ORGANUM VASCULOSUM LAMINA TERMINALIS-EVOKED POSTSYNAPTIC RESPONSES INRAT SUPRAOPTIC NEURONS IN-VITRO

Citation
Cr. Yang et al., ORGANUM VASCULOSUM LAMINA TERMINALIS-EVOKED POSTSYNAPTIC RESPONSES INRAT SUPRAOPTIC NEURONS IN-VITRO, Journal of physiology, 477(1), 1994, pp. 59-74
Citations number
42
Categorie Soggetti
Physiology
Journal title
ISSN journal
00223751
Volume
477
Issue
1
Year of publication
1994
Pages
59 - 74
Database
ISI
SICI code
0022-3751(1994)477:1<59:OVLTPR>2.0.ZU;2-I
Abstract
1. To characterize the organum vasculosum lamina terminalis (OVLT) inn ervation of hypothalamic supraoptic nucleus (SON) neurones, current cl amp recordings were obtained in SON cells in superfused rat hypothalam ic explants. Stimulation of 1 Hz evoked 5-10 mV bicuculline-sensitive IPSPs in forty out of forty-six SON neurones, including both phasic (v asopressin immunoreactive) and continuously firing (oxytocin immunorea ctive) cells. 2. In twenty-four cells, mean IPSP latency was 8.7+/-1 m s (+/-S.D.) and reversal potentials (V-r) ranged between -60 and -75 m V. In the other sixteen cells, V-r ranged between -20 and -55 mV and t he addition of bicuculline revealed underlying EPSPs (latency, 7.8+/-0 .8 ms; mean V-r, -8+/-10 mV) with two components: (a) fast (rise and h alf-decay times of 5.83+/-1.3 ms and 19+/-4.4 ms respectively), with r eversible blockade by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX); (b) slow (4- to 5-fold increase in rise and half-decay time), with revers ible reduction by (-)-aminophosphonovaleric acid (APV). 3. During 10 H z stimulation, EPSPs summated into 3-7 mV depolarizing envelopes lasti ng 1.5-3.0 s and sustaining action potential bursts. Depolarizing enve lopes displayed voltage dependence, and were enhanced after removal of extracellular magnesium, diminished by APV and completely abolished b y APV and CNQX together. 4. Thus, non-NMDA receptors probably mediate fast EPSPs whereas NMDA receptors mediate slow EPSPs and depolarizing envelopes. OVLT-evoked EPSPs were only seen in vasopressin-immunoreact ive neurones. 5. These observations indicate converging inhibitory and target-selective excitatory amino acid-mediated inputs from OVLT to S ON; the latter may modulate the excitability of SON vasopressin neuron es to a hyperosmotic challenge.