Term papers writing service


The influence of neurotransmitters on our body

Impacts of Drugs on Neurotransmission The defining features of drug intoxication and addiction can be traced to disruptions in neuron-to neuron signaling. Scientists continue to build on this essential understanding with experiments to further elucidate the physiological factors that make a person prone to using drugs, as well as the full dimensions and progression of the disorder.

The findings provide powerful leads for developing new medications and behavioral treatments. When inside neurons, the information takes the form of an electrical signal. To cross the tiny gap, or synapse, that separates one neuron from the next, the information takes the form of a chemical signal. The specialized molecules that carry the signals across the synapses are called neurotransmitters.

To grasp the basic idea of neurotransmission, think of a computer. A computer consists of basic units, semiconductors, which are organized into circuits; it processes information by relaying an electric current from unit to unit; the amount of current and its route through the circuitry determine the final output.

The brain relays information from neuron to neuron using electricity and neurotransmitters; the volume of these signals and their routes through the organ determine what we perceive, think, feel, and do. Of course, the brain, a living organ, is much more complex and capable than any machine. The sending cell manufactures neurotransmitter molecules and stores them in packets called vesicles. When stimulated sufficiently, the neuron generates an electric signal and causes some vesicles to migrate to the neuron membrane, merge with it, open up, and release their contents into the synapse.

  • Special cells called neurons are responsible for information transport through the brain;
  • With positron emission tomography PET , researchers can compare people with and without a drug addiction, quantifying differences in their levels of a particular neurotransmitter e;
  • Once these are activated, a number of pathways are activated, resulting in a diverse array of effects, from reduced experience of pain to movement of the digestive tract, as well as having an effect on mood;
  • The nerve impulse travels from the first nerve cell through the axon—a single smooth body arising from the nerve cell— to the axon terminal and the synaptic knobs.

Some of the released molecules drift across the synapse and link up, lock-and-key fashion, with molecules called receptors on the surface of the receiving neuron. If the neurotransmitter is stimulatory e. If the neurotransmitter is inhibitory e. The neurotransmitter molecules drop off the receptors.

  • If the neurotransmitter is stimulatory e;
  • As described above, neurotransmission is a cyclic process that transpires in several steps utilizing specialized components of the sending and receiving neurons.

Loose again in the synapse, they meet one of three fates: Some attach to another receptor. Some encounter an enzyme, a chemical that breaks them apart.

Once back inside the neuron, they are available for re-release in future neurotransmission episodes. The Basic Research Questions Neuroscientists seeking to understand why people use drugs and the consequences of drug use focus on two issues: Which neurotransmitter or neurotransmitters does the drug affect?

How does the drug alter neurotransmission? Each individual neuron manufactures one or more neurotransmitters: Some drugs primarily affect one neurotransmitter or class of neurotransmitters. For example, prescription opioids and heroin produce effects that are similar to but more pronounced than those produced by the neurotransmitters endorphin and enkephalin: Other drugs disrupt more than one type of neurotransmitter.

Cocaine, for example, attaches the influence of neurotransmitters on our body structures that regulate dopamine, leading to increases in dopamine activity and producing euphoria; it also produces changes in norepinephrine and glutamate systems that cause stimulant effects. Because a neurotransmitter can stimulate or inhibit neurons that produce different neurotransmitters, a drug that disrupts one neurotransmitter can have secondary impacts on others.

A key effect that all drugs that cause dependence and addiction appear to have in common—a dramatic increase in dopamine signaling in a brain area called the nucleus accumbens NAcleading to euphoria and a desire to repeat the experience—is in many cases an indirect one. How Does the Drug Alter Neurotransmission?

As described above, neurotransmission is a cyclic process that transpires in several steps utilizing specialized components of the sending and receiving neurons. Some drugs mimic neurotransmitters. Since heroin stimulates many more receptors more strongly than the natural opioids, the result is a massive amplification of opioid receptor activity.

Marijuana mimics cannabinoid neurotransmitters, the most important of which is anandamide. Nicotine attaches to receptors for acetylcholine, the neurotransmitter for the cholinergic system. Other drugs alter neurotransmission by interacting with molecular components of the sending and receiving process other the influence of neurotransmitters on our body receptors.

Cocaine, for example, attaches to the dopamine transporter, the molecular conduit that draws free-floating dopamine out of the synapse and back into the sending neuron. Finally, some drugs alter neurotransmission by means other than increasing or decreasing the quantity of receptors stimulated. These alterations underlie drug tolerance where higher doses of the drug are needed to produce the same effectwithdrawal, addiction, and other persistent consequences.

Some longer-term changes begin as adjustments to compensate for drug-induced increases in neurotransmitter signaling intensity. For example, the brain responds to repeated drug-induced massive dopamine surges in part by reducing its complement of dopamine receptors.

Similarly, methadone and some other opioids induce neurons to retract a portion of their mu opioid receptors, making them unavailable for further stimulation. The retraction is short-lived, after which the receptors return to the neuron surface, restoring normal responsiveness to subsequent stimulation.

  • As the name implies, the drug inhibits the re-uptake of serotonin neurotransmitter from synaptic gaps, thus increasing neurotransmitter action;
  • Physical exercise influences the central dopaminergic, noradrenergic and serotonergic systems;
  • A lack of serotonin in the brain is associated with depression, which is why drugs called SSRIs selective serotonin reuptake inhibitors , such as fluoxetine Prozac , are commonly prescribed to help treat depression.

This dynamic of reducing and then restoring receptor availability may thwart the development of tolerance to these drugs. The drug-related mechanisms producing cumulative changes in neurotransmission sometimes are epigenetic in nature. For example, in mice, cocaine alters important genetic transcription factors and the expression of hundreds of genes.

