Neurons hyperpolarization

Yoshimura M, North RA (1983) Substantia gelatinosa neurones hyperpolarized in vitro by enkephalin. Nature 305(5934) 529-530... 

Within seconds of an ischemic insult, normal brain electrical activity ceases, as a result of the activation of membrane K+ channels and widespread neuronal hyperpolarization [1]. The hyperpolarization may be due to opening of K+ channels responding to acute changes in local concentrations of ATP, H+ or Ca2+, or it may reflect altered nonheme metalloprotein association with and regulation of specific K+ channels [2]. This response, presumably protective, however fails to preserve high-energy phosphate levels in tissue as concentrations of phospho-creatine (PCr) and ATP fall within minutes after ischemia... 

The interaction of delta opioid receptor selective ligands with its respective receptor has been reported to hyperpolarize neurons. Hyperpolarization of neurons in the delta opioid sensitive pathway may play a major... 

Figure 3.6. Schematic model of the GABA/Benzodiaz-epine/Barbiturate receptor complex. The receptor complex surrounds a chloride ion channel. Camma-amin o butyric acid (GABA) is an inhibitory neurotransmitter. GABA binds to the receptor causing chloride influx. The movement of chloride into the neuron hyperpolarizes the neuronal membrane, making it more difficult for excitatory neurotransmitters to depolarize the cell. Benzodiazepines and barbiturates enhance the actions of GABA, but fail to open the chloride channel in the absence of GABA.

Chaplan SR, Guo H-Q, Lee DH, Luo L, Liu C, Kuei C, Velumian AA, Butler MP, Brown SM, Dubin AE (2003) Neuronal hyperpolarization-activated pacemaker channels drive neuropathic pain. J Neurosci 23 1169-1178... 

Opioids bound to MOR on postsynaptic terminals promote the efflnx of potassinm (K ) via K+ channels. The net effect of active MOR receptor resnlts in hyperpolarization of the post-synapse causing inhibition of neuronal firing. Stndies have shown MOR effects at the pre- and post-synapse synergistically decreases the perception of pain (Glanm et al. 1994 Kohno et al. 1999 Williams et al. 2001 Yoshimnra and North 1983). 

Rivera, C, Voipio, J, Payne, JA, Ruusuvuori, E, Lahtinen, H, Lamsa, K, Pirvola, U, Saarma, M and Kaila, K (1999) The K+/CU co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation. Nature 397 251-255. 

The inhibition of firing of catecholamine neurons resulting from amphetamine administration is likely due to activation of somatodendritic autoreceptors. This causes a hyperpolarization of the somatodendritic membrane of both locus coeruleus noradrenergic and substantia nigra dopamine neurons, probably as a consequence of an increase in potassium conductance (Lacey et al. 1987 Williams et al. 1985). 

ANSWER That is Lacey et al., Allan North s group. It was published in the Journal of Physiology last year. It was also an abstract in the Society 2 years ago. It is the consequence of that application of the agonists, recording intracellularly in the slice of the dopamine neuron. He gets the same thing by virtue of application of norepinephrine agonists to noradrene-gic slice preparation. That is a conventional way to create a hyperpolarization of the cell, to increase the potassium conductance, and so forth. 

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