PMID- 8922408
OWN - NLM
STAT- MEDLINE
DCOM- 19970106
LR  - 20191101
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 16
IP  - 23
DP  - 1996 Dec 1
TI  - Atrial natriuretic peptide modulates synaptic transmission from osmoreceptor 
      afferents to the supraoptic nucleus.
PG  - 7526-32
AB  - Atrial natriuretic peptide (ANP) and its receptors are present in hypothalamic 
      nuclei containing the magnocellular neurosecretory cells (MNCs), which release 
      vasopressin and oxytocin. In the rat, intracerebroventricular injections of ANP 
      inhibit the release of both hormones in response to hypertonicity. Although these 
      findings suggest a role for endogenous ANP in the central control of fluid 
      balance, cellular mechanisms underlying the modulatory actions of ANP are 
      unknown. We therefore examined the effects of ANP on the osmoresponsiveness of 
      MNCs impaled in rat hypothalamic explants. Applications of ANP (75-150 nM) over 
      the supraoptic nucleus did not affect depolarizing responses to local 
      hypertonicity, but they reversibly abolished the synaptic excitation of MNCs 
      after hypertonic stimulation of the organum vasculosum laminae terminalis (OVLT). 
      These effects were associated with decreased spontaneous EPSP (sEPSP) amplitude 
      rather than with changes in sEPSP frequency. Accordingly, application of ANP 
      reduced the amplitude of glutamatergic EPSPs evoked by electrical stimulation of 
      the OVLT (IC50 approximately 3 nM). The inhibitory effects of ANP on EPSP 
      amplitude were mimicked by application of 3'-5'-dibutyryl cGMP, consistent with 
      the guanylate cyclase activity of natriuretic peptide receptors. Although 
      depolarizing responses of MNCs to ionotropic glutamate receptor agonists were 
      unaffected by ANP, the peptide reversibly enhanced paired-pulse facilitation of 
      electrically evoked EPSPs. These results indicate that centrally released ANP may 
      inhibit osmotically evoked neurohypophysial hormone release through presynaptic 
      inhibition of glutamate release from osmoreceptor afferents derived from the 
      OVLT.
FAU - Richard, D
AU  - Richard D
AD  - Centre for Research in Neuroscience, Montreal General Hospital Research Institute 
      and McGill University, Quebec, Canada.
FAU - Bourque, C W
AU  - Bourque CW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Excitatory Amino Acid Agonists)
RN  - 0 (Receptors, Glutamate)
RN  - 85637-73-6 (Atrial Natriuretic Factor)
SB  - IM
MH  - Animals
MH  - Atrial Natriuretic Factor/pharmacology/*physiology
MH  - Electric Stimulation
MH  - Excitatory Amino Acid Agonists/pharmacology
MH  - Hypothalamus/cytology/drug effects/metabolism
MH  - Male
MH  - Neurons, Afferent/*physiology
MH  - Neurosecretory Systems/cytology/drug effects/metabolism
MH  - Osmosis
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Receptors, Glutamate/drug effects
MH  - Sensory Receptor Cells/*physiology
MH  - Supraoptic Nucleus/*physiology
MH  - Synaptic Transmission/drug effects/*physiology
PMC - PMC6579099
EDAT- 1996/12/01 00:00
MHDA- 1996/12/01 00:01
PMCR- 1997/06/01
CRDT- 1996/12/01 00:00
PHST- 1996/12/01 00:00 [pubmed]
PHST- 1996/12/01 00:01 [medline]
PHST- 1996/12/01 00:00 [entrez]
PHST- 1997/06/01 00:00 [pmc-release]
AID - 10.1523/JNEUROSCI.16-23-07526.1996 [doi]
PST - ppublish
SO  - J Neurosci. 1996 Dec 1;16(23):7526-32. doi: 10.1523/JNEUROSCI.16-23-07526.1996.