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Effects of α 2 ‐Adrenergic Agonists and Antagonists on Photoreceptor Membrane Currents
Author(s) -
Sakakibara Manabu,
Collin Carlos,
Kuzirian Alan,
Alkon Daniel L.,
Heldman Eliahu,
Naito Shigetaka,
Lederhendler Izja
Publication year - 1987
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1987.tb04108.x
Subject(s) - depolarization , excitatory postsynaptic potential , membrane potential , hyperpolarization (physics) , yohimbine , biophysics , prazosin , chemistry , neuroscience , resting potential , endocrinology , medicine , biology , antagonist , receptor , biochemistry , inhibitory postsynaptic potential , stereochemistry , nuclear magnetic resonance spectroscopy
Type B photoreceptors of the nudibranch mollusc Hermissenda crassicornis receive excitatory synaptic potentials (EPSPs) whose frequency is controlled by potential changes of a neighboring cell known as the S optic ganglion cell which is thought to be electrically coupled to the presyn‐aptic source of these EPSPs, the E optic ganglion cell. The frequency of the EPSPs increases when a conditioned stimulus (light) is paired with an unconditioned stimulus (rotation) during acquisition of a Pavlovian conditioned response. The results of the present study are consistent with an adrenergic origin for these EPSPs. Noradrenergic agonists (≥ 100 μ M ), norepinephrine and clonidine, only slightly depolarize the type B cell but clearly prolong its depolarizing response to light. Serotonin, by contrast, causes hyperpolarization of the type B cell's resting potential as well as after a light step. Clonidine reduces voltage‐dependent outward K + currents (I A , an early current, I ca 2+ ‐K + , a late Ca 2+ ‐dependent current) that control the type B cell's excitability (and thus its light response and membrane potential). These effects of clonidine are reduced or blocked by the α 2 ‐receptor antagonist, yohimbine (0.5 μ M ), but not the α 1 ‐blocker, prazosin. The same yohimbine concentration also blocked depolarizing synaptic excitation of the type B cell in response to depolarization of a simultaneously impaled S optic ganglion cell. Histochemical techniques (both the glyoxylic acid method of de la Torre and Surgeon and the formaldehyde‐induced fluorescence or Falck‐Hillarp method) demonstrated the presence of a biogenic amine(s) within a single neuron in each optic ganglion as well as three or four cells within the vicinity of previously identified visual interneurons. No serotonergic neurons were found within the optic ganglion or in proximity to visual interneurons. A clonidine‐like synaptic effect on type B cells, therefore, could amplify conditioning‐specific changes of membrane currents by increasing type B depolarization and possibly, as well, by elevating intracellular second messengers.