Neurons within the BLA form reciprocal connections with the PFC and the hippocampus (reviewed in Janak and Tye, 2015). Connections with the PFC are sufficient to alter feeding and freezing behavior, as well as reinstatement of fear conditioning. Connections between the BLA and the hippocampus, on the other hand, have been found to affect anxiety-related and social behavior. Neurons in the BNST region of the extended amygdala connect via both glutamatergic and GABAergic projections to DA neurons of the VTA, as well as by GABAergic projections to the lateral hypothalamus [61]. Overall, the actions of alcohol in modulating the excitability of neurons in the amygdala and extended amygdala have the potential to affect social, anxious, and reward behavior as well as associative learning. The critical role of the hippocampus (and related cortical structures such as the entorhinal cortex) in learning and memory makes these brain areas the presumptive site of action for the amnestic actions of medium levels of alcohol.
When to Seek Help for CNS Depression
They’re also a class of drugs with a risk of misuse and addiction, increasing one’s chances of taking too much, which can lead to coma or death. Like depressant drugs, alcohol seems 9 liquor storage ideas for small spaces to affect chemicals that inhibit brain activity. For this reason, doctors often prescribe sedatives to treat insomnia and other sleep disorders, while hypnotics can induce sleep.
What are the most important things I should know about depressants?
Diaz and Valenzuela [13] found that 20mM ethanol increased sIPSC frequency in cerebellar granule neurons from very young animals (pre-weaning), but this concentration had no effect on tonic inhibition in these cells. Despite the negative consequence of drinking alcohol, there is still hope for the recovery of alcohol-induced neurodegeneration. Neuro-regeneration (neuronal stem cell proliferation and formation of new neurons) generally depends on alcohol dosage, drinking duration, nutritional deficiency, stage of neuronal damage, and cellular components that correspond with cognitive functioning impairment.
Opiates and opioids
Addiction to CNS depressants may see a person experience social and family problems, difficulty working, and an inability to function in daily. A person may recover from an overdose, but research in the Journal of Clinical Psychopharmacology shows that some may continue to have problems with everyday functioning after leaving alcohol and weed the hospital. Prescription benzodiazepines and opioids carry the highest level of warning from the U.S. These can treat seizure disorders and anxiety, but doctors rarely prescribe them nowadays. In 2020, the Food and Drug Administration (FDA) strengthened their warning that benzodiazepine use can lead to addiction.
The most common type of GABAA receptor has two α subunits, two β subunits, and one γ subunit, as seen in the diagram below. The primary binding site, also known as the orthosteric site, is where GABA normally binds to the receptor. The classical GABAA receptor is part of what is called the GABAA chloride channel receptor complex. If you are on CNS depressants and suspect it’s making you more lethargic than you should be, don’t stop it until you speak to your doctor.
Recall from Chapter 4 that γ-aminobutyric acid (GABA) is the brain’s main inhibitory neurotransmitter. This is because GABA targets GABA receptors, which promote hyperpolarization of the postsynaptic cell. This inhibits the postsynaptic cell from firing and releasing other neurotransmitters such as glutamate or norepinephrine. As a result, increasing GABA activity will, in general, reduce the activity of other neurons and transmitters. Although many people don’t think of alcohol as a drug, it’s one of the most common and often abused drugs in the world today.
In certain cases, CNS depression could also be caused by a stroke, brain trauma, an aneurysm, or a tumor. Some research shows that even conditions that don’t directly affect the brain, like diabetes or kidney and heart disease, could cause CNS depression. People who develop AUD continue to consume alcohol despite experiencing negative consequences. This condition can have a negative effect on health, relationships, and emotional well-being. A person should speak with a healthcare professional if they think they have AUD.
Disruption of neuron-specific neurofilaments or neuronal death initiates the primary process of alcohol-related neurodegeneration [37]. Alcohol is the most commonly used recreational beverage and drug of abuse among the adult population, alcohol-related death is the third leading preventable cause of death in the United States which accounts for more than 3.3 million global deaths annually [1],[2]. According to the 2018-National Survey on Drug Use and Health (NSDUH), 14.4 million people suffered from alcohol use disorder (AUD) in the US, and over 100,000 deaths were attributable to alcohol [3].
- Although AUD cases may differ in severity, people who receive effective treatment can fully recover.
- The danger is when the CNS is slowed too much, which can lead to unconsciousness, coma, and death.
- Naloxone is administered to people who are suffering from an opioid overdose.
- Another study by[55] aimed to look at the availability of the SERT in patients with AD.
- Long-term overuse of alcohol can cause physical and psychological dependence.
It’s a little less clear why a sometimes crushing low replaces that initial high as your blood alcohol level decreases. When you first begin taking a CNS depressant, you may feel unusually sleepy or uncoordinated as your body adjusts to the medication. For the last chapter in this unit, we will take a detailed look at alcohol, the most infamous depressant of all. Much of the terminology used to describe alcohol’s effects will have already been introduced in this chapter, so make sure you are comfortable with this chapter’s material before moving on. When used in a medical or dental setting, a mixture of nitrous oxide and oxygen is dispensed by an anesthesia machine with a fail-safe system to protect the patient from hypoxia.
