Somatostatin Presynaptically Inhibits Both GABA and Glutamate Release Onto Rat Basal Forebrain Cholinergic Neurons

• Published in: Journal of neurophysiology 2006-08, Vol.96 (2), p.686-694
• Main Authors: Momiyama, Toshihiko, Zaborszky, Laszlo
• Format: Article
• Language: English
• Subjects: Animals; Calcium - physiology; Data Interpretation, Statistical; Electrophysiology; GABA Agonists - pharmacology; GABA Antagonists - pharmacology; gamma-Aminobutyric Acid - metabolism; Glutamic Acid - metabolism; Hormone Antagonists - pharmacology; In Vitro Techniques; Neurons - drug effects; Neurons - metabolism; Parasympathetic Nervous System - cytology; Parasympathetic Nervous System - drug effects; Parasympathetic Nervous System - metabolism; Patch-Clamp Techniques; Prosencephalon - cytology; Prosencephalon - drug effects; Prosencephalon - metabolism; Rats; Receptor, Nerve Growth Factor - metabolism; Receptors, Presynaptic - drug effects; Somatostatin - pharmacology
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.00507.2005

1 Division of Cerebral Structure, National Institute for Physiological Sciences, Okazaki; 2 Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Kawaguchi, Japan; and 3 Center for Molecular and Behavioral Neuroscience, Rutgers, The State University of New Jersey, Newark, New Jersey Submitted 16 May 2005; accepted in final form 24 March 2006 A whole cell patch-clamp study was carried out in slices obtained from young rat brain to elucidate the roles of somatostatin in the modulation of synaptic transmission onto cholinergic neurons in the basal forebrain (BF), a region that contains cholinergic and GABAergic corticopetal neurons and somatostatin (SS)-containing local circuit neurons. Cholinergic neurons within the BF were identified by in vivo prelabeling with Cy3 IgG. Because in many cases SS is contained in GABAergic neurons in the CNS, we investigated whether exogenously applied SS can influence GABAergic transmission onto cholinergic neurons. Bath application of somatostatin (1 µM) reduced the amplitude of the evoked GABAergic inhibitory presynaptic currents (IPSCs) in cholinergic neurons. SS also reduced the frequency of miniature IPSCs (mIPSCs) without affecting their amplitude distribution. SS-induced effect on the mIPSC frequency was significantly larger in the solution containing 7.2 mM Ca 2+ than in the standard (2.4 mM Ca 2+ ) external solution. Similar effects were observed in the case of non-NMDA glutamatergic excitatory postsynaptic currents (EPSCs). SS inhibited the amplitude of evoked EPSCs and reduced the frequency of miniature EPSCs dependent on the external Ca 2+ concentration with no effect on their amplitude distribution. Pharmacological analyses using SS-receptor subtype–specific drugs suggest that SS-induced action of the IPSCs is mediated mostly by the sst 2 subtype, whereas sst subtypes mediating SS-induced inhibition of EPSCs are mainly sst 1 or sst 4 . These findings suggest that SS presynaptically inhibits both GABA and glutamate release onto BF cholinergic neurons in a Ca 2+ -dependent way, and that SS-induced effect on IPSCs and EPSCs are mediated by different sst subtypes. Address for reprint requests and other correspondence: T. Momiyama, Division of Cerebral Structure, National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8787, Japan (E-mail: tmomi{at}nips.ac.jp )