Noradrenaline is released via volume transmission from axons originating in the locus coeruleus and released into the parenchyma to be detected by both neurons and astrocytes. Noradrenergic α-1 receptors are Gq-coupled receptors that induce intracellular calcium release from the endoplasmic reticulum as a key pathway for astrocyte calcium signalling. Due to interactions between astrocytes and synapses including their known roles in structural isolation of synapses, metabolic support, potassium buffering and gliotransmitter release, fluctuations of intracellular calcium in astrocytes can influence neuronal circuits.Here we utilise Fgfr3-iCreERT2 x Adra1Af/f mice in which α-1A receptors are knocked out of astrocytes to investigate how noradrenaline elicits astrocyte-dependent changes to hippocampal neuronal circuits and susceptibility to epileptic seizures. Using slice electrophysiology, we show that astrocyte α-1A receptor activation increases inhibitory synaptic activity onto hippocampal dentate gyrus granule cells. In the kainic acid mouse model of temporal lobe epilepsy, spontaneous seizures were measured through implanted EEG. In these epileptic mice, a single intraperitoneal injection of a specific α-1A agonist transiently reduced the frequency of spontaneous seizures. This demonstrates a role for targeting astrocyte α-1A receptor as a target for controlling hippocampal hyperexcitability.