Intracellular recordings were made from neurons of rat lateral amygdala, nucleus accumbens, and striatum in vitro. Synaptic potentials mediated by Y-aminobutyric acid and by excitatory amino acids were isolated pharmacologically by using receptor antagonists, and their amplitudes were used as a measure oftransmitter release. Mucanrne and acetylcholine inhibited the release of both y-aminobutyric acid and excitatory amino acids, but measurements of the dissociation equilibrium constants for the antagonists piren- ,4]benzodiazepine-6-one, methoctramine, and hexahydrosiladifenidol indicated clearly that different muscarinic receptors were involved (MI and probably M3, respectively). The differential localization of distinct muscarinc receptor subtypes on terminals releasing the major inhibitory and excitatory transmitters of the brain could be exploited therapeutically in some movement disorders and Alzheimer disease.Acetylcholine (AcCho) has diverse functional roles in the mammalian brain, including actions at muscarinic receptors that are important for memory (1). Cholinergic neurons are lost in Alzheimer disease, and one therapeutic approach has been to develop drugs that mimic the neurotransmitter action of missing AcCho (1). However, such drugs, like AcCho itself, will have different effects at different muscarinic receptors in the brain, and not all of these effects may be desired. Three muscarinic receptors (M1-M3) can be distinguished pharmacologically, but five (ml-mS) have been identified by molecular cloning (ml-m3 correspond to M1-M3) (2-8).Fibers containing 'y-aminobutyric acid (GABA) and excitatory amino acids such as glutamate provide synaptic inputs to virtually all central neurons; therefore, in addition to their direct effects on neurons (9, 10), muscarinic agonists will also excite or inhibit cells by acting presynaptically to change release of these neurotransmitters. In the present experiments, the release of GABA and excitatory amino acids (glutamate) was assayed by recording the amplitude of depolarizing synaptic potentials from neurons in three brain regions where AcCho is known to play an important functional role-the amygdala, nucleus accumbens, and striatum. METHODSAdult rats were anesthetized with halothane and killed by a heavy blow to the chest. The brain was rapidly removed, and a block of tissue containing nucleus accumbens, dorsal striatum, or amygdaloid complex was sectioned with a Vibratome. Intracellular recordings were made from slices (300 ,am thick) by using electrodes containing 2 M KCI (11-13).The superfusing solution was a bicarbonate buffer gassed with 95% 02/5% CO2 and contained 2.5 mM KCI, 2.4 mM CaC12, 1.3 mM MgCl2, 1.2 mM NaH2PO4, 26 mM NaHCO3, 126 mM NaCi, and 10 mM glucose. The slice was completely submerged in this flowing solution, which was prewarmed to 370C. Drugs were applied by changing this solution to one that contained the drug. A bipolar tungsten-in-glass stimulating electrode was used for focal stimulation. The components of the synaptic potential...

Rapid eye movement sleep behavior disorder (RBD) is a parasomnia with clinical symptoms that include punching, kicking, yelling and leaping out of bed in sleep. Polysomnographic (PSG) finding showed REM sleep without muscle atonia. Clonazepam is generally used for treating RBD symptoms but melatonin was reported to be effective so we reconfirmed the effect of melatonin on RBD patients in the present study. We used melatonin (3-9 mg/day) which could ameliorate problem sleep behaviors remarkably, as well as %tonic activity in PSG variables. In the present study, melatonin was reconfirmed to be effective in RBD symptoms, especially for patients with low melatonin secretion, while its mechanism was not clearly known in the present study.

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1. Intracellular recordings were made from neurons in slices cut from the rat nucleus accumbens septi. Membrane currents were measured with a single-electrode voltage-clamp amplifier in the potential range -50 to -140 mV. 2. In control conditions (2.5 mM potassium), the resting membrane potential of the neurons was -83.4 +/- 1.1 (SE) mV (n = 157). Steady state membrane conductance was voltage dependent, being 34.8 +/- 1.7 nS (n = 25) at -100 mV and 8.0 +/- 0.7 nS (n = 25) at -60 mV. 3. Barium (1 microM) markedly reduced the inward rectification and caused a small inward current (40.6 +/- 8.7 pA, n = 8) at the resting potential. These effects became larger with higher barium concentrations, and, in 100 microM barium, the current-voltage relation was straight. 4. The block of the inward current by barium (at -130 mV) occurred with an exponential time course; the time constant was approximately 1 s at 1 microM barium and less than 90 ms with 100 microM. Strontium had effects similar to those of barium, but 1000-fold higher concentrations were required. Cesium chloride (2 mM) and rubidium chloride (2 mM) also blocked the inward rectification; their action reached steady state within 50 ms. 5. It is concluded that the nucleus accumbens neurons have a potassium conductance with many features of a typical inward rectifier and that this contributes to the potassium conductance at the resting potential.