Antihistamine: Difference between revisions

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Most antihistamines act as [[Agonist#Agonists|inverse agonists]] on histamine [[receptors]], meaning they inhibit the action of histamine by preventing it from binding to them. They may also inhibit the enzymatic activity of histidine decarboxylase which catalyzes the transformation of histidine into [[histamine]].{{citation needed}}

First-generation antihistamines readily cross the [[blood–brain barrier]] (BBB) and occupy H1-receptors located on postsynaptic membranes of histaminergic neurons throughout the CNS. Most of these drugs have antimuscarinic anticholinergic effects, some have [[adrenaline|alpha-adrenergic]] blocking effects, and others can inhibit both histamine and [[5-HT]] activity. Second-generation H1-antihistamineshave significantly less affinity for muscarinic cholinergic and alpha-adrenergic receptors and cross the BBB to a minimal degree, penetrate poorly into the CNS, and typically occupy fewer than 20% of CNS H1-receptors.<ref ~~name~~=~~"H1~~-~~antihistamines"~~ />

First-generation antihistamines readily cross the [[blood–brain barrier]] (BBB) and occupy H1-receptors located on postsynaptic membranes of histaminergic neurons throughout the central nervous system (CNS). Most of these drugs have antimuscarinic anticholinergic effects, some have [[adrenaline|alpha-adrenergic]] blocking effects, and others can inhibit both histamine and [[5-HT]] activity. Second-generation H1-antihistamineshave significantly less affinity for muscarinic cholinergic and alpha-adrenergic receptors and cross the BBB to a minimal degree, penetrate poorly into the CNS, and typically occupy fewer than 20% of CNS H1-receptors.{{citation needed}}

The promotion of sleep by antihistamines with sedative properties may partially be due to the antagonism of [[histamine]] receptors in the ventrolateral preoptic area (VLPO) located in the hypothalamus. When the VLPO is stimulated, it increases the frequency of [[GABA|GABAergic]] activity within other wake-promoting sites of the brain as an inhibitory process to wakefulness. In contrast, the VLPO is inhibited by [[histamine|histaminergic]] activity, primarily from the tuberomammillary nucleus (TMN); deactivating the VLPO in order to promote wakefulness (primarily in the transition from sleep to wake).<ref>{{cite journal|last1=Yu Wei|first1=Liu|last2=Jing|first2=Li|last3=Jiang-Hong|first3=Ye|title=Histamine regulates activities of neurons in the ventrolateral preoptic nucleus|journal=The Journal of Physiology|volume=588|issue=21|year=2010|pages=4103-4116|issn=0022-3751|doi=10.1113/jphysiol.2010.193904}}</ref>

==Examples==

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 Most antihistamines act as [[Agonist#Agonists|inverse agonists]] on histamine [[receptors]], meaning they inhibit the action of histamine by preventing it from binding to them. They may also inhibit the enzymatic activity of histidine decarboxylase which catalyzes the transformation of histidine into [[histamine]].{{citation needed}}
-First-generation antihistamines readily cross the [[blood–brain barrier]] (BBB) and occupy H1-receptors located on postsynaptic membranes of histaminergic neurons throughout the CNS. Most of these drugs have antimuscarinic anticholinergic effects, some have [[adrenaline|alpha-adrenergic]] blocking effects, and others can inhibit both histamine and [[5-HT]] activity. Second-generation H1-antihistamineshave significantly less affinity for muscarinic cholinergic and alpha-adrenergic receptors and cross the BBB to a minimal degree, penetrate poorly into the CNS, and typically occupy fewer than 20% of CNS H1-receptors.<ref name="H1-antihistamines" />
+First-generation antihistamines readily cross the [[blood–brain barrier]] (BBB) and occupy H1-receptors located on postsynaptic membranes of histaminergic neurons throughout the central nervous system (CNS). Most of these drugs have antimuscarinic anticholinergic effects, some have [[adrenaline|alpha-adrenergic]] blocking effects, and others can inhibit both histamine and [[5-HT]] activity. Second-generation H1-antihistamineshave significantly less affinity for muscarinic cholinergic and alpha-adrenergic receptors and cross the BBB to a minimal degree, penetrate poorly into the CNS, and typically occupy fewer than 20% of CNS H1-receptors.{{citation needed}}
+The promotion of sleep by antihistamines with sedative properties may partially be due to the antagonism of [[histamine]] receptors in the ventrolateral preoptic area (VLPO) located in the hypothalamus. When the VLPO is stimulated, it increases the frequency of [[GABA|GABAergic]] activity within other wake-promoting sites of the brain as an inhibitory process to wakefulness. In contrast, the VLPO is inhibited by [[histamine|histaminergic]] activity, primarily from the tuberomammillary nucleus (TMN); deactivating the VLPO in order to promote wakefulness (primarily in the transition from sleep to wake).<ref>{{cite journal|last1=Yu Wei|first1=Liu|last2=Jing|first2=Li|last3=Jiang-Hong|first3=Ye|title=Histamine regulates activities of neurons in the ventrolateral preoptic nucleus|journal=The Journal of Physiology|volume=588|issue=21|year=2010|pages=4103-4116|issn=0022-3751|doi=10.1113/jphysiol.2010.193904}}</ref>
 ==Examples==