Activation of taste-bud cells on the tongue causes serotonin release onto sensory afferent nerves (59) that transmit taste information to the CNS. Once food enters the GI tract, it is propelled along by peristaltic waves; these waves, as well as intestinal motility and secretion, are modulated by serotonin (reviewed does alcohol release dopamine or serotonin extensively in Reference 8). For example, intestinal serotonin regulates pancreatic enzyme secretion (60), a mechanism by which the gut may communicate exocrine enzyme needs to the pancreas based on GI contents. Indeed, acute blockade of the serotonin transporter by SSRIs can block the development of PAH and subsequent right ventricular hypertrophy in animal models (42), suggesting that intracellular rather than extracellular serotonin may be an etiological factor in PAH. Serotonin regulates several different aspects of cardiac function, ranging from electrical conduction to valvular closure to postMI remodeling (Figure 2). Studies of cardiac abnormalities in patients with serotonin-producing carcinoid tumors provided early evidence that serotonin modulates heart function.
Ethanol, 5-HT3 receptors the mesolimbic dopamine system
Serotonin, along with other neurotransmitters, also may contribute to alcohol’s intoxicating and rewarding effects, and abnormalities in the brain’s serotonin system appear to play an important role in the brain processes underlying alcohol abuse. The role of dopamine in AUD is complex and has been reviewed in detail elsewhere 10,11,12,13. Briefly, acute alcohol increases dopamine release across the striatum 14 primarily due to increased firing of midbrain dopaminergic neurons, an effect that may underlie the initial reinforcing properties of alcohol.
From obesity to substance abuse: Therapeutic opportunities for 5-HT2C receptor agonists
One neurotransmitter used by many neurons throughout the brain is serotonin, also known as 5-hydroxytryptamine (5-HT). Serotonin released by the signal-emitting neuron subtly alters the function of the signal-receiving neurons in a process called neuromodulation. For example, in some neurons serotonin alters the rate at which the cells produce the electrical signals (i.e., action potentials) used for relaying information within the cells, whereas in other neurons it modulates the release of other neurotransmitters. People who constantly deal with anxiety are more likely to develop a problem with alcohol or substance abuse than those who do not have anxiety issues. Because it takes increasing amounts of alcohol to achieve the same effect, it can lead to alcohol dependence. Cortisol is beneficial in short-term stressful situations because it improves focus, attention, and alertness.
- That’s right — 90% of this essential chemical is found “downstairs,” in the gut, where it acts as a hormone.
- This group also found no difference in the quinpirole-mediated inhibition of dopamine release between alcohol and control male cynomolgus macaques 24.
- Serotonin may interact with GABA-mediated signal transmission by exciting the neurons that produce and secrete GABA (i.e., GABAergic neurons).
Social and coping reasons for drinking: Predicting alcohol misuse in adolescents
Alcohol is a depressant, but it’s also an indirect stimulant, and plays a few other roles that might surprise you. Serotonin is a neurotransmitter — a molecule that acts as a chemical messenger, helping neurons communicate with one another. But did you know that only about 10% of serotonin is actually produced in the brain? That’s right — 90% of this essential chemical is found “downstairs,” in the gut, where it acts as a hormone.
- Among the neurotransmitter systems linked to the reinforcing effects of alcohol are dopamine, endogenous opiates (i.e., morphinelike neurotransmitters), GABA, serotonin, and glutamate acting at the NMDA receptor (Koob 1996).
- However, the function of individual neurotransmitters and their receptors cannot entirely explain a syndrome as complex as alcoholism.
Thus, the observed AB changes following P/T depletion reflect not only changes to dopamine transients 57 in response to conditioned cues 18, 19, but also changes to catecholamine systems involved in attention and cognitive control. While data suggest that P/T depletion affects dopamine more than norepinephrine 50, 58, 86, 87, changes to norepinephrine systems could contribute to the effects reported here. This finding may seem surprising given that less than one in a million CNS neurons produce serotonin and the vast majority of total body serotonin is found outside the CNS (8). However, brainstem serotonin neurons send ascending projections that terminate in a defined and organized manner in cortical, limbic, midbrain, and hindbrain regions (Figure 1). Indeed, all brain regions express multiple serotonin receptors in a receptor subtype-specific fashion (9).
