Cholecystokinin activates CCKB receptors to excite cells and depress EPSCs in the rat rostral nucleus accumbens in vitro.

The peptide cholecystokinin (CCK) is abundant in the rat nucleus accumbens (NAc). Although it is colocalized with dopamine (DA) in afferent terminals in this region, neurochemical and behavioural reports are equally divided as to whether CCK enhances or diminishes DA's actions in this nucleus. To better understand the role of this peptide in the physiology of the NAc, we examined the effects of CCK on excitatory synaptic transmission and tested whether these are dependent on DA and/or other neuromodulators.

Dopamine and adenosine mediate substance P-induced depression of evoked IPSCs in the rat nucleus accumbens in vitro.

The major projection cells of the nucleus accumbens (NAc) are under a strong inhibitory influence from GABAergic afferents and depend on afferent excitation to produce their output. We have earlier reported that substance P (SP), a peptide which is colocalized with GABA in these neurons, depresses excitatory synaptic transmission in this nucleus (Kombian, S.B.

Substance P depresses excitatory synaptic transmission in the nucleus accumbens through dopaminergic and purinergic mechanisms.

Substance P (SP) is an undecapeptide that is co-localized with conventional transmitters in the nucleus accumbens (NAc). Its neurochemical and behavioral effects resemble those of cocaine and amphetamine. How SP accomplishes these effects is not known, partly because its cellular and synaptic effects are not well characterized.

Modulation of synaptic transmission by oxytocin and vasopressin in the supraoptic nucleus.

It is now generally accepted that magnocellular neurons of the supraoptic and paraventricular nuclei release the neuropeptides oxytocin and vasopressin from their dendrites. Peptide release from their axon terminals in the posterior pituitary and dendrites differ in dynamics suggesting that they may be independently regulated. The dendritic release of peptide within the supraoptic nucleus (SON) is an important part of its physiological function since the local peptides can regulate the electrical activity of magnocellular neurons (MCNs) which possess receptors for these peptides.

GABA(B) receptors modulate short-term potentiation of spontaneous excitatory postsynaptic currents in the rat supraoptic nucleus in vitro.

High-frequency stimulation of afferents to the supraoptic nucleus (SON) results in a robust increase in the frequency and amplitude of pharmacologically isolated, tetrodotoxin-resistant, miniature excitatory postsynaptic currents (mEPSCs) lasting for 5-20 min. This increase in mEPSC frequency, termed short-term potentiation (STP), is tightly coupled to increases in action potential firing in magnocellular neurons (MCNs) suggesting a functional role for STP. gamma-Aminobutyric acid (GABA), acting selectively on GABA(B) receptors, has been shown to modulate action potential-dependent EPSCs, as well as mEPSCs in this nucleus.