Cl‐ ‐ and K+‐dependent inhibitory postsynaptic potentials evoked by interneurones of the rat lateral geniculate nucleus.

Abstract

1. Hyperpolarizing potentials evoked by electrical stimulation of the optic tract were studied in projection cells of the rat dorsal lateral geniculate nucleus (LGN) in vitro. In the same cells the effects of gamma-amino butyric acid (GABA), baclofen and acetylcholine (ACh) were also investigated. 2. In the majority of cells a short- (SHP) (34 ms) and a long-lasting (LHP) (240 ms) hyperpolarizing potential could be recorded in the presence and in the absence of a preceding EPSP. They were blocked by tetrodotoxin (1 microM) and were more sensitive than the monosynaptic EPSP to a low-Ca2+-high-Mg2+ solution. 3. The SHP was associated with a marked decrease (75%) in input resistance, was blocked by bicuculline (1-100 microM) and its reversal potential (-67 mV) was dependent on the extracellular Cl- concentration. 4. The LHP was associated with a smaller decrease (45%) in input resistance and its reversal potential (-76 mV) was dependent on the extracellular K+ concentration. It was increased by bicuculline (100% at 50 microM) and nipecotic acid (30% at 10 microM), blocked by Ba2+ (1 mM), and unaffected by eserine (1-10 microM), neostigmine (1-10 microM) or by recording with EGTA-filled electrodes. In the presence of bicuculline, a single LHP was able to evoke, as a rebound response, a low-threshold Ca2+ spike that was, however, not followed by another LHP (or any other long-lasting hyperpolarization). 5. Ionophoretic applications of GABA evoked in the same cell a Cl- -dependent hyperpolarization (reversal potential: -65 mV) and/or depolarization, both of which were associated with a marked decrease (91%) in input resistance and abolished by bicuculline. GABA was also able to evoke a bicuculline-insensitive, K+-dependent hyperpolarization that had a reversal potential of -75 mV and was associated with a smaller decrease (43%) in input resistance. 6. Baclofen, applied by ionophoresis, pressure ejection or in the perfusion medium (1-100 microM), produced a hyperpolarization that had a reversal potential of -79 mV and was associated with a decrease (45%) in input resistance. 7. In the majority of cells (thirty-seven out of forty) ACh evoked a slow depolarization and only in three cells a hyperpolarization which had a reversal potential of -80 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

Cellular mechanisms underlying cholinergic and noradrenergic modulation of neuronal firing mode in the cat and guinea pig dorsal lateral geniculate nucleus

“…6D,E). These reversal potentials are identical to that exhibited by the MCh-induced outward current (-101.6 mV) and the GABA,-receptor-mediated increase in outward current (-107.3 mv), both of which we have previously shown to be due to an increase in K+ conductance (McCormick and Prince, 1987;Crunelli et al, 1988). Neurons in the cerebral cortex, hippocampus, and sympathetic ganglia respond to muscarinic receptor activation with a slow depolarization that results in part from a decrease in three distinct K+ currents: ZM, ZAHP, and a resting "leak" potassium current (Brown and Adams, 1980;Madison et al, 1987;McCormick and Williamson, 1989).…”

Leading role of thalamic over cortical neurons during postinhibitory rebound excitation

“…The biphasic inhibitory postsynaptic potential illustrated in Fig. 1 results from activation of ␥-aminobutyric acid type A (GABA A ) and GABA B receptors (15,16). In the simultaneously recorded cortical cells, the VL stimulus gave rise to a short-latency depolarization, and the postinhibitory rebound depolarization was shaped by the spindle sequence ( Fig.…”

Short-Term Plasticity during Intrathalamic Augmenting Responses in Decorticated Cats

“…Despite the demonstration that prolonged, biphasic (Crunelli et al, 1988), or triphasic (Paré et al, 1991) IPSPs can be elicited in TC cells by local interneurons in the absence of RE afferents, several points indicate that thalamic stimulation elicited augmenting responses stemming from postinhibitory rebound phenomena as a result of activation of RE cells, rather than local circuit cells. The activation of local interneurons by recurrent collaterals of TC axons is precluded by the absence of such intranuclear collaterals in intracellularly stained neurons of VL Sawyer et al, 1994) and other principal nuclei of the dorsal thalamus (Yen and Jones, 1983;Kita and Kitai, 1986;Liu et al, 1995).…”

“…4,6), followed by an orthodromic excitation with one or two action potentials at a latency of 1.5 to 6 msec (see also Fig. 4); (2) a long-lasting hyperpolarization with two components, similar to GABA A -and GABA B -mediated IPSPs described in vitro (Hirsch and Burnod, 1987;Crunelli et al, 1988) and in vivo (Paré et al, 1991); and (3) a postinhibitory LT spike, often crowned by a burst of fast Na ϩ action potentials (Fig. 2).…”