Presynaptic, activity-dependent modulation of cannabinoid type 1 receptor-mediated inhibition of GABA release
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Presynaptic, activity-dependent modulation of cannabinoid type 1 receptor-mediated inhibition of GABA release. / Földy, Csaba; Neu, Axel; Jones, Mathew V; Soltesz, Ivan.
In: J NEUROSCI, Vol. 26, No. 5, 01.02.2006, p. 1465-9.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - Presynaptic, activity-dependent modulation of cannabinoid type 1 receptor-mediated inhibition of GABA release
AU - Földy, Csaba
AU - Neu, Axel
AU - Jones, Mathew V
AU - Soltesz, Ivan
PY - 2006/2/1
Y1 - 2006/2/1
N2 - Endocannabinoid signaling couples activity-dependent rises in postsynaptic Ca2+ levels to decreased presynaptic GABA release. Here, we present evidence from paired recording experiments that cannabinoid-mediated inhibition of GABA release depends on the firing rates of the presynaptic interneurons. Low-frequency action potentials in post hoc identified cholecystokinin-positive CA1 basket cells elicited IPSCs in the postsynaptic pyramidal cells that, as expected, were fully abolished by the exogenous application of the cannabinoid receptor agonist WIN55,212-2 [R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)(1-naphthalenyl) methanone monomethanesulfonate] at 5 microM. However, the presynaptic basket cells recovered from the cannabinoid agonist-induced inhibition of GABA release when the presynaptic firing rate was increased to > or =20 Hz. Pharmacological experiments showed that the recovered transmission was exclusively dependent on presynaptic N-type Ca2+ channels. Furthermore, the increased presynaptic firing could also overcome even complete depolarization-induced suppression of inhibition, indicating that the magnitude of DSI markedly depends on the activity levels of basket cells. These results reveal a new locus of activity-dependent modulation for endocannabinoid signaling and suggest that endocannabinoid-mediated inhibition of GABA release may differ in distinct behavioral states.
AB - Endocannabinoid signaling couples activity-dependent rises in postsynaptic Ca2+ levels to decreased presynaptic GABA release. Here, we present evidence from paired recording experiments that cannabinoid-mediated inhibition of GABA release depends on the firing rates of the presynaptic interneurons. Low-frequency action potentials in post hoc identified cholecystokinin-positive CA1 basket cells elicited IPSCs in the postsynaptic pyramidal cells that, as expected, were fully abolished by the exogenous application of the cannabinoid receptor agonist WIN55,212-2 [R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)(1-naphthalenyl) methanone monomethanesulfonate] at 5 microM. However, the presynaptic basket cells recovered from the cannabinoid agonist-induced inhibition of GABA release when the presynaptic firing rate was increased to > or =20 Hz. Pharmacological experiments showed that the recovered transmission was exclusively dependent on presynaptic N-type Ca2+ channels. Furthermore, the increased presynaptic firing could also overcome even complete depolarization-induced suppression of inhibition, indicating that the magnitude of DSI markedly depends on the activity levels of basket cells. These results reveal a new locus of activity-dependent modulation for endocannabinoid signaling and suggest that endocannabinoid-mediated inhibition of GABA release may differ in distinct behavioral states.
KW - Action Potentials
KW - Animals
KW - Benzoxazines
KW - Calcium Channels, N-Type
KW - Cannabinoids
KW - Cholecystokinin
KW - Evoked Potentials
KW - Hippocampus
KW - Interneurons
KW - Morpholines
KW - Naphthalenes
KW - Neural Inhibition
KW - Neuronal Plasticity
KW - Patch-Clamp Techniques
KW - Presynaptic Terminals
KW - Pyramidal Cells
KW - Rats
KW - Rats, Sprague-Dawley
KW - Receptor, Cannabinoid, CB1
KW - Synaptic Transmission
KW - gamma-Aminobutyric Acid
U2 - 10.1523/JNEUROSCI.4587-05.2006
DO - 10.1523/JNEUROSCI.4587-05.2006
M3 - SCORING: Journal article
C2 - 16452670
VL - 26
SP - 1465
EP - 1469
JO - J NEUROSCI
JF - J NEUROSCI
SN - 0270-6474
IS - 5
ER -