems, and they affect the mesolimbic circuit of the DA. DA and glutamate transmitters are stimulatory (encode appetitive actions, like seeking of drugs), GABA and 5-HT neurotransmitters are suppressive (regulate and encode harm-avoidance actions). Studies indicate that more stimulatory transmitters are released in adolescence. These are bound to influence addictive substance experimentation due to the high stimulatory to suppressive aspects ratio in the adolescence stage.
Neurobiological transformations in adolescents influence behavioral factors associated with SUD development like peer affiliation, risk-taking, reduced parental monitoring, impulsivity, impaired decision-making, labile emotions, plus other neurobehavioral changes that are controlled by the frontal lobes. While these are common to all adolescents, they are amplified in those at high risk of SUD. Neurobiological markers of those vulnerable to SUD have been found to correspond to disinhibition, as well as negative effects; thus, they can be useful endophenotypes related to SUD.
This review brings out the etiological factors behind the experimentation and substance use in adolescents leading to SUD. The objective of the study is fully attained. The paper concludes by suggesting future research to dig into the role played by genetic factors in SUD development and further research on contributions of 5-HT, HPA, and the neural circuit of frontal-striatal-thalamus to SUD development.
References
Geva, R., & Feldman R. (2008). A neurobiological model for the effects of early brainstem functioning on the development of behavior and emotion regulation in infants: implications for prenatal risk. Journal of Child Psychology and Psychiatry, 49(10), 1031–1041.
Jutras-Aswad, D., & DiNieri, J. (2009). Neurobiological consequences of maternal cannabis on human fetal development and its neuropsychiatric outcome. Eur Arch Psychiatry Clinical Neuroscience, 259, 395–412.
Schepis, T. S., Adinoff, B., & Rao, U. (2008), Neurobiological process in adolescent addictive disorders. The American Journal on Addictions, 17, 6–23.