CPT1C, a neuron-specific enzyme located at the endoplasmic reticulum, is widely expressed throughout the central nervous system (CNS). Intriguingly, dense expression has been found in discrete brain areas, including the hypothalamus, hippocampus and amygdala. Although its molecular functions remain partially unclear, CPT1c is well known to regulate ceramide metabolism and, more recently, its involvement in dendritic spine maturation and AMPA receptor synthesis and trafficking has also come to light. Consistently, its main roles described to date are related to hypothalamic control of energy homeostasis, motor function and hippocampal-dependent spatial memory. However, its widespread distribution along with the diverse molecular mechanisms attributed invites to consider its potential implication in additional functions associated to different brain regions. Here, we carried out systematic characterization of the physiological role of CPT1C at different levels -molecular, synapses,  neural networks and behavior- of complexity by comparing CPT1C knock-out (KO) mice and wild-type littermates. First, the expression pattern of the protein was examined by fluorescence immunohistochemistry. In behaving mice, we explored the impact of CPT1C deficiency on locomotor activity, energy status, emotional state and different types of learning. Specifically, we evaluated motor learning, hippocampal-dependent spatial memory, and associative instrumental learning. In order to correlate memory processes that rely on hippocampal function with changes in synaptic plasticity, we analyzed dendritic spine maturation in the hippocampus as well as local field potentials from hippocampal slices ex vivo and electroencephalographic recordings obtained in vivo. Our results confirmed the presence of CPT1C across almost all brain regions, with strong expression in the hippocampus and amygdala. When compared to WT mice (n = 25), CPT1C-deficient animals (n = 22) showed energy deficits (tail suspension test (TST); p < 0.001) and locomotor impairments (locomotion test; p < 0.001). More surprisingly, CPT1C deficiency is not associated with anxiety- nor depression-like behaviors (WT, n = 25, vs CPT1C KO, n = 22; elevated plus maze, p = 0.443; TST, p = 0.259). CPT1C-KO mice also exhibited deficits in motor learning (rotarod performance task; WT, n = 25, latency = 148±13.57% of first session, p < 0.001; CPT1C KO, latency = 96.12±7.54%, p = 0.951) and instrumental learning (Skinner-box paradigm; WT, n = 14, vs CPT1C KO, n = 12: p = 0.009), as well as in spatial memory (novel object location test; WT, n = 25, vs CPT1C KO, n = 20: p = 0.846). The latter effects might be attributed to inefficient hippocampal dendritic spine maturation (WT, n = 3, vs CPT1C KO, n = 4: p = 0.002), long-term plasticity impairments observed at the CA3-CA1 synapse (magnitude of LTP: WT, n = 19, vs CPT1C KO, n = 17: p = 0.049) and aberrant cortical oscillatory activity (gamma rhythm: WT, n = 24, vs CPT1C KO, n = 14; p = 0.006) . Together, our results not only support the notion that CPT1C regulates energy homeostasis and motor function, but also reveal that it is required for learning and memory processes taking place in brain areas that underlie motor, associative, and non-associative learning.