Noradrenergic modulation of glutamate release in the cerebellum.
The effect of alpha- and beta-adrenergic agonists has been studied on the release of newly synthesized [3H]glutamate and [3H]GABA from slices of rat cerebellum. The beta 2-adrenergic agonist salbutamol, and also noradrenaline in the presence of the alpha-adrenergic antagonist phentolamine, both potentiated the K+-evoked release of [3H]glutamate. This potentiation appears to be mediated by adenylate cyclase activation. No effects of beta-adrenergic stimulation were observed on [3H]GABA release. The alpha-adrenergic agonist clonidine inhibited both the [3H]glutamate and the [3H]GABA release evoked by K+. The results suggest that noradrenergic modulation of cerebellar activity may have a presynaptic as well as postsynaptic origin.
D000818:Animals; D002525:Cerebellar Cortex / Q000502:physiology; D002531:Cerebellum / Q000502:physiology*; D000242:Cyclic AMP / Q000502:physiology; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D008297:Male; D009638:Norepinephrine / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D011689:Purkinje Cells / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D011941:Receptors, Adrenergic / Q000502:physiology; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects; D013574:Synaptosomes / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D005971:Glutamates; D011941:Receptors, Adrenergic; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D000242:Cyclic AMP; D011188:Potassium; D009638:Norepinephrine