Buprenorphine's Impact: Less Rem Sleep?

Buprenorphine is a partial mu-opioid receptor agonist and kappa-opioid receptor antagonist, and is an effective analgesic. It has been found that buprenorphine increases wakefulness and decreases both non-rapid eye movement sleep and rapid eye movement sleep.

Opioids disrupt sleep

Opioids, including buprenorphine, have been found to negatively impact sleep. They can cause issues with sleep quality, falling asleep, and conditions like sleep apnea. Buprenorphine, for example, has been found to disrupt sleep architecture, increasing wakefulness and decreasing non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep.

Opioids can also cause abnormal behaviours during sleep, such as sleepwalking, speaking, and eating, which are known as parasomnia. These behaviours can be dangerous, for example, sleepwalking can result in falls.

Opioids disrupt the sleep cycle by blocking access to REM sleep and the deeper restorative stages of non-REM sleep. REM sleep is important for learning and retaining memory, so disrupted REM sleep may negatively affect these areas.

Opioids can also cause an increase in sleep apnea, a condition where breathing stops and starts while sleeping. This can have serious health consequences, including hypertension, cardiovascular disease, and metabolic disorders.

Additionally, opioids can alter breathing patterns, even if sleep apnea is not present. Respiratory depression caused by opioids can be fatal in some cases.

The negative impact of opioids on sleep can create a cycle where increased pain leads to greater opioid use, which further disrupts sleep. This cycle can make addiction more severe.

Buprenorphine is an effective analgesic

Buprenorphine has been available in parenteral and sublingual formulations for more than two decades. It is a potent opioid analgesic, with a duration of action for analgesia of 4 to 8 hours. The smallest dose recommended for IM use (0.3 mg) has been shown to be as effective as morphine (10 mg) but has a longer duration of action (6-18 hours). The accepted range for buprenorphine analgesic effects is 0.1-10 mg, and in this range, the drug behaves as an agonist with no flattening of the dose-response curve at less than 100% effect.

Buprenorphine has been widely used and studied for over 20 years and has shown to be an effective opioid analgesic. Its μ-agonistic profile, combined with high analgesic potency and efficacy, good safety profile, ease of opioid switch, and reversibility by μ-antagonists makes this drug a valuable option for long-term treatment in a wide range of chronic pain indications.

Buprenorphine increases wakefulness and decreases non-rapid eye movement sleep and rapid eye movement sleep

Buprenorphine is a partial mu-opioid receptor agonist and kappa-opioid receptor antagonist, and is an effective analgesic. It has been found to disrupt sleep and decrease adenosine levels in sleep-regulating brain regions. An antinociceptive dose of buprenorphine has been found to cause a significant increase in wakefulness and a decrease in both non-rapid eye movement sleep and rapid eye movement sleep.

Buprenorphine has been found to increase the time spent awake, decrease non-rapid eye movement sleep, and increase the latency to sleep onset. These disruptions in sleep architecture can be mitigated by co-administration of the nonbenzodiazepine sedative-hypnotic eszopiclone.

Buprenorphine has been found to decrease adenosine levels in the pontine reticular formation and substantia innominata. The decrease in adenosine levels in these sleep-regulating brain regions is one mechanism by which opioids disrupt sleep.

Buprenorphine increases the time spent awake, decreases non-rapid eye movement sleep, and increases the latency to sleep onset

Buprenorphine is a partial mu-opioid receptor agonist and kappa-opioid receptor antagonist, and is an effective analgesic. The effects of buprenorphine on sleep have not been well characterised. However, studies have shown that an antinociceptive dose of buprenorphine increases the time spent awake, decreases non-rapid eye movement sleep and increases the latency to sleep onset.

An antinociceptive dose of buprenorphine has been shown to cause a significant increase in wakefulness (25.2%) and a decrease in both non-rapid eye movement sleep (−22.1%) and rapid eye movement sleep (−3.1%). Buprenorphine also increases electroencephalographic delta power during non-rapid eye movement sleep.

Co-administration of the sedative/hypnotic eszopiclone diminished the buprenorphine-induced decrease in sleep.

Buprenorphine decreases adenosine levels in the pontine reticular formation and substantia innominata

Buprenorphine, a partial mu-opioid receptor agonist and kappa-opioid receptor antagonist, is an effective analgesic. The effects of buprenorphine on sleep have not been well characterised. This study tested the hypothesis that an antinociceptive dose of buprenorphine decreases sleep and adenosine levels in regions of the basal forebrain and pontine brain stem that regulate sleep.

Male Sprague Dawley rats were implanted with intravenous catheters and electrodes for recording states of wakefulness and sleep. Buprenorphine (1 mg/kg) was administered systemically via an indwelling catheter, and sleep/wake states were recorded for 24 hours. In additional rats, buprenorphine was delivered by microdialysis to the pontine reticular formation and substantia innominata of the basal forebrain while simultaneously measuring adenosine.

An antinociceptive dose of buprenorphine caused a significant increase in wakefulness (25.2%) and a decrease in both non-rapid eye movement sleep (−22.1%) and rapid eye movement sleep (−3.1%). Buprenorphine also increased electroencephalographic delta power during non-rapid eye movement sleep. Co-administration of the sedative/hypnotic eszopiclone diminished the buprenorphine-induced decrease in sleep. Dialysis delivery of buprenorphine significantly decreased adenosine levels in the pontine reticular formation (−14.6%) and substantia innominata (−36.7%). Intravenous administration of buprenorphine significantly decreased (−20%) adenosine in the substantia innominata.

Buprenorphine significantly increased the time spent awake, decreased non-rapid eye movement sleep, and increased the latency to sleep onset. These disruptions in sleep architecture were mitigated by co-administration of the non-benzodiazepine sedative/hypnotic eszopiclone. The buprenorphine-induced decrease in adenosine levels in the basal forebrain and pontine reticular formation is consistent with the interpretation that decreasing adenosine in sleep-regulating brain regions is one mechanism by which opioids disrupt sleep.

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