Mental Wellness & The Neuroscience Perspective
Genes
Inheritance denotes the means of passing along the instructions for building the mechanism of the body from parents to their descendants (children). Genes are the physical mechanism used for the process of inheritance. A gene is simply a recipe for making a protein.
Depending on the recipe we get from our biological parents, we will make a certain variety of proteins. Proteins can be enzymes, and enzymes are the workhorses for making all the other molecules in the body as well as the workhorses for acting on the molecules that we consume in our diet. Proteins can also be structural components of our body. For example, the collagen in our nose or the keratin in our hair. Essentially, the versions of the proteins that we inherit play a significant role in defining the characteristics that differentiate us from others who have had equal experiences and live in comparable environments. Genes are made up of a series of nucleotides. Various genes are threaded together to comprise a longer string of nucleotides called a chromosome. Moreover, for storing the DNA, two strings of nucleotides bond parallel with each other, forming a ladder-type assembly.
The ladder is twisted into the accustomed double helix. The two sequences are effortlessly pulled apart because the connecting bonds between the sides of the treads of the ladders are of a delicate nature. Importantly, the gene recipe is only present on one of the strings. Every cell in the body (excluding red blood cells) contains chromosomes in the nucleus of the cell. In the nucleus, there are 23 pairs of chromosomes, one from the biological mother and the other from the biological father. The chromosome sequence can be long and very narrow. To fit into the small nucleus inside the cell, the string must be compressed. The chromosome is comprised of a DNA string that is wound around other proteins so that it gets compressed into a small space.
The Process of Making a Protein
A nucleotide has a base connected to sugar and phosphate groups. The identity of the nucleotide is determined by its base. There are four DNA bases: adenine, cytosine, thymine, and guanine. The familiar letters A, C, T, and G noted in the lay press signify these bases. To use the recipe in the gene to make a protein, several steps need to happen. Firstly, an enzyme complex sits on top of the beginning of the gene and at the start of the sequence. The machinery uses the DNA template to make a succession of ribonucleic acid (RNA) nucleotides. The subsequent RNA nucleotide string copy of the DNA gene string is called messenger RNA (mRNA). The mRNA can leave the nucleus and move into the cytoplasm of the cell. This is the first step in the protein-making process. The second step occurs when the mRNA meets another complex machinery in the cell cytoplasm. In the second phase, machinery uses the mRNA nucleotides as directives for stringing together individual amino acids) into a sequence of amino acids called a peptide or protein. Moreover, different sequences of three nucleotides in the mRNA string, called a codon, denote which amino acid should be added to the developing chain. The machinery just slides along the mRNA string, acknowledging the appearance of a start codon, and consecutively adds on amino acids according to the instructions from the mRNA.
How the Cell Elects Whether to Make a Protein or Not
Whether a gene will be used to make mRNA is an exceedingly regulated process. Regularly, transcription of the DNA into mRNA is organised by other proteins called transcription factors. Transcription factors help to compile the machinery that will make an mRNA string using the DNA string as the recipe. Many transcription factors, typically proteins, only operate when molecules (for example, hormones like glucocorticoids) are bound to these proteins. The docking of all the machinery for transcribing a DNA nucleotide sequence into mRNA also varies on the DNA sequence in the promoter section.
Several genes are polymorphic in each population, meaning that there are numerous versions of the recipe or nucleotide string in each group of individuals. Occasionally the difference in the nucleotide string is in a single nucleotide in the region, which is used to determine the sequence of amino acids in the protein. Even a single modification in a base can create a significant functional difference in the protein. Sometimes the difference is observed in the promoter area of the gene. A variation in a nucleotide or nucleotides in the promoter region of the gene will not change the version of the protein that gets produced. Though, variation across people in a gene’s promoter region can determine how often the protein gets expressed (made) (Alberts et al., 2008; Schaaf et al., 2012).
Telomeres
Telomeres are a certain sequence of nucleotides at the end of a chromosome. They are formed by telomerase (a specific enzyme). Due to the manner that DNA is copied in the formulation for cell division, each copying event slightly reduces the length of the telomere, unless the cell has activated telomerase. Researchers have recognised that the length of the telomere aids as a marker for stress (Epel et al., 2004). Those individuals who have spent more of their lifecycle in a state of depression have, as a collective group, shorter telomeres in their white blood cells (Wolkowitz et al., 2011). Additionally, those individuals whose diets are higher in omega-3s (fish oil) have longer telomeres in their white blood cells (Kiecolt-Glaser et al., 2013). Meditation is also connected with higher telomerase activity. The higher telomerase activity stimulated by meditation was statistically mediated by an improved sense of purpose in life and greater perceived control (Jacobs et al., 2011).
Summary of Various Key Brain Structures
Gamma-Aminobutyric Acid
Gamma-Aminobutyric Acid (GABA) in our brain’s main inhibitory neurotransmitter. GABA neurons are distributed through the brain. When GABA binds to its receptor, a channel for chloride opens. With further chloride inside the neuron, it is less prone to fire. While GABA largely inhibits neurons, occasionally GABA’s purpose is to ensure that only a robust signal from inputting neurons activates the receiving neurons.
Cannabinoids
Our brain has ligands (binding partners) that will attach to cannabinoid receptors. The molecules formed by the brain that bind at receptors for marijuana are termed endocannabinoids, (“endo” referring to internal or within). Endocannabinoids unlike numerous other neurotransmitters, which are modifications of amino acids, endocannabinoids are altered polyunsaturated fatty acid chains.
