Do Nuerons Dictate BehaviorJoin now to read essay Do Nuerons Dictate BehaviorContemporary behavioral endocrinology and biological neuron psychology claim that neurons play an important role in the production of behavioral differences in human and other animal behaviors. This paper critically examines these claims, which range from simple biologically determinist arguments through to more complex attempts to theorize the connected roles of the hormonal and the social.
Behavioral neuronsSciences rely on a social/biological distinction. Analyzing contemporary feminist work on the body as lived, and innovative scientific views of biologys “coaction” with the behavior, it is suggested that this distinction is limiting and requires rethinking. Rather than accusing science of essentialism and rejecting the role of the biological neuron outright, it may prove more fruitful for neurological biology to theorize the “interimplication” of the biological and the social in attempts to understand sex differences in behavior. (Lavie, 2001)
In spite of the ubiquitous periodic nature of change of behaviors, recognition of the behavior as a biological and neurological rhythm controlled by brain oscillators has been slow to come. Until the 1960s, human behavior was mostly conceptualized within the framework of homeostatic principles.
Another impediment to the recognition of the sleep-wake cycle as an endogenous biological rhythm was Nathaniel Kleitmans firm conviction that bodily rhythms were extrinsic in nature. Researchers believe that to satisfy the definition of a rhythm, a periodic “regularly recurring” change in a biological process should be “extrinsic in origin, depending upon a regular change in the environment, such as light or temperature,” and that “when fully established, it must persist for some time, even when the environmental changes are absent”. Thus, Kleitman considered biological rhythms to be conditioned responses. This explained, in his opinion, their continuation for some time after the extrinsic influences ceased. An expert on neurological functions of human behavior has pointed out in his observation on the biological and neurological functions in human behaviors by saying, The development and maintenance of behavior among human beings stems from being born into, and living in, a family and community run according to alterations of light and darkness, resulting from the period of rotation of the earth around its axis. (Lavie, 2001)
These accumulated findings linking melatonin secretion with increased sleep propensity have led to the suggestion that the endogenous cycle of melatonin is involved in the regulation of the sleep-wake cycle not by actively promoting sleep, but by inhibiting the SCN wakefulness-producing mechanism (Lavie 1997). Thus, the evening onset of melatonin secretion, which coincides with the crest of the SCN-driven arousal cycle, inhibits the wakefulness-generating mechanisms, thereby enabling the brains sleep-related structures to be activated unopposed by the drive for wakefulness. Recent evidence demonstrating that in addition to its well-known phase-shifting effects on SCN neuronal activity, melatonin also exerts acute inhibition of behavioral neurons, provides support for this hypothesis.
A few recent investigations of the circadian clock of cells of the PEA in the brain have demonstrated that melatonin stimulates the neural mechanisms of sleep-wake, with the aim of mimicking that of the endogenous circadian rhythm.
3.5. Epigenetics and Neurogenesis
Melatonin is produced and excreted in the pineal gland in all cells. Melatonin also undergoes an epigenetic response in different brain cell types. Melatonin levels have been found to decline when melatonin supplementation or other systemic administration is combined with melatonin-dependent oxidative stress: decreased TNF-α production by cell-based T cell chemokines (Makoto et al., 2002), increased TNF cell activation by TNF-α-inositol, decreased TNF-β/IL-1-induced TNF-β production, increased TNF+ T cell proliferation time and TNFα and TNF+-1-induced cell death (Sharma-Zorba et al., 1995), a critical step in maintaining cellular energy balance at the low-level (Makoto et al., 2002; Joly et al., 1995), and reduced TNF+ M cells. On the other hand, after acute stimulation of other brain cell types with endogenous melatonin, melatonin does not appear to have any protective effect against oxidative stress. In fact, this hypothesis is a bit controversial and in the current scientific literature there is no clear evidence that melatonin deficiency induces neurogenesis nor has melatonin an effect on neurogenesis. Several neurogenesis studies in the past 20 years, however, have demonstrated that melatonin deficiency and/or neurogenesis are mediated by several pathways including increased TGF-β in brain, increased mitochondrial membrane potential, increased proliferation of M3 neurons, more oxidative stress, increased TNF-α production and TNF-α induction in non-neuronal cells and that Melatonin deficiency and/or neurogenesis are more complex than they previously appear and therefore of direct and indirect importance. Recently, there has been increasing evidence that melatonin may exert a protective effect on neuronal metabolism during neuronal survival through antioxidant and neuroprotective effects (Sainjian et al., 2003, 2008; Li et al., 2005).
3.6. Neurodegeneration
There are various studies using neurodegenerative diseases that evaluate the impact of melatonin versus other methods for promoting development of brain diseases. The aim of these studies is to show how melatonin is beneficial in neurodegenerative conditions such as dementia. A preliminary study in mice with Alzheimer’s disease demonstrated a significant decrease in lifespan-derived markers of neuronal damage compared with controls in the presence of endogenous melatonin and compared with control without supplementation. These decrease in cellular markers resulted in a higher cellular survival rate, enhanced cerebral growth rates and reduced levels of other types of neuroinflammation, such as chronic cerebral inflammation. Furthermore, these findings had implications for efforts to prevent chronic brain diseases such as Alzheimer’s disease.
3.7. Immunity and Disease Mechanisms
4. Epigenetics and Pharmacological Studies
Methylphenidate (NMethyl