Other changes, such as proliferation of new dendrites branchlike structures on neurons that feature neurotransmitter receptors on their surface may be compensatory.

Exercise and brain neurotransmission.

Some epigenetic changes can be passed down to the next generation, and one study found that the offspring of rats exposed to THC—the main psychotropic component of marijuana—have alterations in glutamate and cannabinoid receptor formation that affects their responses to heroin.

Some drugs are toxic to neurons, and the effect accumulates with repeated exposures. Similarly, methamphetamine damage to dopamine-releasing neurons can cause significant defects in thinking and motor skills; with abstinence, dopamine function can partially recoverbut the extent to which cognitive and motor capabilities can recover remains unclear.

To determine whether a drug affects a particular neurotransmitter system, or how, researchers typically will compare animals or people who have a history of drug exposure with others who do not. In experiments with animals, drug exposure often takes place under laboratory conditions designed to mimic human drug consumption. Studies can be divided into those in which measurements are made in living animals or people and those in which animal brain tissue is removed and examined.

Brain Tissue Assays Scientists may perform chemical assays on brain tissue to quantify the presence of a neurotransmitter, receptor, or other structure of interest. Scientists place the tissue in a laboratory solution of nutrients cell culture that enables neurons to survive outside of the body. In both living animals and extracted tissue, the techniques for measuring neurotransmitter quantities and fluctuations include microdialysis and fast-scan cyclic voltammetry FSCV.

Microdialysis involves taking a series of samples of the intercellular fluid containing the neurotransmitter through a microscopic tube inserted into the tissue or living brain. FSCV, which was developed by NIDA-funded scientists, monitors neurotransmitter fluctuations at tenth-of-a-second intervals by measuring electrical changes related to neurotransmitter concentrations.

A common design for experiments with either animals or people is to give study subjects a chemical that has a known effect on a particular neurotransmitter, and then observe the impact on behavior. Typically, the chemical is either an agonist promoter or antagonist blocker of signaling by the neurotransmitter. Another team using a similar strategy showed that nicotine-induced disruption of glutamate signaling contributed to aspects of nicotine withdrawal.

Both findings point to manipulation of the glutamate system as a potential strategy for treating some addictions. Researchers are now attempting to parlay this the influence of neurotransmitters on our body into a novel treatment for cocaine addiction. Brain Scans Brain imaging techniques enable neuroscientists to directly assess neurotransmission in people and living animals.

What Is Neurotransmission?

With positron emission tomography PETresearchers can compare people with and without a drug addiction, quantifying differences in their levels of a particular neurotransmitter e.

The findings indicated that the need to saturate these receptors is the primary driver of smoking behavior, but that sensory aspects of smoking, such as handling and tasting cigarettes, also play a role. Or, they can elicit a drug-related behavior or symptom e.

Researchers use several imaging techniques, including PET, functional magnetic resonance imaging fMRIand computerized tomography to monitor metabolic activity in selected regions of the brain.

Because each neurotransmitter has a unique distribution among the regions of the brain, information on locations of heightened or decreased activity provides clues as to which neurotransmitter is affected under the conditions of the study. Another technique, diffusion tensor imaging, provides information about the white matter neuron fiber pathways through which sending neurons extend to receiving neurons, often over long distances.

Genetic Studies Studies that link genetic variants to contrasting responses to drugs and drug-related behaviors provide another avenue of insight into drugs and neurotransmission. Such studies have shown, for example, that one rare variant of the gene for the mu opioid receptor is twice as common in the general population of European Americans as it is among European Americans who are addicted to cocaine or opioids. The finding suggests that receptors that are built based on the DNA sequence of the variant gene confer resistance to those addictions.

Impacts of Drugs on Neurotransmission

Another study linked a different variant of the same mu opioid receptor gene to reduced incidence and severity of neonatal abstinence syndrome among infants born to mothers who used opioids while pregnant. In another type of study, researchers knock down or knock out specific genes in laboratory animals and observe whether drug-related behavior—for example, pacing restlessly after being given a stimulant—increases or decreases.

Researchers have used this technique to explore how different subtypes of nicotinic acetylcholine receptor influence smoking behaviors, including how much a person smokes and susceptibility to symptoms of nicotine withdrawal. Finally, researchers may implant modified genes into animals. In one such project, researchers, starting from clues provided by a South American caterpillar that eats coca leaves, modified the dopamine transporter gene to produce a transporter that is insensitive to cocaine.

Mice who were implanted with this gene showed no preference for the drug over a saline solution.

  1. Both findings point to manipulation of the glutamate system as a potential strategy for treating some addictions. In another type of study, researchers knock down or knock out specific genes in laboratory animals and observe whether drug-related behavior—for example, pacing restlessly after being given a stimulant—increases or decreases.
  2. Studies, mostly with animals, indicate that the interactions of cocaine with the dopamine and other neurotransmitter systems influence the risk of drug use, progression to addiction, and relapse after abstinence through a variety of pathways.
  3. Some common neurotransmitters are acetylcholine, norepinephrine, dopamine, serotonin and gamma aminobutyric acid GABA. Alongside pleasure, these receptors ensure the involvement of dopamine in a range of activities, from movement and attention to memory.

This result could point researchers toward medications capable of preventing or treating cocaine use disorders. Like all drugs that cause dependence and addiction, cocaine alters dopamine signaling. Studies, mostly with animals, indicate that the interactions of cocaine with the dopamine and other neurotransmitter systems influence the risk of drug use, progression to addiction, and relapse after abstinence through a variety of pathways.

Reward Cocaine causes pleasurable feelings that motivate drug use by sharply elevating dopamine concentrations in the synapses of the reward system.