Cannabinoid receptors, which are metabotropic, are in several regions of the brain. In addition to neurons, receptors are also found on support cells in the brain (astrocytes, microglia, and oligodendrocytes). Cannabinoids play key roles in decreasing anxiety. They are vital for being able to terminate fear memories. They also potentiate GABA inhibition in the amygdala (a structure involved in anxiety) and they decrease the stress hormone (cortisol).
Opioids
Opioid receptors are called this because opium binds to these receptors. Opiate by-products (i.e., morphine, heroin, and codeine) also attach to these receptors. There are likewise, natural opiates in the brain including endorphins, enkephalins, and dynorphins. There are three forms of opioid receptors specifically (1) mu-receptors for the natural endorphin’s binding partners; (2) delta receptors for the natural enkephalin’s binding partners, and (3) kappa receptors for the natural dynorphin’s binding partner.
Opioid receptors are located in several regions, including the spinal cord, where they reduce pain transmission. The dorsal anterior cingulate cortex (an alarm centre in the brain), is packed full of opioid receptors where they function to decrease alarm and somatic pain. Way and associated reported (2009) that individuals with a specific allele for the mu-opioid receptor experience greater physical and emotional pain. They display greater activation of the dorsal anterior cingulate cortex in response to social rejection.
Opioid receptors are located on the GABA interneurons in the caudal dorsal raphe, the serotonergic configuration involved in creating anxiety and defeat after exposure to uncontrollable shock (termed learned helplessness). Opioids increase the release of GABA into the serotonin-releasing neurons, whose cell bodies are in the caudal dorsal raphe. The serotonergic neurons in the caudal dorsal raphe are inhibited by opioids. Maier and Watkins (2005) reported that the anxious behaviour following an inescapable shock is reduced.
In the ventral tegmental area, opioid receptors are positioned on the GABA neurons synapsing onto dopaminergic neurons. GABA inhibits dopamine release from dopaminergic neurons, which release into the nucleus accumbens. The opioids decrease the release of GABA from the GABAnergic neurons. When GABA release is inhibited, the inhibition of dopamine release is gone. Effectively, opiates are a break on a break. Thus, when opiates hit their receptors in VTA, more dopamine is released from VTA neurons into the nucleus accumbens. The effect increases locomotion and movement (Lüscher, 2013).
Gamma-Aminobutyric Acid
Gamma-Aminobutyric Acid (GABA) in our brain’s main inhibitory neurotransmitter. GABA neurons are distributed through the brain. When GABA binds to its receptor, a channel for chloride opens. With further chloride inside the neuron, it is less prone to fire. While GABA largely inhibits neurons, occasionally GABA’s purpose is to ensure that only a robust signal from inputting neurons activates the receiving neurons.
Cannabinoids
Our brain has ligands (binding partners) that will attach to cannabinoid receptors. The molecules formed by the brain that bind at receptors for marijuana are termed endocannabinoids, (“endo” referring to internal or within). Endocannabinoids unlike numerous other neurotransmitters, which are modifications of amino acids, endocannabinoids are altered polyunsaturated fatty acid chains.
Cannabinoid receptors, which are metabotropic, are in several regions of the brain. In addition to neurons, receptors are also found on support cells in the brain (astrocytes, microglia, and oligodendrocytes). Cannabinoids play key roles in decreasing anxiety. They are vital for being able to terminate fear memories. They also potentiate GABA inhibition in the amygdala (a structure involved in anxiety) and they decrease the stress hormone (cortisol).
Opioids
Opioid receptors are called this because opium binds to these receptors. Opiate by-products (i.e., morphine, heroin, and codeine) also attach to these receptors. There are likewise, natural opiates in the brain including endorphins, enkephalins, and dynorphins. There are three forms of opioid receptors specifically (1) mu-receptors for the natural endorphin’s binding partners; (2) delta receptors for the natural enkephalin’s binding partners, and (3) kappa receptors for the natural dynorphin’s binding partner.
Opioid receptors are located in several regions, including the spinal cord, where they reduce pain transmission. The dorsal anterior cingulate cortex (an alarm centre in the brain), is packed full of opioid receptors where they function to decrease alarm and somatic pain. Way and associated reported (2009) that individuals with a specific allele for the mu-opioid receptor experience greater physical and emotional pain. They display greater activation of the dorsal anterior cingulate cortex in response to social rejection.
Opioid receptors are located on the GABA interneurons in the caudal dorsal raphe, the serotonergic configuration involved in creating anxiety and defeat after exposure to uncontrollable shock (termed learned helplessness). Opioids increase the release of GABA into the serotonin-releasing neurons, whose cell bodies are in the caudal dorsal raphe. The serotonergic neurons in the caudal dorsal raphe are inhibited by opioids. Maier and Watkins (2005) reported that the anxious behaviour following an inescapable shock is reduced.
In the ventral tegmental area, opioid receptors are positioned on the GABA neurons synapsing onto dopaminergic neurons. GABA inhibits dopamine release from dopaminergic neurons, which release into the nucleus accumbens. The opioids decrease the release of GABA from the GABAnergic neurons. When GABA release is inhibited, the inhibition of dopamine release is gone. Effectively, opiates are a break on a break. Thus, when opiates hit their receptors in VTA, more dopamine is released from VTA neurons into the nucleus accumbens. The effect increases locomotion and movement (Lüscher, 2013).