Opioids manipulate which of the following neurotransmitters

The words on the page enter the brain through the eyes and are converted into information that is relayed, from one neuron to the next, to regions that process visual input and attach meaning and memory. 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. Neurons respond with greater versatility to more types of input than any semiconductor; they also can change, grow, and reconfigure their own circuits.

The task in neurotransmission is to convey a signal from a sending neuron to a receiving neuron across an open space known as a synapse. All neurons accomplish this in approximately the same way. 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.

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. Once a neurotransmitter has interacted with its receptor on the receiving neuron, neuron to neuron communication is complete.

The neurotransmitter molecules drop off the receptors. Loose again in the synapse, they meet one of three fates:. Normally, when drugs are not present, the cycle of release, breakup, and neuron re-entry maintains the amount of neurotransmitter in the synapse, and hence neurotransmission, within certain limits. In most cases, when an addictive drug enters the brain, it causes neurotransmission to increase or decrease dramatically beyond these limits.

Neuroscientists seeking to understand why people use drugs and the consequences of drug use focus on two issues:. Dopamine, for example, is highly concentrated in regions that regulate motivation and feelings of reward, and is a strong motivator for drug use. 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: increased analgesia, decreased alertness, and slowed respiration.

Other drugs disrupt more than one type of neurotransmitter. Cocaine, for example, attaches to 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.

For example, nicotine stimulates cells directly by activating their receptors for acetylcholine, and indirectly by inducing higher levels of glutamate , a neurotransmitter that acts as an accelerator for neuron activity throughout the brain.

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 NAc , leading to euphoria and a desire to repeat the experience—is in many cases an indirect one.

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

Identifying the precise step that a drug disrupts, and how, provides crucial insight into its impact on users, and is key to developing medical and behavioral interventions to inhibit, counter, or reverse the disruption.

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 than 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. As long as cocaine occupies the transporter, dopamine cannot re-enter the neuron. It builds up in the synapse, stimulating receiving-neuron receptors more copiously and producing much greater dopamine impact on the receiving neurons than occurs naturally.

Finally, some drugs alter neurotransmission by means other than increasing or decreasing the quantity of receptors stimulated. Eventually, however, repeated drug use leads to changes in neuronal structure and function that cause long-lasting or permanent neurotransmission abnormalities. These alterations underlie drug tolerance where higher doses of the drug are needed to produce the same effect , withdrawal, addiction, and other persistent consequences.

The route from the PAG to the spinal cord is not direct. Opioid and serotonergic antagonists reverse both local opiate analgesia and brain-stimulation produced analgesia. In conclusion, in the CNS, much of the information from the nociceptive afferent fibers results from excitatory discharges of multireceptive neurons.

The pain information in the CNS is controlled by ascending and descending inhibitory systems, using endogenous opioids, or other endogenous substances like serotonin as inhibitory mediators. In addition, a powerful inhibition of pain-related information occurs in the spinal cord.

These inhibitory systems can be activated by brain stimulation, intracerebral microinjection of morphine, and peripheral nerve stimulation. Centrally acting analgesic drugs activate these inhibitory control systems. However, pain is a complex perception that is influenced also by prior experience and by the context within which the noxious stimulus occurs.

This sensation is also influenced by emotional state. Therefore, the response to pain varies from subject to subject. Descending corticospinal fibers produce postsynaptic inhibition of nociceptive spinal neurons will not affect pain sensation.

Descending spinothalamic fibers produce presynaptic inhibition of Rexed lamina VII neurons. The spinothalamic fibers are ascending fibers that carry pain information to the thalamus. The descending dorsolateral fasciculus fibers suppress pain in the spinal cord.

Pain stimuli activate descending fibers in the dorsolateral fasciculus. Transection of the dorsal column blocks the descending fibers producing analgesia. The dorsal column does not carry the descending dorsolateral fiber, therefore their transaction will not affect SPH. Ascending pain suppression system. Non-noxious input suppresses pain at the spinal cord. Melzack and Wall assume that peripheral non-noxious stimulation will inhibit presynaptically the pain conducting pulses at the spinal cord target cells T cells and will prevent pain sensation from being transmitted to higher centers.

Electrical simulation-produced analgesia. Cortical control system suppresses pain. Descending pain suppression system.

Stimulation at the central gray and the Raphe nuclei produces analgesia via dorsolateral funiculus descendign fibers. Opiate Analgesia OA The most effective clinically used drugs for producing temporary analgesia and relief from pain are the opioid family, which includes morphine, and heroin. Endogenous Opioids Opioidergic neurotransmission is found throughout the brain and spinal cord and appears to influence many CNS functions, including nociception, cardiovascular functions, thermoregulation, respiration, neuroendocrine functions, neuroimmune functions, food intake, sexual activity, aggressive locomotor behavior as well as learning and memory.

Gate Control theory The first pain modulatory mechanism called the " Gate Control " theory was proposed by Melzack and Wall in the mid s. According to the descending pain suppression theory, A. Mechanical stimulation produces presynaptic inhibition, not postsynaptic inhibition.

Corticospinal fibers innervate motor neurons, and have no effect on nociceptive spinal neurons. The Melzack-Wall gate theory refers to: A. The goal of this article is to assist clinicians to develop pharmacological interventions that better meet their patient's analgesic needs.

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Peptides ;8 3 PubMed Google Scholar. Save Preferences. Privacy Policy Terms of Use. This Issue. Citations View Metrics. Twitter Facebook More LinkedIn. Original Article. October Tiffany M. Love, BS ; Christian S. Personality inventories. Stress challenge. Scanning protocols. Image analyses. Psychophysical measures. Interactions among measures: conjunction analyses. Access your subscriptions. Access through your institution. Add or change institution. Free access to newly published articles.

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