Similarly, studies in AUD patients have shown an elevated level of choline-containing compounds that usually provide evidence of demyelination but it is not consistent with alcohol withdrawal syndrome [71],[11]. According to earlier studies, alcohol withdrawal seizures commonly occur due to an imbalance between glutamatergic and GABAergic neurotransmission which can be detected by MRS of the human brain [107]. In particular, MRI studies of individuals with AUD demonstrate widespread diffuse loss of both cortical white and gray matter thickness where disproportionate deficits of gray and white matter are more visible in older age compared to young patients [86]. The mechanism of neuronal damage and volume deficits in chronic drinking patterns that have been suggested is neuronal death with the destruction of glial structure which may be caused by the induction of pro-inflammatory cytokines and oxidative enzymes [87].
Inhalants, which we will also be examining, do not have any sleep-inducing effects. At the same time, some drugs produce sedative effects through mechanisms other than the GABA receptor. Antihistamines, one such example, act at histamine receptors and cause drowsiness as a side effect. Mild CNS depression is often the goal of taking some CNS depressants, especially sleep and anxiety disorders. It’s important to take the medication exactly as your doctor prescribes to avoid a more severe form of the condition.
Fortunately, the withdrawal symptoms can be suppressed by safer sedative-hypnotic drugs like benzodiazepines. Empirical studies further show that ethanol-induced brain damage is mainly related to oxidative stress response from proinflammatory cytokines activated during alcohol intoxication. Proinflammatory cytokines NF-kB (transcription factor) mediate oxidative stress plays a role in the induction of anti-inflammatory and immune response signals, which appear to underlie neuronal degeneration and tissue atrophy [46],[47]. Cytokines are large families of secreted proteins that are transported from blood serum to neuronal tissue in response to oxidative stress-related alcohol neuroinflammation [47].
Statistics show that liver cirrhosis is one of the top 10 causes of death worldwide and this in itself indicates the severity of the same [16]. The changing lifestyle and also many people turning to prolonged alcohol intake for many years are contributing to the increased number of liver cirrhosis patients in the modern world. In liver cirrhosis patients, there occurs an increased severity of fibrosis due to the loss of parenchyma and fibrous scar proliferation [17]. Alcoholic liver disease (ALD) is an umbrella term which incorporates a wide range of injuries of the liver, spanning from simple steatosis to cirrhosis, and this also includes alcohol-related fatty liver disease (AFLD) and also alcoholic hepatitis [18]. Advancements in the diagnostic modalities have helped to diagnose ALD at an early phase and there is no doubt that newer and better investigations that have helped to detect more cases have led to a surge in the number of ALD patients on whole.
Alcohol seldom leaves any system untouched as far as leaving its impression is concerned, spanning from single tissue involvement to complex organ system manifestations. Almost all the major organs that make up a human’s physiological being are dramatically affected by the overconsumption of alcohol. There is an enormous overall economic cost that is paid for alcohol abuse all over the world. Recently mutations in the SERT gene, commonly known as 5’- hydroxtryptamine transporter linked polymorphic region (5’-HTTLPR), has been implicated in cases of alcoholism. One mutation is known as the “long” allele and the other mutation is known as the “short” allele. The difference between the two alleles is that the “short” version of the allele has a 44 bp deletion in the 5’ regulatory region of the gene.
An increase in the activity of GABA in your brain leads to a slowdown of your brain activity. CNS depression is prevalent among people who use these substances recreationally. Another medication, called disulfiram, causes negative symptoms such as nausea after consuming alcohol. Consuming too much alcohol too quickly can affect breathing, body temperature, and heart rate. Long-term overuse of alcohol can cause physical and psychological dependence. People who are dependent on alcohol may experience withdrawal symptoms when they try to quit drinking.
A standard beer may contain about 5% alcohol, whereas one portion of a distilled spirit could contain 40% alcohol. A psychotropic substance impacts the brain and can affect thoughts, mood, or behavior. The SERT gene or SERT, also known as SLC6A4 has another polymorphism in intron 2. This polymorphism has therefore appropriately been named as serotonin intron 2 (STin2).
It also facilitates dopamine release from the nucleus accumbens, although the effect is not potent. Its actions on dopaminergic and opioid peptidergic systems are implicated in the reinforcing effect of alcohol. After chronic exposure, downregulation of GABAergic and upregulation of NMDA glutamatergic systems typically occur. Normalizing this imbalance might be effective in the treatment of alcohol dependence. Antagonism of the μ-opioid system also reduces the motivation to consume alcohol. New animal models of binge alcohol intake, such as the alcohol deprivation effect (ADE) and the “Drinking-in-the-Dark” technique, would help us to develop new treatment methods against alcohol dependence.
Doing so can help minimize the risk for dependence; although dependence may still occur if you take the medication for an extended period of time. People should take depressants if they have been advised to do so by their healthcare provider. These medications can be safe when taken as prescribed, when not combined with alcohol alcohol withdrawal syndrome or other drugs, and when not used while driving or operating heavy machinery. Sedative-hypnotics include barbiturates, benzodiazepines, and non-benzodiazepines (such as Z-drugs). We will discuss some of these in greater detail during Unit 4 on psychotherapeutic drugs, but, for this chapter, we will focus on barbiturates.