Abstract
1. Intracellular recordings were obtained from neurones in the region of the paraventricular nucleus in slices of rat hypothalamus. Glutamate microdrops were applied to the surface of the slices at sites dorsal, lateral and ventral to the paraventricular nucleus to selectively activate local presynaptic neurones. The gamma-aminobutyric acidA (GABAA)-receptor antagonists picrotoxin or bicuculline were bath-applied to block synaptic inhibition. 2. Glutamate microapplication caused a tonic depolarization and often repetitive action potentials in twenty of forty-seven recorded cells. This was probably caused by the direct exposure of the dendrites of the recorded cells to the glutamate microdrops. 3. Glutamate microstimulation elicited inhibitory synaptic responses in nine of forty-seven neurones tested. Glutamate microdrops caused discrete, hyperpolarizing postsynaptic potentials (PSPs) in four cells recorded with microelectrodes containing potassium acetate and evoked depolarizing PSPs in four cells recorded with KCl-filled microelectrodes. Glutamate microapplication inhibited spontaneous spike firing in another cell recorded with a potassium acetate microelectrode. 4. Bath application of GABAA-receptor antagonists completely blocked the hyperpolarizing PSPs elicited by glutamate microstimulation in three of three cells recorded with potassium acetate electrodes and the depolarizing PSPs in two of two cells recorded with KCl electrodes, indicating they were inhibitory PSPs caused by the release of GABA. Suppression of GABAA-mediated synaptic inhibition did not reveal any glutamate-evoked excitatory PSPs. 5. Recorded cells were identified as magnocellular, parvocellular or non-paraventricular bursting neurones on the basis of their electrophysiological properties. Direct depolarization and local inhibitory synaptic responses were observed in all three cell types. 6. Several conclusions can be drawn from these data: (1) functional glutamate receptors are distributed throughout neuronal populations in the paraventricular region of the hypothalamus, confirming and extending previous observations; (2) local synaptic inputs to neurones in the paraventricular nucleus are primarily inhibitory, supplied by perinuclear GABAergic neurones; (3) both magnocellular and parvocellular subpopulations receive local inhibitory synaptic inputs. The possibility that these local GABAergic circuits mediate inhibitory inputs to paraventricular neurones from limbic structures is discussed.