Cerebral ischemia and brain histamine.

Area of Science:

• Neuroscience
• Neuropharmacology

Background:

• Cerebral ischemia causes neuronal injury via glutamate excitotoxicity and increased intracellular calcium.
• Histamine, a neurotransmitter, is released during ischemia and may offer neuroprotection.
• Histaminergic activity is enhanced during ischemia, suggesting a role in mitigating damage.

Purpose of the Study:

• To investigate the neuroprotective role of histamine and its receptors in cerebral ischemia.
• To determine the effects of preischemic histamine administration and postischemic histidine loading on ischemic brain injury.

Main Methods:

• Administration of histamine (intracerebroventricular) before ischemia.
• Blockade of central histamine H2 receptors.
• Postischemic administration of histidine.
• Assessment of glutamate release, neuronal damage, and brain infarction.

Main Results:

• Preischemic histamine administration suppressed ischemic glutamate release and reduced neuronal damage.
• Blockade of histamine H2 receptors aggravated ischemic injury.
• Postischemic histidine loading alleviated brain infarction and delayed neuronal death, an effect abolished by H2 receptor blockade.
• Histamine H2 receptor stimulation may exert anti-inflammatory effects, contributing to neuroprotection.

Conclusions:

• Histamine, acting via H2 receptors, provides neuroprotection against cerebral ischemic damage.
• Preischemic histamine administration and postischemic histidine loading are beneficial strategies.
• The anti-inflammatory action of histamine H2 receptor stimulation is a potential mechanism for its neuroprotective effects.